PMID-sentid Pub_year Sent_text comp_official_name comp_offset protein_name organism prot_offset 31169725-11 2019 The serum levels of GIP (P = .003) and PP (P = .012) were significantly increased in the AET+ group. 2-(2-Aminoethyl)isothiourea dihydrobromide 89-92 gastric inhibitory polypeptide Homo sapiens 20-23 31063975-1 2019 Glucose-dependent insulinotropic polypeptide (GIP) in combination with hyperinsulinemia increase blood flow and triglyceride clearance in subcutaneous abdominal adipose tissue in lean humans. Triglycerides 112-124 gastric inhibitory polypeptide Homo sapiens 0-44 31063975-1 2019 Glucose-dependent insulinotropic polypeptide (GIP) in combination with hyperinsulinemia increase blood flow and triglyceride clearance in subcutaneous abdominal adipose tissue in lean humans. Triglycerides 112-124 gastric inhibitory polypeptide Homo sapiens 46-49 31063975-6 2019 During GIP infusion and the clamp, ATBF increased ~fourfold to 11.4 +- 1.9 ml/min 100 g/tissue, P<0.001. atbf 35-39 gastric inhibitory polypeptide Homo sapiens 7-10 31169725-13 2019 There was a positive correlation between GIP and triglyceride levels (correlation coefficient 0.279, P = .017). Triglycerides 49-61 gastric inhibitory polypeptide Homo sapiens 41-44 30784161-6 2019 GIPR variants were expressed in COS-7 cells and cAMP production was measured upon stimulation with GIP. Cyclic AMP 48-52 gastric inhibitory polypeptide Homo sapiens 0-3 31169725-2 2019 Gastric inhibitory polypeptide (GIP) and pancreatic polypeptide (PP) participate in the regulation of gastric acid secretion, blood glucose and lipid levels, and food intake. Glucose 132-139 gastric inhibitory polypeptide Homo sapiens 32-35 30928213-7 2019 The solvent evaporation technique provided the better coating of HPMC around DNA-core with gastro-resistant and effervescent property due to presence of NaHCO3 (0.01%) in the formulations that caused delayed delivery of VD as well as nanoparticles to the intestine, increasing the availability time of the drug and nanospheres at the target sites (intestine and blood) where DPP-4 enzyme is most abundant (to degrade the GLP-1 and GIP causing loss of control of the postprandial glycemic levels. Hypromellose Derivatives 65-69 gastric inhibitory polypeptide Homo sapiens 431-434 30259623-7 2019 AUC240 for insulin, C-peptide, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) was also lower after exenatide. Exenatide 139-148 gastric inhibitory polypeptide Homo sapiens 67-111 30626611-1 2019 The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are secreted postprandially and contribute importantly to postprandial glucose tolerance. Glucose 22-29 gastric inhibitory polypeptide Homo sapiens 68-71 30626611-5 2019 In conclusion, endogenous GIP affects postprandial plasma glucose excursions and insulin secretion more than endogenous GLP-1, but the hormones contribute additively to postprandial glucose regulation in healthy individuals. Glucose 58-65 gastric inhibitory polypeptide Homo sapiens 26-29 30259623-7 2019 AUC240 for insulin, C-peptide, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) was also lower after exenatide. Exenatide 139-148 gastric inhibitory polypeptide Homo sapiens 113-116 30293770-0 2018 Efficacy and safety of LY3298176, a novel dual GIP and GLP-1 receptor agonist, in patients with type 2 diabetes: a randomised, placebo-controlled and active comparator-controlled phase 2 trial. ly3298176 23-32 gastric inhibitory polypeptide Homo sapiens 47-50 31237842-6 2019 RESULTS: The serum levels of GIP in the patients with type T1DM were significantly higher, compared to the individuals without carbohydrate disorders (P<0.05), while there was no statistically significant difference in the GLP-1 levels. Carbohydrates 127-139 gastric inhibitory polypeptide Homo sapiens 29-32 30863364-5 2019 The responsible hormones appear to include glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), known as incretin hormones due to their role in regulating glucose homeostasis by enhancing insulin release in response to food intake. Glucose 43-50 gastric inhibitory polypeptide Homo sapiens 89-92 30473097-0 2018 LY3298176, a novel dual GIP and GLP-1 receptor agonist for the treatment of type 2 diabetes mellitus: From discovery to clinical proof of concept. ly3298176 0-9 gastric inhibitory polypeptide Homo sapiens 24-27 30473097-2 2018 METHODS: LY3298176 is a fatty acid modified peptide with dual GIP and GLP-1 receptor agonist activity designed for once-weekly subcutaneous administration. ly3298176 9-18 gastric inhibitory polypeptide Homo sapiens 62-65 29910091-9 2018 Higher meal-induced release of GIP (iAUC0-260min) correlated positively with fasting (r=0.54) and postprandial serum triglyceride concentrations (iAUC0-260min, r=0.54; all P<0.01). Triglycerides 117-129 gastric inhibitory polypeptide Homo sapiens 31-34 30243968-6 2018 The indirect action of trichothecenes in the gastrointestinal tract involved, by enteroendocrine cells, the secretion of several gut hormones such as cholecystokinin (CCK) and peptide YY (PYY) but also glucagon-like peptide 1 (GLP-1), gastric inhibitory peptide (GIP) and 5-hydroxytryptamine (5-HT), which transmitted signals to the brain via the gut-brain axis. Trichothecenes 23-37 gastric inhibitory polypeptide Homo sapiens 235-261 30243968-6 2018 The indirect action of trichothecenes in the gastrointestinal tract involved, by enteroendocrine cells, the secretion of several gut hormones such as cholecystokinin (CCK) and peptide YY (PYY) but also glucagon-like peptide 1 (GLP-1), gastric inhibitory peptide (GIP) and 5-hydroxytryptamine (5-HT), which transmitted signals to the brain via the gut-brain axis. Trichothecenes 23-37 gastric inhibitory polypeptide Homo sapiens 263-266 30765429-0 2019 Comparative Effects of Proximal and Distal Small Intestinal Glucose Exposure on Glycemia, Incretin Hormone Secretion, and the Incretin Effect in Health and Type 2 Diabetes. Glucose 60-67 gastric inhibitory polypeptide Homo sapiens 90-106 30609862-8 2019 CeDD had lower insulin and glucose-dependent insulinotropic polypeptide (GIP) than CeDGF and HS. cedd 0-4 gastric inhibitory polypeptide Homo sapiens 73-76 29438631-8 2018 The iAUC for AEA was positively related to iAUC GIP ( r = 0.384, P = 0.005). anandamide 13-16 gastric inhibitory polypeptide Homo sapiens 48-51 29438631-10 2018 The relationships between plasma AEA with duodenal ZO-1, IAP, and GIP suggest that altered endocannabinoid signaling may contribute to changes in intestinal permeability, inflammation, and incretin release in human obesity. anandamide 33-36 gastric inhibitory polypeptide Homo sapiens 66-69 30143540-6 2018 Injection of glucose into the lumen of organoids caused an increase in both GIP secretion and K-cell number. Glucose 13-20 gastric inhibitory polypeptide Homo sapiens 76-79 30293770-1 2018 BACKGROUND: LY3298176 is a novel dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptor agonist that is being developed for the treatment of type 2 diabetes. ly3298176 12-21 gastric inhibitory polypeptide Homo sapiens 38-82 30293770-1 2018 BACKGROUND: LY3298176 is a novel dual glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptor agonist that is being developed for the treatment of type 2 diabetes. ly3298176 12-21 gastric inhibitory polypeptide Homo sapiens 84-87 30293770-2 2018 We aimed to examine the efficacy and safety of co-stimulation of the GLP-1 and GIP receptors with LY3298176 compared with placebo or selective stimulation of GLP-1 receptors with dulaglutide in patients with poorly controlled type 2 diabetes. ly3298176 98-107 gastric inhibitory polypeptide Homo sapiens 79-82 30293770-30 2018 INTERPRETATION: The dual GIP and GLP-1 receptor agonist, LY3298176, showed significantly better efficacy with regard to glucose control and weight loss than did dulaglutide, with an acceptable safety and tolerability profile. ly3298176 57-66 gastric inhibitory polypeptide Homo sapiens 25-28 30293770-30 2018 INTERPRETATION: The dual GIP and GLP-1 receptor agonist, LY3298176, showed significantly better efficacy with regard to glucose control and weight loss than did dulaglutide, with an acceptable safety and tolerability profile. Glucose 120-127 gastric inhibitory polypeptide Homo sapiens 25-28 29704228-9 2018 After 24 months, the area under the curve (AUC) of GLP1 increased and in the SG + TB group and the AUC of the GIP concentrations was lower in the SG + TB group than in the SMT. Terbium 151-153 gastric inhibitory polypeptide Homo sapiens 110-113 29227575-5 2018 Sitagliptin also increased active glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) and reduced total (reflecting the secretion) GIP, but not total GLP-1 levels. Sitagliptin Phosphate 0-11 gastric inhibitory polypeptide Homo sapiens 34-78 30067625-2 2018 The GIP ceramic employing particularly designed borosilicate glass as adhesive exhibits high thermal conductivity (2.8 W/m K at 80 C) and remarkable improvement in thermal stability (Tg=711 C) and reliability (luminous flux has only a 0.5% drop after 100 h at 300 C). borosilicate 48-60 gastric inhibitory polypeptide Homo sapiens 4-7 30061863-7 2018 Thus, it is likely that incretin comprises additional gastrointestinal hormones, which interact with GIP and GLP-1 during normal meals containing protein, fat and complex carbohydrates (and not just pure glucose). Carbohydrates 171-184 gastric inhibitory polypeptide Homo sapiens 101-104 29138226-1 2018 Sitagliptin, a dipeptidyl peptidase-IV inhibitor (DPP-4), sustains activity of the incretin hormones GLP-1 and GIP and improves hyperglycemia in Type 2 diabetes mellitus (T2DM). Sitagliptin Phosphate 0-11 gastric inhibitory polypeptide Homo sapiens 111-114 29378179-10 2018 Human GIP(3-30)NH2 inhibited GIP(1-42)-induced cAMP and beta-arrestin 1 and 2 recruitment on the human GIPR and Schild plot analysis showed competitive antagonism with a pA2 and Hill slope of 16.8 nM and 1.11 +- 0.02 in cAMP, 10.6 nM and 1.15 +- 0.05 in beta-arrestin 1 recruitment, and 10.2 nM and 1.06 +- 0.05 in beta-arrestin 2 recruitment. Cyclic AMP 47-51 gastric inhibitory polypeptide Homo sapiens 6-9 29378179-10 2018 Human GIP(3-30)NH2 inhibited GIP(1-42)-induced cAMP and beta-arrestin 1 and 2 recruitment on the human GIPR and Schild plot analysis showed competitive antagonism with a pA2 and Hill slope of 16.8 nM and 1.11 +- 0.02 in cAMP, 10.6 nM and 1.15 +- 0.05 in beta-arrestin 1 recruitment, and 10.2 nM and 1.06 +- 0.05 in beta-arrestin 2 recruitment. Cyclic AMP 47-51 gastric inhibitory polypeptide Homo sapiens 29-32 29378179-10 2018 Human GIP(3-30)NH2 inhibited GIP(1-42)-induced cAMP and beta-arrestin 1 and 2 recruitment on the human GIPR and Schild plot analysis showed competitive antagonism with a pA2 and Hill slope of 16.8 nM and 1.11 +- 0.02 in cAMP, 10.6 nM and 1.15 +- 0.05 in beta-arrestin 1 recruitment, and 10.2 nM and 1.06 +- 0.05 in beta-arrestin 2 recruitment. Cyclic AMP 220-224 gastric inhibitory polypeptide Homo sapiens 6-9 29378179-10 2018 Human GIP(3-30)NH2 inhibited GIP(1-42)-induced cAMP and beta-arrestin 1 and 2 recruitment on the human GIPR and Schild plot analysis showed competitive antagonism with a pA2 and Hill slope of 16.8 nM and 1.11 +- 0.02 in cAMP, 10.6 nM and 1.15 +- 0.05 in beta-arrestin 1 recruitment, and 10.2 nM and 1.06 +- 0.05 in beta-arrestin 2 recruitment. Cyclic AMP 220-224 gastric inhibitory polypeptide Homo sapiens 29-32 29548277-10 2018 The minor A- allele of rs36210421 was associated with increased GLP-1 and decreased GIP response to oral glucose stimulation, whereas the minor G-allele of rs1805123 is associated with decreased fasting plasma insulin and glucagon release. Glucose 105-112 gastric inhibitory polypeptide Homo sapiens 84-87 29548277-11 2018 A genetic risk score combining the two gene variants revealed reductions in glucose-stimulated GIP, as well as suppressed glucagon response to increased glucose levels during an OGTT. Glucose 76-83 gastric inhibitory polypeptide Homo sapiens 95-98 29687583-2 2018 We tested the hypothesis that regular LCS consumption is associated with higher postprandial glucose-dependent insulinotropic polypeptide (GIP) secretion, which has been linked to obesity. lcs 38-41 gastric inhibitory polypeptide Homo sapiens 93-137 29687583-2 2018 We tested the hypothesis that regular LCS consumption is associated with higher postprandial glucose-dependent insulinotropic polypeptide (GIP) secretion, which has been linked to obesity. lcs 38-41 gastric inhibitory polypeptide Homo sapiens 139-142 29884547-1 2018 OBJECTIVE: The incretin hormones GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic peptide) are secreted by the gut after food intake leading to pancreatic insulin secretion and glucose lowering. Glucose 74-81 gastric inhibitory polypeptide Homo sapiens 69-72 29846588-7 2018 In cultured human umbilical vein endothelial cells (HUVECs), GIP elevated cytosolic calcium levels without affecting intracellular cAMP levels. Calcium 84-91 gastric inhibitory polypeptide Homo sapiens 61-64 29369529-11 2018 The BCAA stimulate secretion of both insulin and glucagon and, when given orally, of both glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), with oral administration leading to greater and more prolonged insulin and glucagon secretion. Amino Acids, Branched-Chain 4-8 gastric inhibitory polypeptide Homo sapiens 126-170 29369529-11 2018 The BCAA stimulate secretion of both insulin and glucagon and, when given orally, of both glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), with oral administration leading to greater and more prolonged insulin and glucagon secretion. Amino Acids, Branched-Chain 4-8 gastric inhibitory polypeptide Homo sapiens 172-175 29602522-2 2018 This difference requires the presence of intact glucose-induced insulinotropic peptide receptor (GIPR) and is mediated by the rapid uptake of glucose and the stimulation of GIP release from K cells in the upper small intestine. Glucose 48-55 gastric inhibitory polypeptide Homo sapiens 97-100 29602522-4 2018 GIP is similarly required for the detrimental metabolic effects of other high GI carbohydrates. Carbohydrates 81-94 gastric inhibitory polypeptide Homo sapiens 0-3 29602522-5 2018 We therefore propose that the release of GIP in the upper small intestine is an important determinant of the metabolic quality of carbohydrates. Carbohydrates 130-143 gastric inhibitory polypeptide Homo sapiens 41-44 29235553-10 2018 sE-Selectin was found to be a factor influencing GIP response to oral glucose intake (beta (95% CI): 0.47 (0.14-0.81)) and sVCAM was found to be a factor influencing GIP response to high-fat meal intake (beta (95% CI): 0.19 (0.01-0.37)). se-selectin 0-11 gastric inhibitory polypeptide Homo sapiens 49-52 29227575-5 2018 Sitagliptin also increased active glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) and reduced total (reflecting the secretion) GIP, but not total GLP-1 levels. Sitagliptin Phosphate 0-11 gastric inhibitory polypeptide Homo sapiens 80-83 29227575-5 2018 Sitagliptin also increased active glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) and reduced total (reflecting the secretion) GIP, but not total GLP-1 levels. Sitagliptin Phosphate 0-11 gastric inhibitory polypeptide Homo sapiens 166-169 28838782-4 2018 The concept evolved with the discovery by Samols and co-workers that oral glucose stimulated the release of immunoreactive glucagon-like substances from the gut mucosa and the subsequent isolation of glucagon immunoreactive compounds, most notably oxyntomodulin and glicentin, and of gastic inhibitory polypetide (GIP). Glucose 74-81 gastric inhibitory polypeptide Homo sapiens 314-317 29466430-12 2018 However, GIP, but not Xen, rapidly and transiently increased ISRs and glucagon levels. Glucagon 70-78 gastric inhibitory polypeptide Homo sapiens 9-12 29548277-12 2018 CONCLUSIONS: Two common missense polymorphisms of the Kv11.1 voltage-gated hERG potassium channel are associated with alterations in circulating levels of GIP and glucagon, suggesting that hERG potassium channels play a role in fasting and glucose-stimulated release of GIP and glucagon. Glucagon 163-171 gastric inhibitory polypeptide Homo sapiens 270-273 29548277-12 2018 CONCLUSIONS: Two common missense polymorphisms of the Kv11.1 voltage-gated hERG potassium channel are associated with alterations in circulating levels of GIP and glucagon, suggesting that hERG potassium channels play a role in fasting and glucose-stimulated release of GIP and glucagon. Glucose 240-247 gastric inhibitory polypeptide Homo sapiens 155-158 29548277-12 2018 CONCLUSIONS: Two common missense polymorphisms of the Kv11.1 voltage-gated hERG potassium channel are associated with alterations in circulating levels of GIP and glucagon, suggesting that hERG potassium channels play a role in fasting and glucose-stimulated release of GIP and glucagon. Glucose 240-247 gastric inhibitory polypeptide Homo sapiens 270-273 29548277-12 2018 CONCLUSIONS: Two common missense polymorphisms of the Kv11.1 voltage-gated hERG potassium channel are associated with alterations in circulating levels of GIP and glucagon, suggesting that hERG potassium channels play a role in fasting and glucose-stimulated release of GIP and glucagon. Glucagon 278-286 gastric inhibitory polypeptide Homo sapiens 155-158 29548277-12 2018 CONCLUSIONS: Two common missense polymorphisms of the Kv11.1 voltage-gated hERG potassium channel are associated with alterations in circulating levels of GIP and glucagon, suggesting that hERG potassium channels play a role in fasting and glucose-stimulated release of GIP and glucagon. Glucagon 278-286 gastric inhibitory polypeptide Homo sapiens 270-273 28948296-4 2018 METHODS: In transiently transfected COS-7 cells, GIP(3-30)NH2 was evaluated with homologous receptor binding and receptor activation (cAMP accumulation) studies at the glucagon-like peptide 1 (GLP-1), glucagon-like peptide-2 (GLP-2), glucagon, secretin and growth hormone-releasing hormone (GHRH) receptors. carbonyl sulfide 36-39 gastric inhibitory polypeptide Homo sapiens 49-52 28948296-4 2018 METHODS: In transiently transfected COS-7 cells, GIP(3-30)NH2 was evaluated with homologous receptor binding and receptor activation (cAMP accumulation) studies at the glucagon-like peptide 1 (GLP-1), glucagon-like peptide-2 (GLP-2), glucagon, secretin and growth hormone-releasing hormone (GHRH) receptors. Cyclic AMP 134-138 gastric inhibitory polypeptide Homo sapiens 49-52 28948296-12 2018 Markedly larger amounts of glucose were required to maintain the clamp during GIP infusion compared with the other days. Glucose 27-34 gastric inhibitory polypeptide Homo sapiens 78-81 27632019-6 2018 AUC0-120min for glucose-dependent insulinotropic polypeptide was higher after SFA meal compared with MUFA (23 %) and n-6 PUFA meals (20 %) (P = 0.004). Fatty Acids, Monounsaturated 101-105 gastric inhibitory polypeptide Homo sapiens 16-60 28822313-1 2018 A selective nonenzymatic glucose sensor was developed based on the direct oxidation of glucose on hierarchical CuCo bimetal-coated with a glucose-imprinted polymer (GIP). Glucose 25-32 gastric inhibitory polypeptide Homo sapiens 165-168 29412817-3 2018 In addition, GIP increases triacylglycerol (TAG) uptake in adipose tissue and decreases bone resorption. Triglycerides 27-42 gastric inhibitory polypeptide Homo sapiens 13-16 28822313-1 2018 A selective nonenzymatic glucose sensor was developed based on the direct oxidation of glucose on hierarchical CuCo bimetal-coated with a glucose-imprinted polymer (GIP). glucose-imprinted polymer 138-163 gastric inhibitory polypeptide Homo sapiens 165-168 28822313-2 2018 Glucose was introduced into the GIP composed of Nafion and polyurethane along with aminophenyl boronic acid (APBA), which was formed on the bimetal electrode formed on a screen-printed electrode. Glucose 0-7 gastric inhibitory polypeptide Homo sapiens 32-35 28822313-2 2018 Glucose was introduced into the GIP composed of Nafion and polyurethane along with aminophenyl boronic acid (APBA), which was formed on the bimetal electrode formed on a screen-printed electrode. perfluorosulfonic acid 48-54 gastric inhibitory polypeptide Homo sapiens 32-35 28822313-2 2018 Glucose was introduced into the GIP composed of Nafion and polyurethane along with aminophenyl boronic acid (APBA), which was formed on the bimetal electrode formed on a screen-printed electrode. Polyurethanes 59-71 gastric inhibitory polypeptide Homo sapiens 32-35 28822313-2 2018 Glucose was introduced into the GIP composed of Nafion and polyurethane along with aminophenyl boronic acid (APBA), which was formed on the bimetal electrode formed on a screen-printed electrode. 3-aminobenzeneboronic acid 83-107 gastric inhibitory polypeptide Homo sapiens 32-35 28822313-2 2018 Glucose was introduced into the GIP composed of Nafion and polyurethane along with aminophenyl boronic acid (APBA), which was formed on the bimetal electrode formed on a screen-printed electrode. 3-aminobenzeneboronic acid 109-113 gastric inhibitory polypeptide Homo sapiens 32-35 28822313-3 2018 The extraction of glucose from the GIP allowed for the selective permeation of glucose into the bimetal electrode surface for oxidation. Glucose 18-25 gastric inhibitory polypeptide Homo sapiens 35-38 28822313-3 2018 The extraction of glucose from the GIP allowed for the selective permeation of glucose into the bimetal electrode surface for oxidation. Glucose 79-86 gastric inhibitory polypeptide Homo sapiens 35-38 28822313-5 2018 The GIP layer coated on the NaOH pre-treated bimetal electrode exhibited a dynamic range between 1.0microM and 25.0mM with a detection limit of 0.65+-0.10microM in phosphate buffer solution (pH 7.4). Sodium Hydroxide 28-32 gastric inhibitory polypeptide Homo sapiens 4-7 28722834-2 2018 The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are secreted from the intestine in response to nutrient intake and exhibit several physiological functions including regulation of islet hormone secretion and glucose levels. Glucose 254-261 gastric inhibitory polypeptide Homo sapiens 22-52 28722834-2 2018 The incretin hormones gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are secreted from the intestine in response to nutrient intake and exhibit several physiological functions including regulation of islet hormone secretion and glucose levels. Glucose 254-261 gastric inhibitory polypeptide Homo sapiens 54-57 29950546-3 2018 Incretins such as glucose-dependent insulinotropic peptide(GIP)and glucagon-like peptide 1(GLP-1)modulate glucose homeostasis by regulating glucose-dependent insulin release from pancreatic betacells. Glucose 18-25 gastric inhibitory polypeptide Homo sapiens 59-62 28822313-5 2018 The GIP layer coated on the NaOH pre-treated bimetal electrode exhibited a dynamic range between 1.0microM and 25.0mM with a detection limit of 0.65+-0.10microM in phosphate buffer solution (pH 7.4). Phosphates 164-173 gastric inhibitory polypeptide Homo sapiens 4-7 29950546-3 2018 Incretins such as glucose-dependent insulinotropic peptide(GIP)and glucagon-like peptide 1(GLP-1)modulate glucose homeostasis by regulating glucose-dependent insulin release from pancreatic betacells. Glucose 106-113 gastric inhibitory polypeptide Homo sapiens 59-62 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 gastric inhibitory polypeptide Homo sapiens 68-71 30282365-5 2018 Herein, we examine whether the chronic treatment with the novel dual GLP-1/GIP receptor agonist DA-CH3 can restore the cognitive decline and AD-like cerebral pathology of the APPSWE/PS1DeltaE9 mouse model at the age of 10 months old. da-ch3 96-102 gastric inhibitory polypeptide Homo sapiens 75-78 29099978-12 2018 Conclusions: Short-term GIP infusions robustly reduce bone resorption independently of endogenous insulin secretion and during both elevated and low plasma glucose, but have no effect on P1NP or PTH after 90 minutes. Glucose 156-163 gastric inhibitory polypeptide Homo sapiens 24-27 29162361-2 2017 We investigated the relationships between the time course of the incretin effect and that of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) during oral glucose tolerance tests (OGTTs), thereby estimating incretin sensitivity of the beta cell, and its associated factors. Glucose 93-100 gastric inhibitory polypeptide Homo sapiens 139-142 29235507-3 2017 The incretin hormone GLP-1 prevents the decline of cerebral metabolic rate for glucose (CMRglc) in AD, and GLP-1 may serve to raise transporter numbers. Glucose 79-86 gastric inhibitory polypeptide Homo sapiens 4-20 28698280-12 2017 In the latter, the reduction of plasma GIP levels also contributed to the improvement of glucose metabolism. Glucose 89-96 gastric inhibitory polypeptide Homo sapiens 39-42 28374974-1 2017 The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), play an important role in glucose homeostasis by potentiating glucose-induced insulin secretion. Glucose 23-30 gastric inhibitory polypeptide Homo sapiens 69-72 28374974-4 2017 The endogenous secretion of both GIP and GLP-1 is stimulated by glucose in the small intestine, and the release is dependent on the amount. Glucose 64-71 gastric inhibitory polypeptide Homo sapiens 33-36 28374974-5 2017 In this work, we developed a semimechanistic model describing the release of GIP and GLP-1 after ingestion of various glucose doses in healthy volunteers and patients with T2D. Glucose 118-125 gastric inhibitory polypeptide Homo sapiens 77-80 28655715-7 2017 In the nabilone vs. placebo study, when compared with placebo, nabilone resulted in significantly elevated post-dose fasting GIP levels and post-OGTT GIP levels, but no change in post-dose fasting GLP-1 levels together with significantly lower post-OGTT GLP-1 levels. nabilone 63-71 gastric inhibitory polypeptide Homo sapiens 125-128 28870797-2 2017 pGIP/Neo is a genetically selected sub-clone of STC-1 with augmented levels of glucose-dependent insulinotropic peptide (GIP). pgip/neo 0-8 gastric inhibitory polypeptide Homo sapiens 79-119 28655715-7 2017 In the nabilone vs. placebo study, when compared with placebo, nabilone resulted in significantly elevated post-dose fasting GIP levels and post-OGTT GIP levels, but no change in post-dose fasting GLP-1 levels together with significantly lower post-OGTT GLP-1 levels. nabilone 63-71 gastric inhibitory polypeptide Homo sapiens 150-153 28655715-9 2017 We conclude that elevated GIP levels in obesity are likely a consequence of increased endocannabinoid levels. Endocannabinoids 86-101 gastric inhibitory polypeptide Homo sapiens 26-29 28667118-2 2017 This study examined the ability of GIP(3-30)NH2 to antagonize the physiological actions of GIP in glucose metabolism, subcutaneous abdominal adipose tissue blood flow (ATBF), and lipid metabolism in humans. Glucose 98-105 gastric inhibitory polypeptide Homo sapiens 35-38 28630069-6 2017 Matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) analysis showed His/Tyr-Ala dipeptide release from the N termini of incretins, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide, respectively, with the action of microbial DPP4. Histidine 108-111 gastric inhibitory polypeptide Homo sapiens 207-251 28630069-6 2017 Matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) analysis showed His/Tyr-Ala dipeptide release from the N termini of incretins, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide, respectively, with the action of microbial DPP4. Alanine 116-119 gastric inhibitory polypeptide Homo sapiens 207-251 28630069-6 2017 Matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) analysis showed His/Tyr-Ala dipeptide release from the N termini of incretins, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide, respectively, with the action of microbial DPP4. Dipeptides 120-129 gastric inhibitory polypeptide Homo sapiens 207-251 28452237-7 2017 GLP-1 and GIP responses to oral glucose load did not differ significantly between those with hyperthyroidism and controls. Glucose 32-39 gastric inhibitory polypeptide Homo sapiens 10-13 28667118-4 2017 In addition, ATBF remained constant during the antagonist and increased only slightly in combination with GIP, whereas it increased fivefold during GIP alone. atbf 13-17 gastric inhibitory polypeptide Homo sapiens 106-109 28667118-6 2017 The changes in glucose infusion rates and plasma insulin levels demonstrate an inhibitory effect of the antagonist on the incretin effect of GIP. Glucose 15-22 gastric inhibitory polypeptide Homo sapiens 141-144 29632608-5 2017 The studies establish that vildagliptin is a selective DPP-4 inhibitor that blocks GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) inactivation, thereby prolonging their action, resulting in improved glycaemic control. Vildagliptin 27-39 gastric inhibitory polypeptide Homo sapiens 93-137 29632608-5 2017 The studies establish that vildagliptin is a selective DPP-4 inhibitor that blocks GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) inactivation, thereby prolonging their action, resulting in improved glycaemic control. Vildagliptin 27-39 gastric inhibitory polypeptide Homo sapiens 139-142 28073779-3 2017 We hypothesized that GIP is anabolic in human subcutaneous adipose tissue (SAT) promoting triacylglycerol (TAG) deposition through reesterification of nonesterified fatty acids (NEFA), and this effect may differ according to obesity status or glucose tolerance. Triglycerides 90-105 gastric inhibitory polypeptide Homo sapiens 21-24 28385175-12 2017 We show that these gut-derived hormones affect glucagon secretion differently and that OGTT-induced secretion of these hormones may play a role in the inappropriate glucagon response to orally ingested glucose in patients with type 2 diabetes with especially GIP acting to increase glucagon secretion. Glucose 202-209 gastric inhibitory polypeptide Homo sapiens 259-262 28385175-12 2017 We show that these gut-derived hormones affect glucagon secretion differently and that OGTT-induced secretion of these hormones may play a role in the inappropriate glucagon response to orally ingested glucose in patients with type 2 diabetes with especially GIP acting to increase glucagon secretion. Glucagon 165-173 gastric inhibitory polypeptide Homo sapiens 259-262 28530680-1 2017 OBJECTIVES: We aim to validate the effects of glucose-dependent insulinotropic polypeptide (GIP) on fat distribution and glucose metabolism in Han Chinese populations. Glucose 46-53 gastric inhibitory polypeptide Homo sapiens 92-95 28530680-6 2017 However, rs9904288 of GIP was associated with the SFA in males as well as glucose-related traits in all subjects (P range, 0.004-0.049), and the GIPR variants displayed associations with both fat- and glucose-related traits. Glucose 74-81 gastric inhibitory polypeptide Homo sapiens 22-25 28237651-9 2017 In perfused rat pancreata, rat GIP(3-30)NH2 efficiently antagonized rat GIP(1-42)-induced insulin, somatostatin, and glucagon secretion. Glucagon 117-125 gastric inhibitory polypeptide Homo sapiens 72-75 28181363-3 2017 We therefore evaluated the impact of chronic liraglutide therapy on endogenous GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) response to an oral glucose challenge. Glucose 89-96 gastric inhibitory polypeptide Homo sapiens 135-138 28179449-4 2017 RESULTS: Nearly 80% of GIPR-expressing somatotropinomas, all of them negative for gsp mutations, show increased GH secretion upon GIP stimulation, higher sensitivity to Forskolin but not to somatostatin analogs. Colforsin 169-178 gastric inhibitory polypeptide Homo sapiens 23-26 28565879-0 2017 Difference in protective effects of GIP and GLP-1 on endothelial cells according to cyclic adenosine monophosphate response. Cyclic AMP 84-114 gastric inhibitory polypeptide Homo sapiens 36-39 28073779-3 2017 We hypothesized that GIP is anabolic in human subcutaneous adipose tissue (SAT) promoting triacylglycerol (TAG) deposition through reesterification of nonesterified fatty acids (NEFA), and this effect may differ according to obesity status or glucose tolerance. Fatty Acids, Nonesterified 151-176 gastric inhibitory polypeptide Homo sapiens 21-24 28073779-3 2017 We hypothesized that GIP is anabolic in human subcutaneous adipose tissue (SAT) promoting triacylglycerol (TAG) deposition through reesterification of nonesterified fatty acids (NEFA), and this effect may differ according to obesity status or glucose tolerance. Fatty Acids, Nonesterified 178-182 gastric inhibitory polypeptide Homo sapiens 21-24 28073779-3 2017 We hypothesized that GIP is anabolic in human subcutaneous adipose tissue (SAT) promoting triacylglycerol (TAG) deposition through reesterification of nonesterified fatty acids (NEFA), and this effect may differ according to obesity status or glucose tolerance. Glucose 243-250 gastric inhibitory polypeptide Homo sapiens 21-24 28216550-8 2017 The acute ingestion of typical amounts of fructose, in a variety of forms, results in marked differences in circulating GIP and lactate concentration, but no differences in appetite ratings, triglyceride concentration, indicative lipolysis, or NEFA metabolism, when compared to glucose. Fructose 42-50 gastric inhibitory polypeptide Homo sapiens 120-123 27840416-9 2017 Stimulation of GLP-1 and GIP were greater (P<0.001) in response to 3 kcal min-1, compared with 1 kcal min-1 and saline, without any difference between the groups. Sodium Chloride 115-121 gastric inhibitory polypeptide Homo sapiens 25-28 27709794-7 2017 Intact glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) concentrations were augmented by sitagliptin, by 78.4% and 90.2%, respectively (both P < .0001). Sitagliptin Phosphate 127-138 gastric inhibitory polypeptide Homo sapiens 89-92 27709794-9 2017 CONCLUSIONS: Sitagliptin, in patients already treated with a GLP-1 receptor agonist (liraglutide), increased intact GLP-1 and GIP concentrations, but with marginal, non-significant effects on glycaemic control. Sitagliptin Phosphate 13-24 gastric inhibitory polypeptide Homo sapiens 126-129 28166771-8 2017 RESULTS: Trehalose ingestion did not evoke rapid increases in blood glucose levels, and had a lower stimulatory potency of insulin and active GIP secretion compared with glucose ingestion. Trehalose 9-18 gastric inhibitory polypeptide Homo sapiens 142-145 28166771-10 2017 Specifically, active GIP secretion, which induces fat accumulation, was markedly lower after trehalose ingestion. Trehalose 93-102 gastric inhibitory polypeptide Homo sapiens 21-24 27840416-10 2017 In the obese, glycaemic, insulinaemic and GIP, but not GLP-1, responses to oral and intraduodenal glucose were related (P<0.05). Glucose 98-105 gastric inhibitory polypeptide Homo sapiens 42-45 27598511-1 2016 CONTEXT: The rate of gastric emptying is an important determinant of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) secretion and may influence the magnitude of glucose lowering by dipeptidyl peptidase-4 (DPP-4) inhibitors. Glucose 69-76 gastric inhibitory polypeptide Homo sapiens 115-118 28115026-7 2017 Acylated ghrelin, GLP-1 and GIP responses to the MTT were all unaffected by the high-fat, high-energy diet. monooxyethylene trimethylolpropane tristearate 49-52 gastric inhibitory polypeptide Homo sapiens 28-31 27780736-0 2016 Add-on therapy with anagliptin in Japanese patients with type-2 diabetes mellitus treated with metformin and miglitol can maintain higher concentrations of biologically active GLP-1/total GIP and a lower concentration of leptin. anagliptin 20-30 gastric inhibitory polypeptide Homo sapiens 188-191 27780736-0 2016 Add-on therapy with anagliptin in Japanese patients with type-2 diabetes mellitus treated with metformin and miglitol can maintain higher concentrations of biologically active GLP-1/total GIP and a lower concentration of leptin. Metformin 95-104 gastric inhibitory polypeptide Homo sapiens 188-191 27780736-9 2016 Add-on therapy with anagliptin in Japanese T2DM patients treated with metformin and miglitol for 52 weeks improved glycemic control and enhanced postprandial concentrations of active GLP-1/total GIP, and reduce the leptin concentration. anagliptin 20-30 gastric inhibitory polypeptide Homo sapiens 195-198 27780736-2 2016 We assessed add-on therapeutic effects of DPP-4I anagliptin in Japanese T2DM patients treated with metformin, an alpha-GI miglitol, or both drugs on postprandial responses of GLP-1 and glucose-dependent insulinotropic polypeptide (GIP), and on plasma concentration of the appetite-suppressing hormone leptin. dpp-4i anagliptin 42-59 gastric inhibitory polypeptide Homo sapiens 185-229 27439698-6 2016 The significant results from the experiments are as follows: higher level of c-Fos induction in presence of GIP, obestatin (p = 0.019 and p = 0.011 respectively), and GIP combined with ATP (p < 0.001) using the luciferase assay; GLP-1 and GLP-2 combined with ATP (p = 0.034 and p = 0.002, respectively) and GLP-2 alone (p < 0.001) using qPCR. Adenosine Triphosphate 262-265 gastric inhibitory polypeptide Homo sapiens 108-111 27439698-6 2016 The significant results from the experiments are as follows: higher level of c-Fos induction in presence of GIP, obestatin (p = 0.019 and p = 0.011 respectively), and GIP combined with ATP (p < 0.001) using the luciferase assay; GLP-1 and GLP-2 combined with ATP (p = 0.034 and p = 0.002, respectively) and GLP-2 alone (p < 0.001) using qPCR. Adenosine Triphosphate 262-265 gastric inhibitory polypeptide Homo sapiens 167-170 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 gastric inhibitory polypeptide Homo sapiens 170-200 27641811-3 2016 Direct evidence is based on identification of the active form of Galphas in early endosomes containing GIPR using a genetically encoded GFP tagged nanobody, and on detection of a distinct FRET signal accounting for cAMP production at the surface of endosomes containing GIP, compared to endosomes without GIP. galphas 65-72 gastric inhibitory polypeptide Homo sapiens 103-106 27641811-3 2016 Direct evidence is based on identification of the active form of Galphas in early endosomes containing GIPR using a genetically encoded GFP tagged nanobody, and on detection of a distinct FRET signal accounting for cAMP production at the surface of endosomes containing GIP, compared to endosomes without GIP. Cyclic AMP 215-219 gastric inhibitory polypeptide Homo sapiens 270-273 27484974-2 2016 It is involved in the inactivation of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), having in this way a profound influence on glucose metabolism. Glucose 74-81 gastric inhibitory polypeptide Homo sapiens 120-123 27798656-0 2016 Third Exposure to a Reduced Carbohydrate Meal Lowers Evening Postprandial Insulin and GIP Responses and HOMA-IR Estimate of Insulin Resistance. Carbohydrates 28-40 gastric inhibitory polypeptide Homo sapiens 86-89 27798656-3 2016 We hypothesized the involvement of dietary carbohydrate load, especially when timed after exercise, and mediation by the glucose-dependent insulinotropic peptide (GIP) in this phenomenon, as this incretin promotes insulin secretion after carbohydrate intake in insulin-sensitive, but not in insulin-resistant states. Carbohydrates 238-250 gastric inhibitory polypeptide Homo sapiens 121-161 27798656-3 2016 We hypothesized the involvement of dietary carbohydrate load, especially when timed after exercise, and mediation by the glucose-dependent insulinotropic peptide (GIP) in this phenomenon, as this incretin promotes insulin secretion after carbohydrate intake in insulin-sensitive, but not in insulin-resistant states. Carbohydrates 238-250 gastric inhibitory polypeptide Homo sapiens 163-166 27412483-12 2016 GLP-1, GIP and dual incretin receptor agonists showed protective effects in SH-SY5Y cells treated with the stressor Rotenone. Rotenone 116-124 gastric inhibitory polypeptide Homo sapiens 7-10 27798656-6 2016 RESULTS: The third low-carbohydrate meal, but not the high-carbohydrate meal, reduced: (1) evening insulin AUC by 39% without exercise and by 31% after exercise; (2) GIP AUC by 48% without exercise and by 45% after exercise, and (3) evening insulin resistance by 37% without exercise and by 24% after exercise. Carbohydrates 23-35 gastric inhibitory polypeptide Homo sapiens 166-169 27798656-9 2016 The parallel timing and magnitude of postprandial insulin and GIP changes suggest their dependence on a delayed intestinal adaptation to a low-carbohydrate diet. Carbohydrates 143-155 gastric inhibitory polypeptide Homo sapiens 62-65 27104640-1 2016 RATIONALE: Incretin hormones, namely glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide/glucose-dependent insulinotropic polypeptide (GIP), and dipeptidyl peptidase-4 (DPP-4) activity are important factors in glucose metabolism and have not been investigated in patients with obstructive sleep apnea (OSA). Glucose 104-111 gastric inhibitory polypeptide Homo sapiens 150-153 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 gastric inhibitory polypeptide Homo sapiens 202-205 27207543-5 2016 Vildagliptin treatment more than doubled responses of intact GLP-1 and glucose-dependent insulinotropic polypeptide and lowered glucose responses without changing AUCISR/AUCglucose in healthy subjects. Vildagliptin 0-12 gastric inhibitory polypeptide Homo sapiens 71-115 26919392-2 2016 It plays a major role in glucose metabolism by N-terminal truncation and inactivation of the incretins glucagon-like peptide-1 (GLP) and gastric inhibitory protein (GIP). Glucose 25-32 gastric inhibitory polypeptide Homo sapiens 137-163 27258938-1 2016 CONTEXT AND OBJECTIVE: Glucose-dependent insulinotropic polypeptide (GIP) in combination with hyperinsulinemia increases blood flow and triglyceride (TAG) clearance in subcutaneous (sc) abdominal adipose tissue in lean humans. Triglycerides 136-148 gastric inhibitory polypeptide Homo sapiens 23-67 27258938-1 2016 CONTEXT AND OBJECTIVE: Glucose-dependent insulinotropic polypeptide (GIP) in combination with hyperinsulinemia increases blood flow and triglyceride (TAG) clearance in subcutaneous (sc) abdominal adipose tissue in lean humans. Triglycerides 136-148 gastric inhibitory polypeptide Homo sapiens 69-72 27686734-0 2016 Single-dose acarbose decreased glucose-dependent insulinotropic peptide and glucagon levels in Chinese patients with newly diagnosed type 2 diabetes mellitus after a mixed meal. Acarbose 12-20 gastric inhibitory polypeptide Homo sapiens 31-71 27686734-10 2016 CONCLUSIONS: Single-dose acarbose could reduce the secretion of GIP and glucagon after a mixed meal in patients with newly diagnosed T2DM. Acarbose 25-33 gastric inhibitory polypeptide Homo sapiens 64-67 26919392-2 2016 It plays a major role in glucose metabolism by N-terminal truncation and inactivation of the incretins glucagon-like peptide-1 (GLP) and gastric inhibitory protein (GIP). Glucose 25-32 gastric inhibitory polypeptide Homo sapiens 165-168 27181102-15 2016 In diabetic patients, GIP is expected to have a direct anti-inflammatory effect on periodontitis in addition to its glucose-lowering effect. Glucose 116-123 gastric inhibitory polypeptide Homo sapiens 22-25 27034187-0 2016 Glucose-dependent insulinotropic polypeptide: effects on insulin and glucagon secretion in humans. Glucagon 69-77 gastric inhibitory polypeptide Homo sapiens 0-44 27304975-7 2016 The 150 mg dose of bethanechol increased the PP response 2-fold only in the IGT group, amplified GLP-1 release in the IGT and T2DM groups, and augmented the GIP response only in the NGT group. Bethanechol 19-30 gastric inhibitory polypeptide Homo sapiens 157-160 26652227-7 2016 Moreover, glucose-dependent insulinotropic polypeptide (GIP) mediated augmentation of glucagon by DPP-4 inhibitors could also protect against hypoglycemia. Glucagon 86-94 gastric inhibitory polypeptide Homo sapiens 10-54 26652227-7 2016 Moreover, glucose-dependent insulinotropic polypeptide (GIP) mediated augmentation of glucagon by DPP-4 inhibitors could also protect against hypoglycemia. Glucagon 86-94 gastric inhibitory polypeptide Homo sapiens 56-59 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 gastric inhibitory polypeptide Homo sapiens 28-31 27186349-1 2016 Glucose-dependent insulinotropic polypeptide (GIP) was established as a gut hormone more than 40 years ago, and there is good experimental support for its role as an incretin hormone although deletion of the GIP receptor or the GIP cells or GIP receptor mutations have only minor effects on glucose metabolism. Glucose 291-298 gastric inhibitory polypeptide Homo sapiens 46-49 27001281-9 2016 A lower carbohydrate and higher fat and protein content provides greater satiety and attenuation of C-peptide, glucose, insulin, and GIP responses compared with the reference breakfast but does not affect adipokines, ghrelin, glucagon, glucagon-like peptide-1, and plasminogen activator inhibitor-1. Carbohydrates 8-20 gastric inhibitory polypeptide Homo sapiens 133-136 26650343-8 2016 CONCLUSIONS: These results suggest that decreased maternal 25OHD may be associated with decreased cord 25OHD and increased cord GLP-1 and GIP levels, which may be involved with the transfer of maternal glucose to the fetus. Glucose 202-209 gastric inhibitory polypeptide Homo sapiens 138-141 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 gastric inhibitory polypeptide Homo sapiens 258-298 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 gastric inhibitory polypeptide Homo sapiens 300-303 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 gastric inhibitory polypeptide Homo sapiens 258-298 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 gastric inhibitory polypeptide Homo sapiens 300-303 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 gastric inhibitory polypeptide Homo sapiens 258-298 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 gastric inhibitory polypeptide Homo sapiens 300-303 26453833-0 2016 A novel dual GLP-1 and GIP receptor agonist is neuroprotective in the MPTP mouse model of Parkinson"s disease by increasing expression of BNDF. 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine 70-74 gastric inhibitory polypeptide Homo sapiens 23-26 26453833-0 2016 A novel dual GLP-1 and GIP receptor agonist is neuroprotective in the MPTP mouse model of Parkinson"s disease by increasing expression of BNDF. bndf 138-142 gastric inhibitory polypeptide Homo sapiens 23-26 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. Cyclic AMP 93-97 gastric inhibitory polypeptide Homo sapiens 166-169 26786780-2 2016 We aimed to explore the relative importance of endogenously secreted GLP-1 and GIP on glucose tolerance and beta-cell function after RYGB. Glucose 86-93 gastric inhibitory polypeptide Homo sapiens 79-82 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. Glucagon 139-147 gastric inhibitory polypeptide Homo sapiens 36-39 26786687-1 2016 The gut-derived incretin hormone, glucagon-like peptide 1 (GLP-1) lowers postprandial blood glucose levels by stimulating insulin and inhibiting glucagon secretion. Glucose 92-99 gastric inhibitory polypeptide Homo sapiens 16-32 27186349-2 2016 Unlike the related hormone, GLP-1, GIP stimulates the secretion of glucagon, which in healthy individuals may help to stabilize glucose levels, but in people with type 2 diabetes may contribute to glucose intolerance. Glucose 128-135 gastric inhibitory polypeptide Homo sapiens 35-38 27186349-2 2016 Unlike the related hormone, GLP-1, GIP stimulates the secretion of glucagon, which in healthy individuals may help to stabilize glucose levels, but in people with type 2 diabetes may contribute to glucose intolerance. Glucose 197-204 gastric inhibitory polypeptide Homo sapiens 35-38 27034187-4 2016 While GLP-1 decreases glucagon levels, the effect of GIP on glucagon levels has been unclear. Glucagon 60-68 gastric inhibitory polypeptide Homo sapiens 53-56 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 gastric inhibitory polypeptide Homo sapiens 128-131 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. Glucagon 80-88 gastric inhibitory polypeptide Homo sapiens 49-52 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 gastric inhibitory polypeptide Homo sapiens 49-52 27034187-14 2016 At fasting glycaemia and lower levels of glycaemia, GIP acts to increase glucagon with little effect on insulin release. Glucagon 73-81 gastric inhibitory polypeptide Homo sapiens 52-55 27034187-15 2016 At hyperglycaemia the insulin releasing effect of GIP prevail, which lead to an increase in glucose disposal by approximately 75% in healthy subjects (Study 1) and 25% in patients with Type 2 diabetes (Study 2) relative to placebo. Glucose 92-99 gastric inhibitory polypeptide Homo sapiens 50-53 27034187-16 2016 After insulin-induced hypoglycaemia in patients with type 1 diabetes (Study 3), GIP increase glucagon release, which probably augments endogenous glucose production. Glucagon 93-101 gastric inhibitory polypeptide Homo sapiens 80-83 27034187-16 2016 After insulin-induced hypoglycaemia in patients with type 1 diabetes (Study 3), GIP increase glucagon release, which probably augments endogenous glucose production. Glucose 146-153 gastric inhibitory polypeptide Homo sapiens 80-83 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 64-71 gastric inhibitory polypeptide Homo sapiens 36-39 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 gastric inhibitory polypeptide Homo sapiens 36-39 26702848-1 2016 PURPOSE OF REVIEW: Glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) are gastrointestinal peptides that play an important role as incretin hormones in the regulation of plasma glucose and insulin secretion. Glucose 199-206 gastric inhibitory polypeptide Homo sapiens 55-85 26702848-1 2016 PURPOSE OF REVIEW: Glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP) are gastrointestinal peptides that play an important role as incretin hormones in the regulation of plasma glucose and insulin secretion. Glucose 199-206 gastric inhibitory polypeptide Homo sapiens 87-90 26752550-1 2016 CONTEXT: Glucose and lipids stimulate the gut-hormones glucagon-like peptide (GLP)-1, GLP-2 and glucose-dependent insulinotropic polypeptide (GIP) but the effect of these on human postprandial lipid metabolism is not fully clarified. Glucose 9-16 gastric inhibitory polypeptide Homo sapiens 96-140 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 gastric inhibitory polypeptide Homo sapiens 11-51 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 gastric inhibitory polypeptide Homo sapiens 53-56 26885360-1 2016 The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon like peptide-1 (GLP-1) are secreted from enteroendocrine cells in the gut and regulate physiological and homeostatic functions related to glucose control, metabolism and food intake. Glucose 22-29 gastric inhibitory polypeptide Homo sapiens 68-71 26752550-1 2016 CONTEXT: Glucose and lipids stimulate the gut-hormones glucagon-like peptide (GLP)-1, GLP-2 and glucose-dependent insulinotropic polypeptide (GIP) but the effect of these on human postprandial lipid metabolism is not fully clarified. Glucose 9-16 gastric inhibitory polypeptide Homo sapiens 142-145 26359804-8 2016 In perfused pancreata in the presence of 7 mM glucose, both rodent (Pro3)GIP analogues induced modest insulin, glucagon and somatostatin secretion, corresponding to the partial agonist activities observed in cAMP production. Cyclic AMP 208-212 gastric inhibitory polypeptide Homo sapiens 73-76 26359804-6 2016 KEY RESULTS: Human (Pro3)GIP is a full agonist at human GIP receptors with similar efficacy (Emax ) for cAMP production as human GIP, while both rat and mouse(Pro3)GIP were partial agonists on their corresponding receptors. Cyclic AMP 104-108 gastric inhibitory polypeptide Homo sapiens 25-28 26264451-6 2016 Recent findings in the Edwards lab indicate that Cd causes timedependent and statistically significant changes in fasting leptin, Glucose-dependent Insulinotropic Polypeptide (GIP) and pancreas polypeptide hormone levels in a subchronic animal model of Cd-induced hyperglycemia. Cadmium 49-51 gastric inhibitory polypeptide Homo sapiens 130-174 26359804-8 2016 In perfused pancreata in the presence of 7 mM glucose, both rodent (Pro3)GIP analogues induced modest insulin, glucagon and somatostatin secretion, corresponding to the partial agonist activities observed in cAMP production. Glucose 46-53 gastric inhibitory polypeptide Homo sapiens 73-76 26359804-8 2016 In perfused pancreata in the presence of 7 mM glucose, both rodent (Pro3)GIP analogues induced modest insulin, glucagon and somatostatin secretion, corresponding to the partial agonist activities observed in cAMP production. Glucagon 111-119 gastric inhibitory polypeptide Homo sapiens 73-76 26264451-6 2016 Recent findings in the Edwards lab indicate that Cd causes timedependent and statistically significant changes in fasting leptin, Glucose-dependent Insulinotropic Polypeptide (GIP) and pancreas polypeptide hormone levels in a subchronic animal model of Cd-induced hyperglycemia. Cadmium 49-51 gastric inhibitory polypeptide Homo sapiens 176-179 26225752-6 2015 Finally, N-acetyl-GIP recognized as a dipeptidyl-IV resistant analogue, fully stimulated cAMP production with a ~15-fold lower potency than GIP and weakly stimulated GIPR internalization and desensitization of cAMP response. Cysteine 11-17 gastric inhibitory polypeptide Homo sapiens 18-21 27426125-8 2016 However use of metformin is associated with an increase in ghrelin, PYY, GLP-1 and GIP in women with PCOS. Metformin 15-24 gastric inhibitory polypeptide Homo sapiens 83-86 26354383-7 2016 GLP-1 and GIP levels increased after all challenges and GIP secretion was markedly higher after the mixed meal than after glucose alone. Glucose 122-129 gastric inhibitory polypeptide Homo sapiens 56-59 27040341-4 2016 Two incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), stimulate glucose-mediated insulin production in pancreatic beta cells. Glucose 59-66 gastric inhibitory polypeptide Homo sapiens 105-108 28326339-10 2016 CONCLUSIONS: This first exploratory association study between polymorphisms in GIP and GIPR in relation to bone phenotypes and serum-GIP in women at different ages indicates a possible, albeit complex link between glucose metabolism genes and bone, while recognizing that further studies are warranted. Glucose 214-221 gastric inhibitory polypeptide Homo sapiens 79-82 28326339-10 2016 CONCLUSIONS: This first exploratory association study between polymorphisms in GIP and GIPR in relation to bone phenotypes and serum-GIP in women at different ages indicates a possible, albeit complex link between glucose metabolism genes and bone, while recognizing that further studies are warranted. Glucose 214-221 gastric inhibitory polypeptide Homo sapiens 87-90 26487006-4 2015 Administration of mAb (30 mg/kg body wt, BW) to mice attenuated the insulin response to oral glucose by 70% and completely eliminated the response to ip glucose coadministered with human GIP. Glucose 153-160 gastric inhibitory polypeptide Homo sapiens 187-190 26254594-8 2015 In hBMSC and SaOS-2 cells, activation of the GIP receptor increased intracellular cAMP levels. Cyclic AMP 82-86 gastric inhibitory polypeptide Homo sapiens 45-48 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 gastric inhibitory polypeptide Homo sapiens 355-358 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 gastric inhibitory polypeptide Homo sapiens 355-358 26225752-6 2015 Finally, N-acetyl-GIP recognized as a dipeptidyl-IV resistant analogue, fully stimulated cAMP production with a ~15-fold lower potency than GIP and weakly stimulated GIPR internalization and desensitization of cAMP response. Cyclic AMP 210-214 gastric inhibitory polypeptide Homo sapiens 18-21 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 gastric inhibitory polypeptide Homo sapiens 93-137 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 gastric inhibitory polypeptide Homo sapiens 139-142 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 gastric inhibitory polypeptide Homo sapiens 139-142 26225752-6 2015 Finally, N-acetyl-GIP recognized as a dipeptidyl-IV resistant analogue, fully stimulated cAMP production with a ~15-fold lower potency than GIP and weakly stimulated GIPR internalization and desensitization of cAMP response. dipeptidyl 38-48 gastric inhibitory polypeptide Homo sapiens 18-21 26225752-6 2015 Finally, N-acetyl-GIP recognized as a dipeptidyl-IV resistant analogue, fully stimulated cAMP production with a ~15-fold lower potency than GIP and weakly stimulated GIPR internalization and desensitization of cAMP response. Cyclic AMP 89-93 gastric inhibitory polypeptide Homo sapiens 18-21 25399343-0 2015 Ethnic disparities in insulin and glucose-dependent insulinotropic peptide (GIP) responses to intraduodenal glucose in health. Glucose 34-41 gastric inhibitory polypeptide Homo sapiens 76-79 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 gastric inhibitory polypeptide Homo sapiens 276-279 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 gastric inhibitory polypeptide Homo sapiens 60-63 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). Alcohols 159-166 gastric inhibitory polypeptide Homo sapiens 115-118 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 gastric inhibitory polypeptide Homo sapiens 115-118 26178726-12 2015 In contrast, both oleic acid and 2-OG contributed to the GIP response. Oleic Acid 18-28 gastric inhibitory polypeptide Homo sapiens 57-60 26178726-12 2015 In contrast, both oleic acid and 2-OG contributed to the GIP response. 2-oleoylglycerol 33-37 gastric inhibitory polypeptide Homo sapiens 57-60 26043830-5 2015 Mutants on these amino acids were expressed in HEKT 293 cells and characterized in terms of GIP-induced cAMP production. Cyclic AMP 104-108 gastric inhibitory polypeptide Homo sapiens 92-95 26055217-9 2015 Postprandial plasma total GIP levels increased following sitagliptin but decreased after acarbose and miglitol. Acarbose 89-97 gastric inhibitory polypeptide Homo sapiens 26-29 25767259-13 2015 Incremental concentrations of insulin, C-peptide, and GIP were reduced for 2 h with premeal GSK-1614235. gsk 92-95 gastric inhibitory polypeptide Homo sapiens 54-57 26055217-9 2015 Postprandial plasma total GIP levels increased following sitagliptin but decreased after acarbose and miglitol. Sitagliptin Phosphate 57-68 gastric inhibitory polypeptide Homo sapiens 26-29 25835510-0 2015 Improvement of dumping syndrome and oversecretion of glucose-dependent insulinotropic polypeptide following a switch from olanzapine to quetiapine in a patient with schizophrenia. Olanzapine 122-132 gastric inhibitory polypeptide Homo sapiens 53-97 25835510-0 2015 Improvement of dumping syndrome and oversecretion of glucose-dependent insulinotropic polypeptide following a switch from olanzapine to quetiapine in a patient with schizophrenia. Quetiapine Fumarate 136-146 gastric inhibitory polypeptide Homo sapiens 53-97 25835510-4 2015 We describe here a patient with schizophrenia under treatment of olanzapine and an anamnesis of gastric surgery, who experienced late dumping syndrome, hyperinsulinemia and overactivation of glucose-dependent insulinotropic polypeptide. Olanzapine 65-75 gastric inhibitory polypeptide Homo sapiens 191-235 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 gastric inhibitory polypeptide Homo sapiens 97-100 25767259-15 2015 SGLT1 inhibitors block intestinal glucose absorption and reduce GIP secretion in rats and humans, suggesting SGLT1 glucose transport is critical for GIP release. Glucose 115-122 gastric inhibitory polypeptide Homo sapiens 149-152 25969715-7 2015 In contrast, plasma GIP levels at both 30 and 60 min, and area under the curve-GIP value after glucose loading were significantly higher than those after GFO loading. Glucose 95-102 gastric inhibitory polypeptide Homo sapiens 79-82 26925376-2 2015 The aim of this study was to assess the influence of a low calorie diet with or without n-3 PUFA supplementation on glucose dependent insulinotropic polypeptide (GIP) output and insulin sensitivity markers in obese subjects. Nitrogen 41-42 gastric inhibitory polypeptide Homo sapiens 116-160 26925376-2 2015 The aim of this study was to assess the influence of a low calorie diet with or without n-3 PUFA supplementation on glucose dependent insulinotropic polypeptide (GIP) output and insulin sensitivity markers in obese subjects. Nitrogen 41-42 gastric inhibitory polypeptide Homo sapiens 162-165 26925376-2 2015 The aim of this study was to assess the influence of a low calorie diet with or without n-3 PUFA supplementation on glucose dependent insulinotropic polypeptide (GIP) output and insulin sensitivity markers in obese subjects. Fatty Acids, Unsaturated 92-96 gastric inhibitory polypeptide Homo sapiens 116-160 26925376-8 2015 Blood triglyceride level was lowered by caloric restriction with a greater effect when n-3 PUFA were included and correlated positively with fasting GIP level. Triglycerides 6-18 gastric inhibitory polypeptide Homo sapiens 149-152 26925376-9 2015 CONCLUSIONS: Three months of caloric restriction with DHA + EPA supplementation exerts beneficial effects on insulin resistance, GIP and triglycerides. dehydroacetic acid 54-57 gastric inhibitory polypeptide Homo sapiens 129-132 25388434-7 2015 CONCLUSIONS: Sitagliptin increased the heart rate response to intraduodenal glucose infusion at 2 kcal/min in people with Type 2 diabetes, which was associated with augmentation of plasma intact glucose-dependent insulinotropic polypeptide concentrations. Sitagliptin Phosphate 13-24 gastric inhibitory polypeptide Homo sapiens 195-239 25388434-7 2015 CONCLUSIONS: Sitagliptin increased the heart rate response to intraduodenal glucose infusion at 2 kcal/min in people with Type 2 diabetes, which was associated with augmentation of plasma intact glucose-dependent insulinotropic polypeptide concentrations. Glucose 76-83 gastric inhibitory polypeptide Homo sapiens 195-239 26925376-10 2015 GENERAL SIGNIFICANCE: Combining caloric restriction and n-3 PUFA improves insulin sensitivity, which may be related to a decrease of GIP levels. Fatty Acids, Omega-3 56-64 gastric inhibitory polypeptide Homo sapiens 133-136 25388434-5 2015 During intraduodenal glucose infusion, there was a substantial increase in plasma total glucose-dependent insulinotropic polypeptide on both days (time effect: P < 0.001), but not in total glucagon-like peptide-1. Glucose 21-28 gastric inhibitory polypeptide Homo sapiens 88-132 25388434-6 2015 After sitagliptin, plasma intact glucagon-like peptide-1 concentration increased slightly (treatment x time interaction: P = 0.044) and glucose-dependent insulinotropic polypeptide concentration increased substantially (treatment x time interaction: P = 0.003).The heart rate response to intraduodenal glucose was related directly to plasma intact glucose-dependent insulinotropic polypeptide concentrations (r = 0.75, P = 0.008). Sitagliptin Phosphate 6-17 gastric inhibitory polypeptide Homo sapiens 348-392 25969715-8 2015 CONCLUSIONS: These results show that GFO ingestion stimulates GLP-1 and GLP-2 secretion, and reduces GIP secretion compared with glucose ingestion. 2-(4-tert-butylphenyl)-5-[(quinolin-2-ylamino)methyl]-6H-[1,2,4]triazolo[1,5-a]pyrimidin-7-one 37-40 gastric inhibitory polypeptide Homo sapiens 101-104 25498624-1 2015 Extraction was optimized of polysaccharides from Gleoestereum incarnatum (GIP). Polysaccharides 28-43 gastric inhibitory polypeptide Homo sapiens 74-77 25613093-3 2015 METHODS: The responses of glucagon and insulin as well as those of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were examined before and after ingestion of glucose or mixed meal in Japanese subjects with normal or impaired glucose tolerance (NGT and IGT) and in non-obese, untreated T2DM of short duration. Glucose 67-74 gastric inhibitory polypeptide Homo sapiens 113-116 25498624-5 2015 GIP-II was composed of galactose, glucose, xylose, and mannose, with glucose was the predominant monosaccharide. Monosaccharides 97-111 gastric inhibitory polypeptide Homo sapiens 0-3 25786106-14 2015 Aspartame and control bars affected GLP-1, GIP, tyrosine and phenylalanine levels equally in both aspartame sensitive and non-sensitive subjects. Aspartame 0-9 gastric inhibitory polypeptide Homo sapiens 43-46 25498624-5 2015 GIP-II was composed of galactose, glucose, xylose, and mannose, with glucose was the predominant monosaccharide. Galactose 23-32 gastric inhibitory polypeptide Homo sapiens 0-3 25498624-5 2015 GIP-II was composed of galactose, glucose, xylose, and mannose, with glucose was the predominant monosaccharide. Glucose 34-41 gastric inhibitory polypeptide Homo sapiens 0-3 25498624-5 2015 GIP-II was composed of galactose, glucose, xylose, and mannose, with glucose was the predominant monosaccharide. Xylose 43-49 gastric inhibitory polypeptide Homo sapiens 0-3 25498624-5 2015 GIP-II was composed of galactose, glucose, xylose, and mannose, with glucose was the predominant monosaccharide. Mannose 55-62 gastric inhibitory polypeptide Homo sapiens 0-3 25498624-5 2015 GIP-II was composed of galactose, glucose, xylose, and mannose, with glucose was the predominant monosaccharide. Glucose 69-76 gastric inhibitory polypeptide Homo sapiens 0-3 25406260-1 2015 This study was conducted to investigate whether a high-fat/high-carbohydrate (HFHC) meal induces an increase in plasma concentrations of glucagon, dipeptidyl peptidase-IV (DPP-IV), and CD26 expression in mononuclear cells (MNC) while reducing insulin, C-peptide, proinsulin, GIP, and GLP-1 concentrations. Carbohydrates 64-76 gastric inhibitory polypeptide Homo sapiens 275-278 25498624-6 2015 GIP-II exhibited strong scavenging activities against DPPH and hydroxyl radials in vitro, as well as a strong inhibitory effect on the growth of HepG2 cells. 1,1-diphenyl-2-picrylhydrazyl 54-58 gastric inhibitory polypeptide Homo sapiens 0-3 25423571-8 2015 In response to intraduodenal glucose, plasma GIP (P < .001), glucagon (P < .001), and insulin (P < .001) were higher, but GLP-1 (P < .001) was less in the obese compared with lean. Glucose 29-36 gastric inhibitory polypeptide Homo sapiens 45-48 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 gastric inhibitory polypeptide Homo sapiens 24-27 25406260-1 2015 This study was conducted to investigate whether a high-fat/high-carbohydrate (HFHC) meal induces an increase in plasma concentrations of glucagon, dipeptidyl peptidase-IV (DPP-IV), and CD26 expression in mononuclear cells (MNC) while reducing insulin, C-peptide, proinsulin, GIP, and GLP-1 concentrations. hfhc 78-82 gastric inhibitory polypeptide Homo sapiens 275-278 25053587-0 2015 Glucose-dependent insulinotropic polypeptide augments glucagon responses to hypoglycemia in type 1 diabetes. Glucagon 54-62 gastric inhibitory polypeptide Homo sapiens 0-44 25613747-2 2015 In health glucose-dependent insulinotropic polypeptide (GIP) is a potent glucose-lowering peptide that does not cause hypoglycaemia. Glucose 10-17 gastric inhibitory polypeptide Homo sapiens 56-59 25613747-3 2015 The objectives of this study were to determine the effects of exogenous GIP infusion on blood glucose concentrations, glucose absorption, insulinaemia and gastric emptying in critically ill patients without known diabetes. Glucose 94-101 gastric inhibitory polypeptide Homo sapiens 72-75 25582643-5 2015 Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are incretins, gut hormones secreted from the intestine in response to food intake, both of which augment glucose-induced insulin release, suppress glucagon secretion, and slow gastric emptying. Glucose 36-43 gastric inhibitory polypeptide Homo sapiens 82-85 25053587-6 2015 On the GIP days, significantly less exogenous glucose was needed to keep plasma glucose above 2 mmol/L (155 +- 36 [GIP] vs. 232 +- 40 [GLP-1] vs. 212 +- 56 [saline] mg kg(-1), P < 0.05). Glucose 46-53 gastric inhibitory polypeptide Homo sapiens 115-118 25243647-1 2015 AIMS: To examine whether 12 weeks of treatment with a dipeptidyl peptidase-4 (DPP-4) inhibitor, sitagliptin, influences the insulin secretion induced by glucose, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) during a hyperglycaemic clamp in patients with type 2 diabetes (T2DM). Sitagliptin Phosphate 96-107 gastric inhibitory polypeptide Homo sapiens 162-206 25053587-2 2015 We studied the effects of GIP and GLP-1 on glucagon responses to insulin-induced hypoglycemia in patients with type 1 diabetes mellitus (T1DM). Glucagon 43-51 gastric inhibitory polypeptide Homo sapiens 26-29 25243647-1 2015 AIMS: To examine whether 12 weeks of treatment with a dipeptidyl peptidase-4 (DPP-4) inhibitor, sitagliptin, influences the insulin secretion induced by glucose, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) during a hyperglycaemic clamp in patients with type 2 diabetes (T2DM). Sitagliptin Phosphate 96-107 gastric inhibitory polypeptide Homo sapiens 208-211 25243647-10 2015 The total beta-cell response during GIP infusion improved significantly from week 1 to week 12, both within the sitagliptin group (p = 0.004) and when compared with the placebo group (p = 0.04). Sitagliptin Phosphate 112-123 gastric inhibitory polypeptide Homo sapiens 36-39 25053587-6 2015 On the GIP days, significantly less exogenous glucose was needed to keep plasma glucose above 2 mmol/L (155 +- 36 [GIP] vs. 232 +- 40 [GLP-1] vs. 212 +- 56 [saline] mg kg(-1), P < 0.05). Glucose 80-87 gastric inhibitory polypeptide Homo sapiens 7-10 25053587-6 2015 On the GIP days, significantly less exogenous glucose was needed to keep plasma glucose above 2 mmol/L (155 +- 36 [GIP] vs. 232 +- 40 [GLP-1] vs. 212 +- 56 [saline] mg kg(-1), P < 0.05). Sodium Chloride 157-163 gastric inhibitory polypeptide Homo sapiens 7-10 25053587-8 2015 Our results suggest that during hypoglycemia in patients with T1DM, exogenous GIP increases glucagon responses during the recovery phase after hypoglycemia and reduces the need for glucose administration. Glucagon 92-100 gastric inhibitory polypeptide Homo sapiens 78-81 25053587-8 2015 Our results suggest that during hypoglycemia in patients with T1DM, exogenous GIP increases glucagon responses during the recovery phase after hypoglycemia and reduces the need for glucose administration. Glucose 181-188 gastric inhibitory polypeptide Homo sapiens 78-81 25243647-13 2015 CONCLUSIONS: Treatment with the DPP-4 inhibitor sitagliptin over 12 weeks in patients with T2DM partially restored the lost insulinotropic effect of GIP, whereas the preserved insulinotropic effect of GLP-1 was not further improved. Sitagliptin Phosphate 48-59 gastric inhibitory polypeptide Homo sapiens 149-152 25053587-5 2015 During the recovery phase, GIP infusions elicited larger glucagon responses (164 +- 50 [GIP] vs. 23 +- 25 [GLP-1] vs. 17 +- 46 [saline] min pmol/L, P < 0.03) and endogenous glucose production was higher with GIP and lower with GLP-1 compared with saline (P < 0.02). Glucagon 57-65 gastric inhibitory polypeptide Homo sapiens 27-30 25053587-5 2015 During the recovery phase, GIP infusions elicited larger glucagon responses (164 +- 50 [GIP] vs. 23 +- 25 [GLP-1] vs. 17 +- 46 [saline] min pmol/L, P < 0.03) and endogenous glucose production was higher with GIP and lower with GLP-1 compared with saline (P < 0.02). Sodium Chloride 128-134 gastric inhibitory polypeptide Homo sapiens 27-30 25053587-5 2015 During the recovery phase, GIP infusions elicited larger glucagon responses (164 +- 50 [GIP] vs. 23 +- 25 [GLP-1] vs. 17 +- 46 [saline] min pmol/L, P < 0.03) and endogenous glucose production was higher with GIP and lower with GLP-1 compared with saline (P < 0.02). Glucose 178-185 gastric inhibitory polypeptide Homo sapiens 27-30 25053587-5 2015 During the recovery phase, GIP infusions elicited larger glucagon responses (164 +- 50 [GIP] vs. 23 +- 25 [GLP-1] vs. 17 +- 46 [saline] min pmol/L, P < 0.03) and endogenous glucose production was higher with GIP and lower with GLP-1 compared with saline (P < 0.02). Sodium Chloride 252-258 gastric inhibitory polypeptide Homo sapiens 27-30 25053587-6 2015 On the GIP days, significantly less exogenous glucose was needed to keep plasma glucose above 2 mmol/L (155 +- 36 [GIP] vs. 232 +- 40 [GLP-1] vs. 212 +- 56 [saline] mg kg(-1), P < 0.05). Glucose 46-53 gastric inhibitory polypeptide Homo sapiens 7-10 25328079-7 2015 In the sitagliptin group, glucose excursion during a meal tolerance test was reduced and accompanied by elevations in active GLP-1 and active GIP concentrations. Sitagliptin Phosphate 7-18 gastric inhibitory polypeptide Homo sapiens 142-145 25328079-7 2015 In the sitagliptin group, glucose excursion during a meal tolerance test was reduced and accompanied by elevations in active GLP-1 and active GIP concentrations. Glucose 26-33 gastric inhibitory polypeptide Homo sapiens 142-145 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 gastric inhibitory polypeptide Homo sapiens 123-126 25029417-9 2014 In addition, fasting irisin level (P < .001) and glucose-induced GIP response (P = .013) in PCOS patients were significantly elevated as compared to those of control women. Glucose 52-59 gastric inhibitory polypeptide Homo sapiens 68-71 25029417-10 2014 Remarkably, levels of fasting irisin and glucose-induced GIP response remained significantly elevated in ATP III [-] PCOS and healthy-weight PCOS patients when compared to matched controls. Glucose 41-48 gastric inhibitory polypeptide Homo sapiens 57-60 25029417-10 2014 Remarkably, levels of fasting irisin and glucose-induced GIP response remained significantly elevated in ATP III [-] PCOS and healthy-weight PCOS patients when compared to matched controls. Adenosine Triphosphate 105-108 gastric inhibitory polypeptide Homo sapiens 57-60 25029417-11 2014 Analysis of the effect size indicated that both fasting irisin and glucose-induced GIP response are significant risk factors for PCOS with odds ratios of 6.63 and 4.21, respectively. Glucose 67-74 gastric inhibitory polypeptide Homo sapiens 83-86 25500886-6 2015 Dibenzazepine also increased K cell numbers, resulting in increased gastric inhibitory polypeptide (GIP) secretion. dibenzazepine 0-13 gastric inhibitory polypeptide Homo sapiens 100-103 26221611-0 2015 Effects of High Glucose Levels and Glycated Serum on GIP Responsiveness in the Pancreatic Beta Cell Line HIT-T15. Glucose 16-23 gastric inhibitory polypeptide Homo sapiens 53-56 25420579-1 2014 BACKGROUND: Sitagliptin inhibits dipeptidyl peptidase-4, which inactivates the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide. Sitagliptin Phosphate 12-23 gastric inhibitory polypeptide Homo sapiens 133-177 25288806-1 2014 PI3Kgamma, a G-protein-coupled type 1B phosphoinositol 3-kinase, exhibits a basal glucose-independent activity in beta-cells and can be activated by the glucose-dependent insulinotropic polypeptide (GIP). Glucose 82-89 gastric inhibitory polypeptide Homo sapiens 153-197 25288806-5 2014 Downstream, we find that GIP, much like glucose stimulation, activates the small GTPase protein Rac1 to induce actin remodeling. Glucose 40-47 gastric inhibitory polypeptide Homo sapiens 25-28 25288806-8 2014 Finally, forced actin depolymerization with latrunculin B restored the exocytotic and secretory responses to GIP during PI3Kgamma inhibition, demonstrating that the loss of GIP-induced actin depolymerization was indeed limiting insulin exocytosis. latrunculin B 44-57 gastric inhibitory polypeptide Homo sapiens 109-112 25288806-8 2014 Finally, forced actin depolymerization with latrunculin B restored the exocytotic and secretory responses to GIP during PI3Kgamma inhibition, demonstrating that the loss of GIP-induced actin depolymerization was indeed limiting insulin exocytosis. latrunculin B 44-57 gastric inhibitory polypeptide Homo sapiens 173-176 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 gastric inhibitory polypeptide Homo sapiens 138-141 25091498-4 2014 Akt-dependent release of FoxO1 and glucose-dependent binding of LEF1/beta-catenin mediate induction of Gip expression while insulin-induced phosphorylation of beta-catenin does not alter its localization or transcriptional activity in enteroendocrine cells. Glucose 35-42 gastric inhibitory polypeptide Homo sapiens 103-106 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 gastric inhibitory polypeptide Homo sapiens 138-141 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 gastric inhibitory polypeptide Homo sapiens 154-157 25144635-10 2014 During hyperglycemia, GIP infusion significantly (P < .001) augmented the decremental area under the curve to 2785 +- 446 % x minutes, compared to 1308 +- 448 % x minutes during saline infusion, with CTX values corresponding to 49% of basal values. Sodium Chloride 181-187 gastric inhibitory polypeptide Homo sapiens 22-25 25271113-0 2014 Response of incretins (GIP and GLP-1) to an oral glucose load in female and male subjects with normal glucose tolerance. Glucose 49-56 gastric inhibitory polypeptide Homo sapiens 23-26 24828362-9 2014 GIP appears to offer an additional survival benefit by not only stimulating intestinal glucose transport and maximally releasing insulin to facilitate nutrient storage but also by its insulin-mimetic properties, including enhanced uptake of glucose by adipocytes. Glucose 87-94 gastric inhibitory polypeptide Homo sapiens 0-3 24828362-9 2014 GIP appears to offer an additional survival benefit by not only stimulating intestinal glucose transport and maximally releasing insulin to facilitate nutrient storage but also by its insulin-mimetic properties, including enhanced uptake of glucose by adipocytes. Glucose 241-248 gastric inhibitory polypeptide Homo sapiens 0-3 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 gastric inhibitory polypeptide Homo sapiens 203-206 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 gastric inhibitory polypeptide Homo sapiens 262-306 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 gastric inhibitory polypeptide Homo sapiens 308-311 25179575-3 2014 Both the GLP-1 receptor and the GIP receptor are members of the secretin family of G protein-coupled receptors and couple positively with adenylate cyclase, resulting in an increase in intracellular cAMP. Cyclic AMP 199-203 gastric inhibitory polypeptide Homo sapiens 32-35 25227623-1 2014 INTRODUCTION: Dipeptidyl peptidase-4 (DPP-4) inhibitors including alogliptin are categorised as a newer class of oral hypoglycaemic, antidiabetic drugs to suppress the degradation of incretin hormones ((glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP)) by DPP-4. alogliptin 66-76 gastric inhibitory polypeptide Homo sapiens 239-283 25227623-1 2014 INTRODUCTION: Dipeptidyl peptidase-4 (DPP-4) inhibitors including alogliptin are categorised as a newer class of oral hypoglycaemic, antidiabetic drugs to suppress the degradation of incretin hormones ((glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP)) by DPP-4. alogliptin 66-76 gastric inhibitory polypeptide Homo sapiens 285-288 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 gastric inhibitory polypeptide Homo sapiens 112-115 24612221-11 2014 Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) levels were significantly elevated by vildagliptin compared to placebo during meal, hypoglycaemia and food re-challenge. Vildagliptin 125-137 gastric inhibitory polypeptide Homo sapiens 36-80 24612221-11 2014 Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) levels were significantly elevated by vildagliptin compared to placebo during meal, hypoglycaemia and food re-challenge. Vildagliptin 125-137 gastric inhibitory polypeptide Homo sapiens 82-85 24612221-12 2014 CONCLUSIONS: Vildagliptin action to block GLP-1 and GIP inactivation by DPP-4 improves glucagon dynamics during hypoglycaemia, hyperglycaemia and food re-challenge. Vildagliptin 13-25 gastric inhibitory polypeptide Homo sapiens 52-55 25334044-0 2014 Marked cortisol production by intracrine ACTH in GIP-treated cultured adrenal cells in which the GIP receptor was exogenously introduced. Hydrocortisone 7-15 gastric inhibitory polypeptide Homo sapiens 49-52 25334044-0 2014 Marked cortisol production by intracrine ACTH in GIP-treated cultured adrenal cells in which the GIP receptor was exogenously introduced. Hydrocortisone 7-15 gastric inhibitory polypeptide Homo sapiens 97-100 25334044-6 2014 The mRNA levels of a cholesterol transport protein required for all steroidogenesis, StAR, and steroidogenic enzymes, HSD3beta2, CYP11A1, CYP21A2, and CYP17A1 increased 1.2-2.1-fold in GIP-stimulated H295R-GIPR cells. Cholesterol 21-32 gastric inhibitory polypeptide Homo sapiens 185-188 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 gastric inhibitory polypeptide Homo sapiens 0-44 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 gastric inhibitory polypeptide Homo sapiens 46-49 28324382-3 2014 In order to probe this interaction on cells, the current study attempts towards expressing 15N-labeled GIP using classical molecular biology tools. 15n 91-94 gastric inhibitory polypeptide Homo sapiens 103-106 28324382-7 2014 Subsequently, the (15N)GIP was obtained using the aforementioned procedure and confirmed by MALDI-TOF. 15n 19-22 gastric inhibitory polypeptide Homo sapiens 23-26 24925644-7 2014 Characterization of mSCP1/GIP activity with the artificial substrate p-NPP (p-nitrophenylphosphate) yielded kinetic parameters comparable to those of DeltaN-rmSCP1/GIP and the truncated human ortholog DeltaN-hSCP1. nitrophenylphosphate 76-98 gastric inhibitory polypeptide Homo sapiens 26-29 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 gastric inhibitory polypeptide Homo sapiens 203-206 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 gastric inhibitory polypeptide Homo sapiens 203-206 24647737-2 2014 We evaluated responses to intraduodenal glucose infusion (60 g over 120 min [i.e., 2 kcal/min], a rate that predominantly stimulates GIP but not GLP-1) after sitagliptin versus control in 12 healthy lean, 12 obese, and 12 type 2 diabetic subjects taking metformin 850 mg b.i.d. Glucose 40-47 gastric inhibitory polypeptide Homo sapiens 133-136 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 gastric inhibitory polypeptide Homo sapiens 53-56 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 gastric inhibitory polypeptide Homo sapiens 53-56 25141237-9 2014 There was a positive correlation between changes in GIP and PYY and changes in ascorbic acid in patients with T2D (p<0.05 and p<0.001, respectively). Ascorbic Acid 79-92 gastric inhibitory polypeptide Homo sapiens 52-55 25141237-10 2014 CONCLUSION/INTERPRETATION: Apart from a positive relationship of postprandial changes in GIP and PYY with changes in ascorbic acid, there was no direct link observed between gastrointestinal hormones and oxidative stress markers in diabetic patients. Ascorbic Acid 117-130 gastric inhibitory polypeptide Homo sapiens 89-92 24647737-6 2014 In contrast, metformin reduced fasting and glucose-stimulated glycemia, suppressed energy intake, and augmented total and intact GLP-1, total GIP, and glucagon in type 2 diabetic subjects, with no additional glucose lowering when combined with sitagliptin. Metformin 13-22 gastric inhibitory polypeptide Homo sapiens 142-145 24696447-6 2014 Based on these data, we conclude that the rate of small intestinal glucose exposure (i.e., glucose load) is a major determinant of the comparative secretion of GIP and GLP-1, as well as the magnitude of the incretin effect and GIGD in health and type 2 diabetes. Glucose 67-74 gastric inhibitory polypeptide Homo sapiens 160-163 24696447-6 2014 Based on these data, we conclude that the rate of small intestinal glucose exposure (i.e., glucose load) is a major determinant of the comparative secretion of GIP and GLP-1, as well as the magnitude of the incretin effect and GIGD in health and type 2 diabetes. Glucose 91-98 gastric inhibitory polypeptide Homo sapiens 160-163 24647737-6 2014 In contrast, metformin reduced fasting and glucose-stimulated glycemia, suppressed energy intake, and augmented total and intact GLP-1, total GIP, and glucagon in type 2 diabetic subjects, with no additional glucose lowering when combined with sitagliptin. Glucose 43-50 gastric inhibitory polypeptide Homo sapiens 142-145 24647737-4 2014 As expected, sitagliptin augmented plasma-intact GIP substantially and intact GLP-1 modestly. Sitagliptin Phosphate 13-24 gastric inhibitory polypeptide Homo sapiens 49-52 25172378-0 2014 High saturated fatty acid intake induces insulin secretion by elevating gastric inhibitory polypeptide levels in healthy individuals. Fatty Acids 5-25 gastric inhibitory polypeptide Homo sapiens 72-102 25172378-3 2014 We hypothesized that high saturated fatty acid intake increases insulin and gastric inhibitory polypeptide (GIP) secretion. Fatty Acids 26-46 gastric inhibitory polypeptide Homo sapiens 64-106 25172378-3 2014 We hypothesized that high saturated fatty acid intake increases insulin and gastric inhibitory polypeptide (GIP) secretion. Fatty Acids 26-46 gastric inhibitory polypeptide Homo sapiens 108-111 25172378-12 2014 These results suggest that a high saturated fatty acid content stimulates postprandial insulin release via increased GIP secretion. Fatty Acids 34-54 gastric inhibitory polypeptide Homo sapiens 117-120 24210541-11 2014 Oral glucose-stimulated GIP levels decreased sharply. Glucose 5-12 gastric inhibitory polypeptide Homo sapiens 24-27 24442463-8 2014 After 1 year of exenatide treatment, decreased glucagon, active GLP-1, and total GIP levels were observed following a meal, suggesting that exenatide might affect these hormonal reactions. Exenatide 140-149 gastric inhibitory polypeptide Homo sapiens 81-84 24382171-5 2014 A number of studies have demonstrated that activation of T1R2-T1R3 by natural sugars and artificial sweeteners leads to secretion of glucagon-like peptides 1&2 (GLP-1 and GLP-2) and glucose dependent insulinotropic peptide (GIP). Sugars 78-84 gastric inhibitory polypeptide Homo sapiens 186-226 24382171-5 2014 A number of studies have demonstrated that activation of T1R2-T1R3 by natural sugars and artificial sweeteners leads to secretion of glucagon-like peptides 1&2 (GLP-1 and GLP-2) and glucose dependent insulinotropic peptide (GIP). Sugars 78-84 gastric inhibitory polypeptide Homo sapiens 228-231 24442463-6 2014 The patient"s levels of insulin, glucagon, active GLP-1, and total GIP also decreased after 1 year of exenatide treatment. Exenatide 102-111 gastric inhibitory polypeptide Homo sapiens 67-70 24442463-8 2014 After 1 year of exenatide treatment, decreased glucagon, active GLP-1, and total GIP levels were observed following a meal, suggesting that exenatide might affect these hormonal reactions. Exenatide 16-25 gastric inhibitory polypeptide Homo sapiens 81-84 24667753-0 2014 Palmitic acid in the sn-2 position decreases glucose-dependent insulinotropic polypeptide secretion in healthy adults. Palmitic Acid 0-13 gastric inhibitory polypeptide Homo sapiens 45-89 24595454-0 2014 Combining gemcitabine, cisplatin, and ifosfamide (GIP) is active in patients with relapsed metastatic germ-cell tumors (GCT): a prospective multicenter GETUG phase II trial. gemcitabine 10-21 gastric inhibitory polypeptide Homo sapiens 50-53 24595454-0 2014 Combining gemcitabine, cisplatin, and ifosfamide (GIP) is active in patients with relapsed metastatic germ-cell tumors (GCT): a prospective multicenter GETUG phase II trial. Ifosfamide 38-48 gastric inhibitory polypeptide Homo sapiens 50-53 24595454-11 2014 CONCLUSION: In a multicenter context, four cycles of the GIP regimen achieved a high CR rate in patients with relapsed testicular GCT. Chromium 85-87 gastric inhibitory polypeptide Homo sapiens 57-60 24667753-6 2014 GIP release was lower (P<0.001) for IPO and lard compared with HOS and PO meals; the maximal increments (geometric mean and 95% confidence interval) for HOS, PO, IPO and lard were 515 (468, 569), 492 (448, 540), 398 (350, 452) and 395 (364, 429) ng/l, respectively. PARA-IODO-D-PHENYLALANINE HYDROXAMIC ACID 39-42 gastric inhibitory polypeptide Homo sapiens 0-3 24512489-8 2014 Glucose uptake studies and insulin signaling in human adipocytes revealed GIP as an insulin-sensitizer incretin. Glucose 0-7 gastric inhibitory polypeptide Homo sapiens 74-77 24667753-6 2014 GIP release was lower (P<0.001) for IPO and lard compared with HOS and PO meals; the maximal increments (geometric mean and 95% confidence interval) for HOS, PO, IPO and lard were 515 (468, 569), 492 (448, 540), 398 (350, 452) and 395 (364, 429) ng/l, respectively. PARA-IODO-D-PHENYLALANINE HYDROXAMIC ACID 165-168 gastric inhibitory polypeptide Homo sapiens 0-3 24667753-8 2014 CONCLUSIONS: Dietary TAGs with an increased proportion of palmitic acid in the sn-2 position do not have acute adverse effects on the insulin and glucose response to meals in healthy men and women, but they decrease GIP release. Palmitic Acid 58-71 gastric inhibitory polypeptide Homo sapiens 216-219 24307436-10 2014 CONCLUSION: During the initial 6-month postoperative period, LGCP induces significant weight loss and improves the metabolic profile of morbidly obese T2DM patients, while it also decreases circulating postprandial ghrelin levels and increases the meal-induced GIP response. lgcp 61-65 gastric inhibitory polypeptide Homo sapiens 261-264 24699248-11 2014 Sitagliptin increased active GLP-1, but caused a profound suppression of total PYY, GLP-1, and GIP when dosed alone or with GSK263. Sitagliptin Phosphate 0-11 gastric inhibitory polypeptide Homo sapiens 95-98 24446656-3 2014 Carriers of the functional variant GIPR Glu354Gln (rs1800437) have higher plasma glucose 2 hours after glucose ingestion, suggesting that the variant encoding GIPR 354Gln decreases the effect of GIP. Glucose 81-88 gastric inhibitory polypeptide Homo sapiens 35-38 24446656-3 2014 Carriers of the functional variant GIPR Glu354Gln (rs1800437) have higher plasma glucose 2 hours after glucose ingestion, suggesting that the variant encoding GIPR 354Gln decreases the effect of GIP. Glucose 103-110 gastric inhibitory polypeptide Homo sapiens 35-38 24354574-3 2014 The insulin secretion rate is higher after oral compared with intravenous glucose administration due to the release of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) enhancing the glucose-induced insulin secretion (the incretin effect). Glucose 74-81 gastric inhibitory polypeptide Homo sapiens 155-199 24354574-3 2014 The insulin secretion rate is higher after oral compared with intravenous glucose administration due to the release of glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) enhancing the glucose-induced insulin secretion (the incretin effect). Glucose 74-81 gastric inhibitory polypeptide Homo sapiens 201-204 24186866-1 2014 Dipeptidyl peptidase-4 (DPP-4) inhibitors prevent degradation of incretin hormones (glucagon-like peptide 1 [GLP-1] and glucose-dependent insulinotropic polypeptide [GIP]), whereas metformin may increase GLP-1 levels. Metformin 181-190 gastric inhibitory polypeptide Homo sapiens 166-169 24423311-0 2014 Glucose-dependent insulinotropic polypeptide: blood glucose stabilizing effects in patients with type 2 diabetes. Glucose 52-59 gastric inhibitory polypeptide Homo sapiens 0-44 24423311-2 2014 OBJECTIVE: We aimed to evaluate the importance of the prevailing plasma glucose levels for the effect of GIP on responses of glucagon and insulin and glucose disposal in patients with T2DM. Glucose 72-79 gastric inhibitory polypeptide Homo sapiens 105-108 24423311-2 2014 OBJECTIVE: We aimed to evaluate the importance of the prevailing plasma glucose levels for the effect of GIP on responses of glucagon and insulin and glucose disposal in patients with T2DM. Glucagon 125-133 gastric inhibitory polypeptide Homo sapiens 105-108 24423311-7 2014 RESULTS: During fasting glycemia (plasma glucose ~8 mmol/L), GIP elicited significant increments in both insulin and glucagon levels, resulting in neutral effects on plasma glucose. Glucose 41-48 gastric inhibitory polypeptide Homo sapiens 61-64 24423311-7 2014 RESULTS: During fasting glycemia (plasma glucose ~8 mmol/L), GIP elicited significant increments in both insulin and glucagon levels, resulting in neutral effects on plasma glucose. Glucagon 117-125 gastric inhibitory polypeptide Homo sapiens 61-64 24423311-7 2014 RESULTS: During fasting glycemia (plasma glucose ~8 mmol/L), GIP elicited significant increments in both insulin and glucagon levels, resulting in neutral effects on plasma glucose. Glucose 173-180 gastric inhibitory polypeptide Homo sapiens 61-64 24423311-8 2014 During insulin-induced hypoglycemia (plasma glucose ~3 mmol/L), GIP elicited a minor early-phase insulin response and increased glucagon levels during the initial 30 minutes, resulting in less glucose needed to be infused to maintain the clamp (29 +- 8 vs 49 +- 12 mg x kg(-1), P < .03). Glucose 44-51 gastric inhibitory polypeptide Homo sapiens 64-67 24423311-8 2014 During insulin-induced hypoglycemia (plasma glucose ~3 mmol/L), GIP elicited a minor early-phase insulin response and increased glucagon levels during the initial 30 minutes, resulting in less glucose needed to be infused to maintain the clamp (29 +- 8 vs 49 +- 12 mg x kg(-1), P < .03). Glucagon 128-136 gastric inhibitory polypeptide Homo sapiens 64-67 24423311-8 2014 During insulin-induced hypoglycemia (plasma glucose ~3 mmol/L), GIP elicited a minor early-phase insulin response and increased glucagon levels during the initial 30 minutes, resulting in less glucose needed to be infused to maintain the clamp (29 +- 8 vs 49 +- 12 mg x kg(-1), P < .03). Glucose 193-200 gastric inhibitory polypeptide Homo sapiens 64-67 24423311-9 2014 During hyperglycemia (1.5 x fasting plasma glucose ~12 mmol/L), GIP augmented insulin secretion throughout the clamp, with slightly less glucagon suppression compared with saline, resulting in more glucose needed to maintain the clamp during GIP infusions (265 +- 21 vs 213 +- 13 mg x kg(-1), P < .001). Glucose 43-50 gastric inhibitory polypeptide Homo sapiens 64-67 24423311-9 2014 During hyperglycemia (1.5 x fasting plasma glucose ~12 mmol/L), GIP augmented insulin secretion throughout the clamp, with slightly less glucagon suppression compared with saline, resulting in more glucose needed to maintain the clamp during GIP infusions (265 +- 21 vs 213 +- 13 mg x kg(-1), P < .001). Glucose 198-205 gastric inhibitory polypeptide Homo sapiens 64-67 24423311-11 2014 In contrast, during hyperglycemia, GIP increases glucose disposal through a predominant effect on insulin release. Glucose 49-56 gastric inhibitory polypeptide Homo sapiens 35-38 23736366-2 2014 Recently, we showed that GIP in combination with hyperinsulinemia and hyperglycemia increases triglyceride uptake in abdominal, subcutaneous adipose tissue in lean humans. Triglycerides 94-106 gastric inhibitory polypeptide Homo sapiens 25-28 24186866-8 2014 In conclusion, sitagliptin increased intact GLP-1 and GIP through DPP-4 inhibition but reduced total GLP-1 and GIP (feedback inhibition) without affecting the numerical contribution of the incretin effect. Sitagliptin Phosphate 15-26 gastric inhibitory polypeptide Homo sapiens 54-57 24186866-8 2014 In conclusion, sitagliptin increased intact GLP-1 and GIP through DPP-4 inhibition but reduced total GLP-1 and GIP (feedback inhibition) without affecting the numerical contribution of the incretin effect. Sitagliptin Phosphate 15-26 gastric inhibitory polypeptide Homo sapiens 111-114 24489924-1 2014 BACKGROUND & AIMS: The incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal peptide hormones regulating postprandial insulin release from pancreatic beta-cells. Adenosine Monophosphate 12-15 gastric inhibitory polypeptide Homo sapiens 73-117 24489924-1 2014 BACKGROUND & AIMS: The incretins glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gastrointestinal peptide hormones regulating postprandial insulin release from pancreatic beta-cells. Adenosine Monophosphate 12-15 gastric inhibitory polypeptide Homo sapiens 119-122 23835687-6 2013 GIP increased glucagon concentrations slightly before nutrient delivery (P=0.03), but not thereafter. Glucagon 14-22 gastric inhibitory polypeptide Homo sapiens 0-3 24195618-0 2013 Resistant starch intake at breakfast affects postprandial responses in type 2 diabetics and enhances the glucose-dependent insulinotropic polypeptide--insulin relationship following a second meal. Starch 10-16 gastric inhibitory polypeptide Homo sapiens 105-149 24843724-1 2013 Dipeptidyl peptidase (DPP)-4 inhibitors are a new class of antidiabetic drugs that increase incretin hormone levels to enhance blood sugar level-dependent insulinotropic effects, suppress glucagon action, and reduce bowel motility. Sugars 133-138 gastric inhibitory polypeptide Homo sapiens 92-108 24843724-1 2013 Dipeptidyl peptidase (DPP)-4 inhibitors are a new class of antidiabetic drugs that increase incretin hormone levels to enhance blood sugar level-dependent insulinotropic effects, suppress glucagon action, and reduce bowel motility. Glucagon 188-196 gastric inhibitory polypeptide Homo sapiens 92-108 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. Glucagon 148-156 gastric inhibitory polypeptide Homo sapiens 36-80 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. Glucagon 148-156 gastric inhibitory polypeptide Homo sapiens 82-85 24151959-8 2014 Amylin and GIP levels were strongly associated with triglycerides concentrations (P < 0.001, for both peptides) in children with CD. Triglycerides 52-65 gastric inhibitory polypeptide Homo sapiens 11-14 25509885-1 2014 AIM: To study the secretion of glucagon-like peptide 1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP),and glucagon- like peptide 2 (GLP-2) in response to a carbohydrate load in people with risk factors for type 2 diabetes mellitus (DM2) in relation to the type of carbohydrate metabolic disturbances and age. Carbohydrates 169-181 gastric inhibitory polypeptide Homo sapiens 64-108 25509885-8 2014 This may suggest that GLP-1 and the two other hormones (GLP-2 and GIP) show opposite effect in the regulatory mechanisms of carbohydrate metabolism. Carbohydrates 124-136 gastric inhibitory polypeptide Homo sapiens 66-69 24321717-10 2013 Total plasma GIP was higher in the pre-lunch period (p=0.05), but not in the post-lunch period (p=0.95), with metformin compared with placebo. Metformin 110-119 gastric inhibitory polypeptide Homo sapiens 13-16 24321717-12 2013 Metformin, independent of exercise, significantly increased total plasma GLP-1 and GIP concentrations in these patients. Metformin 0-9 gastric inhibitory polypeptide Homo sapiens 83-86 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 gastric inhibitory polypeptide Homo sapiens 123-126 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 gastric inhibitory polypeptide Homo sapiens 77-121 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 gastric inhibitory polypeptide Homo sapiens 123-126 24065842-1 2013 OBJECTIVE: To investigate glucose-dependent insulinotropic polypeptide (GIP) secretion in patients with type 2 diabetes and nondiabetic control subjects during oral glucose or meal tests. Glucose 26-33 gastric inhibitory polypeptide Homo sapiens 72-75 24065842-8 2013 CONCLUSIONS: Our results suggest that patients with type 2 diabetes are characterized by preserved GIP secretion in response to oral glucose and meal tests. Glucose 133-140 gastric inhibitory polypeptide Homo sapiens 99-102 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 gastric inhibitory polypeptide Homo sapiens 82-85 24018562-2 2013 beta cell responses to glucose and to incretins such as glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are altered in the disease state. Glucose 23-30 gastric inhibitory polypeptide Homo sapiens 138-141 23559122-1 2013 PURPOSE: The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) help regulate postprandial triacylglycerol (TAG) and insulin concentrations, but the effects of acute aerobic exercise on GLP-1 or GIP responses are unclear. Triglycerides 145-160 gastric inhibitory polypeptide Homo sapiens 67-111 23559122-1 2013 PURPOSE: The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) help regulate postprandial triacylglycerol (TAG) and insulin concentrations, but the effects of acute aerobic exercise on GLP-1 or GIP responses are unclear. Triglycerides 145-160 gastric inhibitory polypeptide Homo sapiens 113-116 23179201-10 2013 Ghrelin, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) production were lower after intake of the CHO constituent (P ranging from <0.001 to 0.019) compared with glucose, and GIP was lower after ingestion of the new DSF (P = 0.002) than after the control product. CAV protocol 134-137 gastric inhibitory polypeptide Homo sapiens 45-85 23864340-7 2013 GIP secretion among diabetic patients was increased on both occasions (82.9 pmol/l (55.9-109.8) vs 47.1 (43.8-50.4) for oral glucose and 130.6 (92.5-168.7) vs 83.2 (77.5-88.9) for mixed meal, both P<0.05). Glucose 125-132 gastric inhibitory polypeptide Homo sapiens 0-3 23864340-9 2013 GIP (tAUC per hour) was positively related to fasting and postprandial triglycerides. Triglycerides 71-84 gastric inhibitory polypeptide Homo sapiens 0-3 23864340-10 2013 Higher fasting GIP levels were related to higher fasting and postprandial triglyceride levels and ALT. Triglycerides 74-86 gastric inhibitory polypeptide Homo sapiens 15-18 23707531-2 2013 The incretin hormones such as glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are released from the small intestine into the vasculature during a meal, and these incretins have a potential to release insulin from pancreatic beta cells of islets of Langerhans, affording a glucose-lowering action. Glucose 66-73 gastric inhibitory polypeptide Homo sapiens 112-115 23179201-10 2013 Ghrelin, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) production were lower after intake of the CHO constituent (P ranging from <0.001 to 0.019) compared with glucose, and GIP was lower after ingestion of the new DSF (P = 0.002) than after the control product. CAV protocol 134-137 gastric inhibitory polypeptide Homo sapiens 87-90 23179201-10 2013 Ghrelin, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) production were lower after intake of the CHO constituent (P ranging from <0.001 to 0.019) compared with glucose, and GIP was lower after ingestion of the new DSF (P = 0.002) than after the control product. CAV protocol 134-137 gastric inhibitory polypeptide Homo sapiens 213-216 23179201-10 2013 Ghrelin, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) production were lower after intake of the CHO constituent (P ranging from <0.001 to 0.019) compared with glucose, and GIP was lower after ingestion of the new DSF (P = 0.002) than after the control product. Glucose 45-52 gastric inhibitory polypeptide Homo sapiens 87-90 23564914-6 2013 CONCLUSIONS: Glutamine does not lower glycemia after ID glucose, despite stimulating GLP-1, GIP, and insulin, probably due to increased glucagon. Glutamine 13-22 gastric inhibitory polypeptide Homo sapiens 92-95 23663508-9 2013 CONCLUSIONS & INFERENCES: Patients with idiopathic gastroparesis exhibit abnormal GIP levels associated with impaired insulin sensitivity during oral glucose load. Adenosine Monophosphate 13-16 gastric inhibitory polypeptide Homo sapiens 86-89 23663508-9 2013 CONCLUSIONS & INFERENCES: Patients with idiopathic gastroparesis exhibit abnormal GIP levels associated with impaired insulin sensitivity during oral glucose load. Glucose 154-161 gastric inhibitory polypeptide Homo sapiens 86-89 23689510-6 2013 A crystal structure of Gipg013 Fab in complex with the human GIPr extracellular domain (ECD) shows that the antibody binds through a series of hydrogen bonds from the complementarity-determining regions of Gipg013 Fab to the N-terminal alpha-helix of GIPr ECD as well as to residues around its highly conserved glucagon receptor subfamily recognition fold. Hydrogen 143-151 gastric inhibitory polypeptide Homo sapiens 251-259 23684623-1 2013 Incretin peptides, principally GLP-1 and GIP, regulate islet hormone secretion, glucose concentrations, lipid metabolism, gut motility, appetite and body weight, and immune function, providing a scientific basis for utilizing incretin-based therapies in the treatment of type 2 diabetes. Glucose 80-87 gastric inhibitory polypeptide Homo sapiens 41-44 23433601-12 2013 The LX4211 + sitagliptin combination was associated with significantly increased active GLP-1, total GLP-1, and total PYY; with a significant reduction in total GIP; and with a significantly improved blood glucose level, with less insulin, compared with sitagliptin monotherapy. (2S,3R,4R,5S,6R)-2-(4-chloro-3-(4-ethoxybenzyl)phenyl)-6-(methylthio)tetrahydro-2H-pyran-3,4,5-triol 4-10 gastric inhibitory polypeptide Homo sapiens 161-164 23697612-4 2013 By inhibiting the dipeptidyl peptidase-4 (DPP-4) enzyme, it is possible to slow the inactivation of GLP-1 and GIP, promoting blood glucose level reduction in a glucose-dependent manner. Glucose 131-138 gastric inhibitory polypeptide Homo sapiens 110-113 23697612-4 2013 By inhibiting the dipeptidyl peptidase-4 (DPP-4) enzyme, it is possible to slow the inactivation of GLP-1 and GIP, promoting blood glucose level reduction in a glucose-dependent manner. Glucose 160-167 gastric inhibitory polypeptide Homo sapiens 110-113 23433601-12 2013 The LX4211 + sitagliptin combination was associated with significantly increased active GLP-1, total GLP-1, and total PYY; with a significant reduction in total GIP; and with a significantly improved blood glucose level, with less insulin, compared with sitagliptin monotherapy. Sitagliptin Phosphate 13-24 gastric inhibitory polypeptide Homo sapiens 161-164 23231438-0 2013 Discovery and development of exenatide: the first antidiabetic agent to leverage the multiple benefits of the incretin hormone, GLP-1. Exenatide 29-38 gastric inhibitory polypeptide Homo sapiens 110-126 23404781-9 2013 At-risk obese individuals present increased GIP levels that might play a role in determining increased glucagon secretion and inappropriate glucagon responses after glucose load, thus contributing to impaired glucose homeostasis. Glucagon 103-111 gastric inhibitory polypeptide Homo sapiens 44-47 23404781-9 2013 At-risk obese individuals present increased GIP levels that might play a role in determining increased glucagon secretion and inappropriate glucagon responses after glucose load, thus contributing to impaired glucose homeostasis. Glucagon 140-148 gastric inhibitory polypeptide Homo sapiens 44-47 23404781-9 2013 At-risk obese individuals present increased GIP levels that might play a role in determining increased glucagon secretion and inappropriate glucagon responses after glucose load, thus contributing to impaired glucose homeostasis. Glucose 165-172 gastric inhibitory polypeptide Homo sapiens 44-47 23092914-10 2013 In conclusion, GIP induces an inflammatory and prolipolytic response via the PKA -NF-kappaB-IL-1 pathway and impairs insulin sensitivity of glucose uptake in human adipocytes. Glucose 140-147 gastric inhibitory polypeptide Homo sapiens 15-18 23708181-8 2013 Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) were completely suppressed during the 75 g-OGTT following subcutaneous injection of octreotide. Octreotide 171-181 gastric inhibitory polypeptide Homo sapiens 36-80 23708181-8 2013 Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) were completely suppressed during the 75 g-OGTT following subcutaneous injection of octreotide. Octreotide 171-181 gastric inhibitory polypeptide Homo sapiens 82-85 23220949-6 2013 In the meal tolerance test, active GLP-1 values before and after acarbose administration were 17.0 +- 5.8 and 24.1 +- 9.3 pmol hr/mL (p=0.054), respectively, showing an increasing tendency, and total GIP(AUC0-180) values were 685.9 +- 209.7 and 404.4 +- 173.7 pmol hr/mL, respectively, showing a significant decrease (p=0.010). Acarbose 65-73 gastric inhibitory polypeptide Homo sapiens 200-203 23055336-8 2012 GIP levels decreased when sitagliptin or miglitol, or both, were added to insulin therapy. Sitagliptin Phosphate 26-37 gastric inhibitory polypeptide Homo sapiens 0-3 23280845-13 2012 Frataxin deficiency sensitized beta cells to oleate-induced and endoplasmic reticulum stress-induced apoptosis, which could be prevented by the incretins glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide. Oleic Acid 45-51 gastric inhibitory polypeptide Homo sapiens 182-226 22960196-0 2012 In vivo effect of glucose-dependent insulinotropic peptide (GIP) on the gene expression of calcitonin peptides in human subcutaneous adipose tissue. Glucose 18-25 gastric inhibitory polypeptide Homo sapiens 60-63 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 gastric inhibitory polypeptide Homo sapiens 122-125 22302537-10 2012 The postsurgical GIP response was significantly associated with the glucagon response throughout the meal test (rho = 0.747; P < 0.01). Glucagon 68-76 gastric inhibitory polypeptide Homo sapiens 17-20 23110260-3 2012 The DPP IV inhibitors saxagliptin, vildagliptin, linagliptin, alogliptin and sitagliptin function by inhibiting the enzyme DPP IV, which breaks down GLP-1 and GIP, and have had significant success. Vildagliptin 35-47 gastric inhibitory polypeptide Homo sapiens 159-162 23110260-3 2012 The DPP IV inhibitors saxagliptin, vildagliptin, linagliptin, alogliptin and sitagliptin function by inhibiting the enzyme DPP IV, which breaks down GLP-1 and GIP, and have had significant success. Linagliptin 49-60 gastric inhibitory polypeptide Homo sapiens 159-162 23110260-3 2012 The DPP IV inhibitors saxagliptin, vildagliptin, linagliptin, alogliptin and sitagliptin function by inhibiting the enzyme DPP IV, which breaks down GLP-1 and GIP, and have had significant success. alogliptin 62-72 gastric inhibitory polypeptide Homo sapiens 159-162 23110260-3 2012 The DPP IV inhibitors saxagliptin, vildagliptin, linagliptin, alogliptin and sitagliptin function by inhibiting the enzyme DPP IV, which breaks down GLP-1 and GIP, and have had significant success. Sitagliptin Phosphate 77-88 gastric inhibitory polypeptide Homo sapiens 159-162 22923655-1 2012 Glucose-dependent insulinotropic polypeptide reduces fat-specific expression and activity of 11beta-hydroxysteroid dehydrogenase type 1 and inhibits release of free fatty acids. Fatty Acids, Nonesterified 160-176 gastric inhibitory polypeptide Homo sapiens 0-44 23110260-3 2012 The DPP IV inhibitors saxagliptin, vildagliptin, linagliptin, alogliptin and sitagliptin function by inhibiting the enzyme DPP IV, which breaks down GLP-1 and GIP, and have had significant success. saxagliptin 22-33 gastric inhibitory polypeptide Homo sapiens 159-162 22876914-7 2012 Leu and Asp residues in the consensus sequence were identified to be critical for binding to GIP through site-directed mutagenesis studies. Leucine 0-3 gastric inhibitory polypeptide Homo sapiens 93-96 22876914-7 2012 Leu and Asp residues in the consensus sequence were identified to be critical for binding to GIP through site-directed mutagenesis studies. Aspartic Acid 8-11 gastric inhibitory polypeptide Homo sapiens 93-96 22876914-8 2012 Structure-based models of GIP bound to two different surrogate peptides determined from nuclear magnetic resonance constraints revealed that the binding pocket is flexible enough to accommodate either the smaller carboxylate (COO(-)) group of a C-terminal recognition motif or the bulkier aspartate side chain (CH(2)COO(-)) of an internal motif. carboxylate 213-224 gastric inhibitory polypeptide Homo sapiens 26-29 22876914-8 2012 Structure-based models of GIP bound to two different surrogate peptides determined from nuclear magnetic resonance constraints revealed that the binding pocket is flexible enough to accommodate either the smaller carboxylate (COO(-)) group of a C-terminal recognition motif or the bulkier aspartate side chain (CH(2)COO(-)) of an internal motif. carboxyl radical 226-233 gastric inhibitory polypeptide Homo sapiens 26-29 22876914-8 2012 Structure-based models of GIP bound to two different surrogate peptides determined from nuclear magnetic resonance constraints revealed that the binding pocket is flexible enough to accommodate either the smaller carboxylate (COO(-)) group of a C-terminal recognition motif or the bulkier aspartate side chain (CH(2)COO(-)) of an internal motif. Aspartic Acid 289-298 gastric inhibitory polypeptide Homo sapiens 26-29 22745245-1 2012 CONTEXT: Sitagliptin is an inhibitor of the enzyme dipeptidyl peptidase-IV (DPP-IV), which degrades the incretins, glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide, and thus, sitagliptin increases their bioavailability. Sitagliptin Phosphate 9-20 gastric inhibitory polypeptide Homo sapiens 143-187 22745245-1 2012 CONTEXT: Sitagliptin is an inhibitor of the enzyme dipeptidyl peptidase-IV (DPP-IV), which degrades the incretins, glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide, and thus, sitagliptin increases their bioavailability. Sitagliptin Phosphate 199-210 gastric inhibitory polypeptide Homo sapiens 143-187 22738299-8 2012 Sitagliptin reduced plasma glucagon between 75 and 120 min (P < 0.05), and increased intact GLP-1 (P = 0.0002) and intact GIP (P = 0.0001) by approximately twofold, but reduced total GIP (P = 0.0003) and had no effect on total GLP-1 (P = 0.16) or insulin (P = 0.75). Sitagliptin Phosphate 0-11 gastric inhibitory polypeptide Homo sapiens 125-128 22738299-8 2012 Sitagliptin reduced plasma glucagon between 75 and 120 min (P < 0.05), and increased intact GLP-1 (P = 0.0002) and intact GIP (P = 0.0001) by approximately twofold, but reduced total GIP (P = 0.0003) and had no effect on total GLP-1 (P = 0.16) or insulin (P = 0.75). Sitagliptin Phosphate 0-11 gastric inhibitory polypeptide Homo sapiens 186-189 22738299-9 2012 On sitagliptin the initial rise in blood glucose (r = -0.66, P = 0.008) and the intact GIP response (r = -0.66, P = 0.007) were inversely related, whereas the intact GLP-1 response was related directly (r = 0.52, P = 0.05) to the T50. Sitagliptin Phosphate 3-14 gastric inhibitory polypeptide Homo sapiens 87-90 22192426-7 2012 RESULT: SKL-14959 selectively bound to GIP receptor and inhibited GIP-stimulated cAMP production with the Ki value of 55 nM and an IC(50) value of 2.9 microM, respectively. skl-14959 8-17 gastric inhibitory polypeptide Homo sapiens 39-42 22587735-2 2012 By inhibiting the DPP-4 enzyme, these drugs slow the inactivation of the endogenous incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), in turn reducing blood glucose levels in a glucose-dependent manner. Glucose 213-220 gastric inhibitory polypeptide Homo sapiens 138-182 22587735-2 2012 By inhibiting the DPP-4 enzyme, these drugs slow the inactivation of the endogenous incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), in turn reducing blood glucose levels in a glucose-dependent manner. Glucose 213-220 gastric inhibitory polypeptide Homo sapiens 184-187 22192426-2 2012 GIP plays a role in the glucose and lipid metabolism, and is associated with obesity and insulin resistance. Glucose 24-31 gastric inhibitory polypeptide Homo sapiens 0-3 22934027-2 2012 In addition to insulin and glucagon produced by pancreatic islets, two incretin hormones, namely glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP, also known as glucose-dependent insulinotropic peptide), also play important roles in blood glucose homeostasis. Glucose 184-191 gastric inhibitory polypeptide Homo sapiens 165-168 22522617-1 2012 Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion (GSIS). Glucose 63-70 gastric inhibitory polypeptide Homo sapiens 0-44 22522617-1 2012 Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-stimulated insulin secretion (GSIS). Glucose 63-70 gastric inhibitory polypeptide Homo sapiens 46-49 22192426-7 2012 RESULT: SKL-14959 selectively bound to GIP receptor and inhibited GIP-stimulated cAMP production with the Ki value of 55 nM and an IC(50) value of 2.9 microM, respectively. skl-14959 8-17 gastric inhibitory polypeptide Homo sapiens 66-69 22192426-7 2012 RESULT: SKL-14959 selectively bound to GIP receptor and inhibited GIP-stimulated cAMP production with the Ki value of 55 nM and an IC(50) value of 2.9 microM, respectively. Cyclic AMP 81-85 gastric inhibitory polypeptide Homo sapiens 66-69 22192426-8 2012 SKL-14959 Na significantly increased blood glucose levels, inhibited insulin secretion in OGTT and inhibited the plasma glucose lowering of exogenous GIP in IPGTT. skl-14959 0-9 gastric inhibitory polypeptide Homo sapiens 150-153 22192426-8 2012 SKL-14959 Na significantly increased blood glucose levels, inhibited insulin secretion in OGTT and inhibited the plasma glucose lowering of exogenous GIP in IPGTT. Glucose 120-127 gastric inhibitory polypeptide Homo sapiens 150-153 22297815-4 2012 Peak concentrations of GLP-1 and GIP following an enteral lipid stimulus (Liposyn) were significantly higher in intestinal lymph than portal venous plasma. safflower oil, soybean oil, lecithin emulsion 74-81 gastric inhibitory polypeptide Homo sapiens 33-36 22581648-6 2012 GIP, an analogue of cyclic AMP or inhibitors of NADPH oxidase inhibited the AGE-induced reactive oxygen species (ROS) generation in HUVECs. Cyclic AMP 20-30 gastric inhibitory polypeptide Homo sapiens 0-3 22581648-6 2012 GIP, an analogue of cyclic AMP or inhibitors of NADPH oxidase inhibited the AGE-induced reactive oxygen species (ROS) generation in HUVECs. Reactive Oxygen Species 88-111 gastric inhibitory polypeptide Homo sapiens 0-3 22581648-6 2012 GIP, an analogue of cyclic AMP or inhibitors of NADPH oxidase inhibited the AGE-induced reactive oxygen species (ROS) generation in HUVECs. Reactive Oxygen Species 113-116 gastric inhibitory polypeptide Homo sapiens 0-3 22581648-9 2012 In addition, an antioxidant N-acetylcysteine mimicked the effects of GIP on RAGE and VCAM-1 gene expression in HUVECs. Acetylcysteine 28-44 gastric inhibitory polypeptide Homo sapiens 69-72 22581648-10 2012 Our present study suggests that GIP could block the signal pathways of AGEs in HUVECs by reducing ROS generation and subsequent RAGE expression probably via GIP receptor-cyclic AMP axis. Reactive Oxygen Species 98-101 gastric inhibitory polypeptide Homo sapiens 32-35 22581648-10 2012 Our present study suggests that GIP could block the signal pathways of AGEs in HUVECs by reducing ROS generation and subsequent RAGE expression probably via GIP receptor-cyclic AMP axis. Cyclic AMP 170-180 gastric inhibitory polypeptide Homo sapiens 32-35 22581648-10 2012 Our present study suggests that GIP could block the signal pathways of AGEs in HUVECs by reducing ROS generation and subsequent RAGE expression probably via GIP receptor-cyclic AMP axis. Cyclic AMP 170-180 gastric inhibitory polypeptide Homo sapiens 157-160 22297815-8 2012 The effect of L-81 relative to Liposyn alone had an even greater effect on GIP secretion, which was completely abolished (P = 0.004). l-81 14-18 gastric inhibitory polypeptide Homo sapiens 75-78 22297815-8 2012 The effect of L-81 relative to Liposyn alone had an even greater effect on GIP secretion, which was completely abolished (P = 0.004). safflower oil, soybean oil, lecithin emulsion 31-38 gastric inhibitory polypeptide Homo sapiens 75-78 22297815-9 2012 These findings of a dramatic effect of L-81 on lymph levels of GLP-1 and GIP support a strong link between intestinal lipid absorption and incretin secretion. l-81 39-43 gastric inhibitory polypeptide Homo sapiens 73-76 22297815-10 2012 The relative difference in the effect of L-81 on the two incretins provides further support that nutrient-stimulation of GIP and GLP-1 is via distinct mechanisms. l-81 41-45 gastric inhibitory polypeptide Homo sapiens 121-124 22429011-2 2012 Their mechanism of action is to decrease the inactivation of glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide, both of which are involved in maintaining euglycemia subsequent to carbohydrate intake. Carbohydrates 202-214 gastric inhibitory polypeptide Homo sapiens 89-133 22158727-7 2012 RESULTS: Both glucose and 3OMG stimulated GLP-1 and GIP release in advance of the meal (each P < 0.05), whereas TIM and sucralose did not. Glucose 14-21 gastric inhibitory polypeptide Homo sapiens 52-55 22391044-6 2012 CONCLUSION: NGT subjects with MS showed increased GIP secretion that could be responsible for the delayed glucagon suppression during the OGTT, thereby suggesting a role for incretins in regulating glucose homeostasis in this condition. Glucagon 106-114 gastric inhibitory polypeptide Homo sapiens 50-53 22391044-6 2012 CONCLUSION: NGT subjects with MS showed increased GIP secretion that could be responsible for the delayed glucagon suppression during the OGTT, thereby suggesting a role for incretins in regulating glucose homeostasis in this condition. Glucose 198-205 gastric inhibitory polypeptide Homo sapiens 50-53 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 gastric inhibitory polypeptide Homo sapiens 50-53 21752172-4 2012 This class of glucose-lowering agents enhances endogenous glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) levels by blocking the incretin-degrading enzyme DPP-4. Glucose 14-21 gastric inhibitory polypeptide Homo sapiens 94-138 21752172-4 2012 This class of glucose-lowering agents enhances endogenous glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) levels by blocking the incretin-degrading enzyme DPP-4. Glucose 14-21 gastric inhibitory polypeptide Homo sapiens 140-143 22349073-0 2012 Fasting and oral glucose-stimulated levels of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are highly familial traits. Glucose 17-24 gastric inhibitory polypeptide Homo sapiens 46-90 22349073-0 2012 Fasting and oral glucose-stimulated levels of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are highly familial traits. Glucose 17-24 gastric inhibitory polypeptide Homo sapiens 92-95 22385133-7 2012 Postprandial TAG, insulin, and GIP concentrations were significantly lower after the DAG meal compared with the TAG meal in 26 subjects with fasting serum TAG levels between 1.36 and 2.83 mmol/L. Diglycerides 85-88 gastric inhibitory polypeptide Homo sapiens 31-34 22339447-23 2012 Vildagliptin significantly increases the active glucagon-like peptide 1 (GLP-1) levels by approximately 2- to 3-fold and glucose-dependent insulinotropic polypeptide (GIP) levels by approximately 5-fold, and significantly suppresses the postprandial glucagon levels in response to a meal or following an oral glucose tolerance test (OGTT) in patients with T2DM. Glucose 121-128 gastric inhibitory polypeptide Homo sapiens 167-170 24843549-6 2012 RESULTS: Area under the curve (AUC)-GIP was increased in proportion to the amount of glucose, and was highest in MTT, showing that GIP secretion is also stimulated by nutrients other than glucose, such as lipid. Glucose 87-94 gastric inhibitory polypeptide Homo sapiens 38-41 24843549-6 2012 RESULTS: Area under the curve (AUC)-GIP was increased in proportion to the amount of glucose, and was highest in MTT, showing that GIP secretion is also stimulated by nutrients other than glucose, such as lipid. Glucose 87-94 gastric inhibitory polypeptide Homo sapiens 133-136 24843549-6 2012 RESULTS: Area under the curve (AUC)-GIP was increased in proportion to the amount of glucose, and was highest in MTT, showing that GIP secretion is also stimulated by nutrients other than glucose, such as lipid. monooxyethylene trimethylolpropane tristearate 115-118 gastric inhibitory polypeptide Homo sapiens 38-41 24843549-6 2012 RESULTS: Area under the curve (AUC)-GIP was increased in proportion to the amount of glucose, and was highest in MTT, showing that GIP secretion is also stimulated by nutrients other than glucose, such as lipid. monooxyethylene trimethylolpropane tristearate 115-118 gastric inhibitory polypeptide Homo sapiens 133-136 24843549-6 2012 RESULTS: Area under the curve (AUC)-GIP was increased in proportion to the amount of glucose, and was highest in MTT, showing that GIP secretion is also stimulated by nutrients other than glucose, such as lipid. Glucose 190-197 gastric inhibitory polypeptide Homo sapiens 38-41 24843549-6 2012 RESULTS: Area under the curve (AUC)-GIP was increased in proportion to the amount of glucose, and was highest in MTT, showing that GIP secretion is also stimulated by nutrients other than glucose, such as lipid. Glucose 190-197 gastric inhibitory polypeptide Homo sapiens 133-136 22105074-5 2012 Application of chimeric GLP-1/GIP peptides together with molecular modeling suggests that His(1) of GLP-1 interacts with Asn(302) of GLP1R and that Thr(7) of GLP-1 has close contact with a binding pocket formed by Ile(196), Leu(232), and Met(233) of GLP1R. Threonine 148-151 gastric inhibitory polypeptide Homo sapiens 30-33 22179810-0 2012 Glucose-dependent insulinotropic polypeptide reduces fat-specific expression and activity of 11beta-hydroxysteroid dehydrogenase type 1 and inhibits release of free fatty acids. Fatty Acids, Nonesterified 160-176 gastric inhibitory polypeptide Homo sapiens 0-44 22179810-2 2012 GIP also reportedly increased glucose uptake and inhibition of lipolysis in adipocytes after inhibition of the intracellular cortisone-cortisol shuttle 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1). Glucose 30-37 gastric inhibitory polypeptide Homo sapiens 0-3 22179810-2 2012 GIP also reportedly increased glucose uptake and inhibition of lipolysis in adipocytes after inhibition of the intracellular cortisone-cortisol shuttle 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1). cortisone-cortisol 125-143 gastric inhibitory polypeptide Homo sapiens 0-3 22179810-6 2012 Preinhibition of 11beta-HSD1 completely abolished GIP-induced effects on FFA release. Fatty Acids, Nonesterified 73-76 gastric inhibitory polypeptide Homo sapiens 50-53 22179810-8 2012 GIP lowered circulating FFAs compared with saline control and reduced expression and ex vivo activity of 11beta-HSD1 and adipose triglyceride lipase expression in subcutaneous fat biopsies. Sodium Chloride 43-49 gastric inhibitory polypeptide Homo sapiens 0-3 21958333-2 2012 The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) stimulate glucose-induced insulin secretion; however, in patients with type 2 diabetes, the incretin system is impaired by loss of the insulinotropic effects of GIP as well as a possible reduction in secretion of GLP-1. Glucose 22-29 gastric inhibitory polypeptide Homo sapiens 68-71 21917634-8 2012 Reduced increments in response to HFO of fasting plasma leptin, PP, and GIP levels may contribute to insulin resistance, lower satiety, and impaired insulin secretion in LBW subjects. 1,3,3,3-tetrafluoropropene 34-37 gastric inhibitory polypeptide Homo sapiens 72-75 21958333-2 2012 The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) stimulate glucose-induced insulin secretion; however, in patients with type 2 diabetes, the incretin system is impaired by loss of the insulinotropic effects of GIP as well as a possible reduction in secretion of GLP-1. Glucose 22-29 gastric inhibitory polypeptide Homo sapiens 270-273 21984584-0 2011 Glucose-dependent insulinotropic polypeptide: a bifunctional glucose-dependent regulator of glucagon and insulin secretion in humans. Glucose 61-68 gastric inhibitory polypeptide Homo sapiens 0-44 22509144-10 2012 There was also a significant (p < 0.05) difference at T30 in GIP levels in response to the control compared to starch gelatinised with alpha- or beta-casein. Starch 114-120 gastric inhibitory polypeptide Homo sapiens 64-67 23125920-5 2012 DPP-4 inhibitors such as sitagliptin and linagliptin prevent the inactivation of endogenous GLP-1 and GIP through competitive inhibition of the DPP-4 enzyme. Sitagliptin Phosphate 25-36 gastric inhibitory polypeptide Homo sapiens 102-105 23125920-5 2012 DPP-4 inhibitors such as sitagliptin and linagliptin prevent the inactivation of endogenous GLP-1 and GIP through competitive inhibition of the DPP-4 enzyme. Linagliptin 41-52 gastric inhibitory polypeptide Homo sapiens 102-105 22412906-0 2012 Regulation of GIP and GLP1 receptor cell surface expression by N-glycosylation and receptor heteromerization. Nitrogen 63-64 gastric inhibitory polypeptide Homo sapiens 14-17 22412906-5 2012 Like many family B GPCRs, both the GIP and GLP-1 receptors possess a large extracellular N-terminus with multiple consensus sites for Asn-linked (N)-glycosylation. Asparagine 134-137 gastric inhibitory polypeptide Homo sapiens 35-38 22412906-7 2012 N-glycosylation enhances cell surface expression and function in parallel but exerts stronger control over the GIP receptor than the GLP-1 receptor. Nitrogen 0-1 gastric inhibitory polypeptide Homo sapiens 111-114 27933595-2 2012 The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) stimulate glucose-induced insulin secretion; however, in patients with type 2 diabetes, the incretin system is impaired by loss of the insulinotropic effects of GIP as well as a possible reduction in secretion of GLP-1. Glucose 22-29 gastric inhibitory polypeptide Homo sapiens 68-71 27933595-2 2012 The incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) stimulate glucose-induced insulin secretion; however, in patients with type 2 diabetes, the incretin system is impaired by loss of the insulinotropic effects of GIP as well as a possible reduction in secretion of GLP-1. Glucose 22-29 gastric inhibitory polypeptide Homo sapiens 270-273 22027830-7 2011 This insulin-sensitizing effect is specific for GIP because isoproterenol, which elevates adipocyte cAMP and activates PKA/CREB signaling, does not affect adipocyte insulin sensitivity. Isoproterenol 60-73 gastric inhibitory polypeptide Homo sapiens 48-51 21984584-1 2011 OBJECTIVE: To evaluate the glucose dependency of glucose-dependent insulinotropic polypeptide (GIP) effects on insulin and glucagon release in 10 healthy male subjects ([means +- SEM] aged 23 +- 1 years, BMI 23 +- 1 kg/m(2), and HbA(1c) 5.5 +- 0.1%). Glucagon 123-131 gastric inhibitory polypeptide Homo sapiens 95-98 21984584-3 2011 RESULTS: During hypoglycemia, GIP infusion caused greater glucagon responses during the first 30 min compared with saline (76 +- 17 vs. 28 +- 16 pmol/L per 30 min, P < 0.008), with similar peak levels of glucagon reached after 60 min. Glucagon 58-66 gastric inhibitory polypeptide Homo sapiens 30-33 21984584-3 2011 RESULTS: During hypoglycemia, GIP infusion caused greater glucagon responses during the first 30 min compared with saline (76 +- 17 vs. 28 +- 16 pmol/L per 30 min, P < 0.008), with similar peak levels of glucagon reached after 60 min. Glucagon 207-215 gastric inhibitory polypeptide Homo sapiens 30-33 21984584-4 2011 During euglycemia, GIP infusion elicited larger glucagon responses (62 +- 18 vs. -11 +- 8 pmol/L per 90 min, P < 0.005). Glucagon 48-56 gastric inhibitory polypeptide Homo sapiens 19-22 21984584-8 2011 In contrast, GIP increases glucagon levels during fasting and hypoglycemic conditions, where it has little or no effect on insulin secretion. Glucagon 27-35 gastric inhibitory polypeptide Homo sapiens 13-16 21984584-9 2011 Thus, GIP seems to be a physiological bifunctional blood glucose stabilizer with diverging glucose-dependent effects on the two main pancreatic glucoregulatory hormones. Glucose 57-64 gastric inhibitory polypeptide Homo sapiens 6-9 21984584-9 2011 Thus, GIP seems to be a physiological bifunctional blood glucose stabilizer with diverging glucose-dependent effects on the two main pancreatic glucoregulatory hormones. Glucose 91-98 gastric inhibitory polypeptide Homo sapiens 6-9 21338535-0 2011 Dietary supplementation with hydroxypropyl-distarch phosphate from waxy maize starch increases resting energy expenditure by lowering the postprandial glucose-dependent insulinotropic polypeptide response in human subjects. hydroxypropyl distarch phosphate 29-61 gastric inhibitory polypeptide Homo sapiens 151-195 22200706-1 2011 OBJECTIVE: To investigate the secretion patterns of glucose-dependent insulinotropic polypeptide (GIP) after different dietary loads in subjects with normal glucose tolerance (NGT) and their relation to insulin secretion and plasma glucose levels. Glucose 52-59 gastric inhibitory polypeptide Homo sapiens 98-101 22200706-1 2011 OBJECTIVE: To investigate the secretion patterns of glucose-dependent insulinotropic polypeptide (GIP) after different dietary loads in subjects with normal glucose tolerance (NGT) and their relation to insulin secretion and plasma glucose levels. Glucose 157-164 gastric inhibitory polypeptide Homo sapiens 52-96 22200706-1 2011 OBJECTIVE: To investigate the secretion patterns of glucose-dependent insulinotropic polypeptide (GIP) after different dietary loads in subjects with normal glucose tolerance (NGT) and their relation to insulin secretion and plasma glucose levels. Glucose 157-164 gastric inhibitory polypeptide Homo sapiens 98-101 22200706-4 2011 RESULTS: The first peak value of GIP after glucose load occurred at 15 min (45.09-+4.67 pmol/L). Glucose 43-50 gastric inhibitory polypeptide Homo sapiens 33-36 22200706-6 2011 After the mixed meal load, GIP secretion presented with two peaks: the first peak appeared at 15 min (71.69-+14.19 pmol/L) with a level significantly higher than that at 15 min following glucose load (P<0.05), and the second occurred at 90 min (55.35-+13.19 pmol/L). Glucose 187-194 gastric inhibitory polypeptide Homo sapiens 27-30 22167829-1 2011 The discovery of incretins-glucagon-like peptide (GLP)-1 and glucose-dependent insulinotrop peptide (GIP)-, clarification of their physiological properties as well as therapeutic application of incretin-based blood glucose lowering drugs opened new perspectives in the medical management of type 2 diabetes. Glucose 61-68 gastric inhibitory polypeptide Homo sapiens 101-104 22093196-1 2011 OBJECTIVES: Saxagliptin, a dipeptidyl peptidase 4 inhibitor, improves glycemic control in patients with type 2 diabetes mellitus (T2DM) by increasing endogenous active, intact glucagon-like peptide 1 and glucose-dependent insulinotropic polypeptide in response to food, which augments insulin secretion and decreases glucagon release. saxagliptin 12-23 gastric inhibitory polypeptide Homo sapiens 204-248 21586700-0 2011 Metabolomic linkage reveals functional interaction between glucose-dependent insulinotropic polypeptide and ghrelin in humans. Ghrelin 108-115 gastric inhibitory polypeptide Homo sapiens 59-103 21586700-3 2011 On the basis of the growing evidence that glucose-dependent insulinotropic polypeptide (GIP) is involved in the control of fuel metabolism, we hypothesized that GIP and/or insulin, directly or via changes in plasma metabolites, might affect circulating ghrelin. Ghrelin 253-260 gastric inhibitory polypeptide Homo sapiens 42-86 21586700-3 2011 On the basis of the growing evidence that glucose-dependent insulinotropic polypeptide (GIP) is involved in the control of fuel metabolism, we hypothesized that GIP and/or insulin, directly or via changes in plasma metabolites, might affect circulating ghrelin. Ghrelin 253-260 gastric inhibitory polypeptide Homo sapiens 88-91 21586700-3 2011 On the basis of the growing evidence that glucose-dependent insulinotropic polypeptide (GIP) is involved in the control of fuel metabolism, we hypothesized that GIP and/or insulin, directly or via changes in plasma metabolites, might affect circulating ghrelin. Ghrelin 253-260 gastric inhibitory polypeptide Homo sapiens 161-164 21586700-6 2011 The GIP and insulin effects on circulating ghrelin were analyzed within the framework of those networks. Ghrelin 43-50 gastric inhibitory polypeptide Homo sapiens 4-7 21586700-7 2011 In the HC, ghrelin levels decreased in the absence (19.2% vs. baseline, P = 0.028) as well as in the presence of GIP (33.8%, P = 0.018). Ghrelin 11-18 gastric inhibitory polypeptide Homo sapiens 113-116 21586700-8 2011 Ghrelin levels were significantly lower during HC with GIP than with placebo, despite insulin levels not differing significantly. Ghrelin 0-7 gastric inhibitory polypeptide Homo sapiens 55-58 21586700-9 2011 In the GIP network combining data on GIP-infusion, EC+GIP and HC+GIP experiments, ghrelin was integrated into hormone-metabolite networks through a connection to a group of long-chain fatty acids. Ghrelin 82-89 gastric inhibitory polypeptide Homo sapiens 7-10 21586700-9 2011 In the GIP network combining data on GIP-infusion, EC+GIP and HC+GIP experiments, ghrelin was integrated into hormone-metabolite networks through a connection to a group of long-chain fatty acids. Ghrelin 82-89 gastric inhibitory polypeptide Homo sapiens 37-40 21586700-9 2011 In the GIP network combining data on GIP-infusion, EC+GIP and HC+GIP experiments, ghrelin was integrated into hormone-metabolite networks through a connection to a group of long-chain fatty acids. Ghrelin 82-89 gastric inhibitory polypeptide Homo sapiens 37-40 21586700-9 2011 In the GIP network combining data on GIP-infusion, EC+GIP and HC+GIP experiments, ghrelin was integrated into hormone-metabolite networks through a connection to a group of long-chain fatty acids. Ghrelin 82-89 gastric inhibitory polypeptide Homo sapiens 37-40 21586700-9 2011 In the GIP network combining data on GIP-infusion, EC+GIP and HC+GIP experiments, ghrelin was integrated into hormone-metabolite networks through a connection to a group of long-chain fatty acids. long-chain fatty acids 173-195 gastric inhibitory polypeptide Homo sapiens 7-10 21586700-10 2011 In contrast, ghrelin was excluded from the network of experiments without GIP. Ghrelin 13-20 gastric inhibitory polypeptide Homo sapiens 74-77 21586700-11 2011 GIP decreased circulating ghrelin and might have affected the ghrelin system via modification of long-chain fatty acid pools. Ghrelin 26-33 gastric inhibitory polypeptide Homo sapiens 0-3 21586700-11 2011 GIP decreased circulating ghrelin and might have affected the ghrelin system via modification of long-chain fatty acid pools. Ghrelin 62-69 gastric inhibitory polypeptide Homo sapiens 0-3 21586700-11 2011 GIP decreased circulating ghrelin and might have affected the ghrelin system via modification of long-chain fatty acid pools. long-chain fatty acid 97-118 gastric inhibitory polypeptide Homo sapiens 0-3 21820006-1 2011 Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the two primary incretin hormones secreted from the intestine upon ingestion of glucose or nutrients to stimulate insulin secretion from pancreatic beta cells. Glucose 157-164 gastric inhibitory polypeptide Homo sapiens 32-35 21824261-3 2011 Gastrointestinal hormones that are secreted in response to oral glucose include glucagon-like peptide-1 (GLP-1) that strongly inhibits glucagon secretion, and GLP-2 and GIP, both of which stimulate secretion. Glucose 64-71 gastric inhibitory polypeptide Homo sapiens 169-172 21815989-2 2011 However, the GIP receptor is widely distributed in peripheral organs, including the adipose tissue, gut, bone and brain, where GIP modulates energy intake, cell metabolism and proliferation, and lipid and glucose metabolism, eventually promoting lipid and glucose storage. Glucose 205-212 gastric inhibitory polypeptide Homo sapiens 13-16 22262068-2 2011 Their plasma concentrations increase quickly following food ingestion, and carbohydrate, fat, and protein have all been shown to stimulate GLP-1 and GIP secretion. Carbohydrates 75-87 gastric inhibitory polypeptide Homo sapiens 149-152 21810601-8 2011 RESULTS: The A allele of GIPR rs10423928 was associated with impaired glucose- and GIP-stimulated insulin secretion and a decrease in BMI, lean body mass, and waist circumference. Glucose 70-77 gastric inhibitory polypeptide Homo sapiens 25-28 21913887-3 2011 These hormones perform several functions: they stimulate insulin secretion in the pancreatic beta cells; they inhibit glucagon release from the alpha cells of the pancreas (GIP not in humans); they slow down gastric emptying and may directly suppress appetite; and, moreover, they indirectly increase peripheral glucose tolerance/insulin sensitivity. Glucagon 118-126 gastric inhibitory polypeptide Homo sapiens 173-176 21677059-10 2011 In the human studies, supplementation with 4% l-arabinose produced an 11% lower glucose peak, a 33% lower and delayed insulin peak, a 23% reduction in the incremental area under the curve (iAUC) for insulin, a 23% lower and delayed C-peptide peak, a 9% reduction in the iAUC for C-peptide, a 53% increase in the iAUC for glucagon-like peptide-1 (GLP-1), and a 28% reduction in the iAUC for glucose-dependent insulinotropic polypeptide. Arabinose 46-57 gastric inhibitory polypeptide Homo sapiens 390-434 21593115-3 2011 OBJECTIVE: The aim of the study was to examine whether insulin and incretin hormone responses are higher after oral vs. iv challenge of a lipid emulsion with matching triglyceride levels in humans. Triglycerides 167-179 gastric inhibitory polypeptide Homo sapiens 67-83 21338535-0 2011 Dietary supplementation with hydroxypropyl-distarch phosphate from waxy maize starch increases resting energy expenditure by lowering the postprandial glucose-dependent insulinotropic polypeptide response in human subjects. Starch 45-51 gastric inhibitory polypeptide Homo sapiens 151-195 21338535-1 2011 The aim of the present study was to investigate the effects of hydroxypropyl-distarch phosphate (HDP) supplementation on postprandial energy metabolism and glucose-dependent insulinotropic polypeptide (GIP) in human subjects. hydroxypropyl distarch phosphate 63-95 gastric inhibitory polypeptide Homo sapiens 156-200 21338535-1 2011 The aim of the present study was to investigate the effects of hydroxypropyl-distarch phosphate (HDP) supplementation on postprandial energy metabolism and glucose-dependent insulinotropic polypeptide (GIP) in human subjects. hydroxypropyl distarch phosphate 97-100 gastric inhibitory polypeptide Homo sapiens 156-200 21386059-7 2011 The glucagon response during the IIGI + GIP + GLP-1 + GLP-2 infusion (day F) equaled the inappropriate glucagon response to OGTT (P = not significant). Glucagon 4-12 gastric inhibitory polypeptide Homo sapiens 40-43 24843483-0 2011 Plasma gastric inhibitory polypeptide and glucagon-like peptide-1 levels after glucose loading are associated with different factors in Japanese subjects. Glucose 79-86 gastric inhibitory polypeptide Homo sapiens 7-37 24843483-5 2011 RESULTS: GIP secretion (AUC-GIP) was positively associated with body mass index (P < 0.05), and area under the curve (AUC) of C-peptide (P < 0.05) and glucagon (P < 0.01), whereas GLP-1 secretion (AUC-GLP-1) was negatively associated with AUC of plasma glucose (P < 0.05). Glucose 264-271 gastric inhibitory polypeptide Homo sapiens 11-14 24843483-5 2011 RESULTS: GIP secretion (AUC-GIP) was positively associated with body mass index (P < 0.05), and area under the curve (AUC) of C-peptide (P < 0.05) and glucagon (P < 0.01), whereas GLP-1 secretion (AUC-GLP-1) was negatively associated with AUC of plasma glucose (P < 0.05). Glucose 264-271 gastric inhibitory polypeptide Homo sapiens 30-33 21386059-8 2011 The separate GIP infusion (day C) elicited significant hypersecretion of glucagon, whereas GLP-1 infusion (day D) resulted in enhancement of glucagon suppression during IIGI. Glucagon 73-81 gastric inhibitory polypeptide Homo sapiens 13-16 21386059-10 2011 Our results indicate that the intestinal hormones, GIP, GLP-1, and GLP-2, may play a role in the inappropriate glucagon response to orally ingested glucose in T2DM with, especially, GIP, acting to increase glucagon secretion. Glucagon 111-119 gastric inhibitory polypeptide Homo sapiens 51-54 21386059-10 2011 Our results indicate that the intestinal hormones, GIP, GLP-1, and GLP-2, may play a role in the inappropriate glucagon response to orally ingested glucose in T2DM with, especially, GIP, acting to increase glucagon secretion. Glucagon 111-119 gastric inhibitory polypeptide Homo sapiens 182-185 21386059-10 2011 Our results indicate that the intestinal hormones, GIP, GLP-1, and GLP-2, may play a role in the inappropriate glucagon response to orally ingested glucose in T2DM with, especially, GIP, acting to increase glucagon secretion. Glucose 148-155 gastric inhibitory polypeptide Homo sapiens 51-54 21386059-10 2011 Our results indicate that the intestinal hormones, GIP, GLP-1, and GLP-2, may play a role in the inappropriate glucagon response to orally ingested glucose in T2DM with, especially, GIP, acting to increase glucagon secretion. Glucose 148-155 gastric inhibitory polypeptide Homo sapiens 182-185 21386059-10 2011 Our results indicate that the intestinal hormones, GIP, GLP-1, and GLP-2, may play a role in the inappropriate glucagon response to orally ingested glucose in T2DM with, especially, GIP, acting to increase glucagon secretion. Glucagon 206-214 gastric inhibitory polypeptide Homo sapiens 51-54 21386059-10 2011 Our results indicate that the intestinal hormones, GIP, GLP-1, and GLP-2, may play a role in the inappropriate glucagon response to orally ingested glucose in T2DM with, especially, GIP, acting to increase glucagon secretion. Glucagon 206-214 gastric inhibitory polypeptide Homo sapiens 182-185 21595271-3 2011 Glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide(GIP) function as incretin and stimulate glucose-mediated insulin production by pancreatic beta cells. Glucose 36-43 gastric inhibitory polypeptide Homo sapiens 81-84 21595285-2 2011 As indicated in GIP receptor deficient experimental animals, GIP receptor antagonists possess favorable effects such as, decreased body adiposity or improvement of glucose intolerance through change of fat metabolism in high-fat diet induced or genetically induced obese experimental animals. Glucose 164-171 gastric inhibitory polypeptide Homo sapiens 61-64 21515744-0 2011 Dual-monoclonal, sandwich immunoassay specific for glucose-dependent insulinotropic peptide1-42, the active form of the incretin hormone. Glucose 51-58 gastric inhibitory polypeptide Homo sapiens 120-136 21515744-1 2011 BACKGROUND: Glucose-dependent insulinotropic peptide (GIP) is an incretin peptide secreted by intestinal K cells that stimulates insulin secretion in a glucose-dependent manner. Glucose 152-159 gastric inhibitory polypeptide Homo sapiens 12-52 21515744-1 2011 BACKGROUND: Glucose-dependent insulinotropic peptide (GIP) is an incretin peptide secreted by intestinal K cells that stimulates insulin secretion in a glucose-dependent manner. Glucose 152-159 gastric inhibitory polypeptide Homo sapiens 54-57 21330636-8 2011 With GIP alone, glucose was lowered slightly (P = 0.0021); insulin and C-peptide were stimulated to a lesser degree than with GLP-1 (P < 0.001). Glucose 16-23 gastric inhibitory polypeptide Homo sapiens 5-8 21595261-1 2011 Incretin hormones, GLP-1 and GIP, contribute to whole body glucose homeostasis by modulating secretion of islet hormones, insulin, glucagon and somatostatin. Glucose 59-66 gastric inhibitory polypeptide Homo sapiens 29-32 21595261-1 2011 Incretin hormones, GLP-1 and GIP, contribute to whole body glucose homeostasis by modulating secretion of islet hormones, insulin, glucagon and somatostatin. Glucagon 131-139 gastric inhibitory polypeptide Homo sapiens 29-32 21595261-3 2011 While glucagon secretion is stimulated by GIP, GLP-1 suppresses glucagon secretion. Glucagon 6-14 gastric inhibitory polypeptide Homo sapiens 42-45 21292338-5 2011 The secretions of intact glucagon-like peptide-1 (iGLP-1) and total glucose-dependent insulinotropic polypeptide (tGIP) during MTT were calculated by total and incremental area under the curve (TAUC and IAUC) values. monooxyethylene trimethylolpropane tristearate 127-130 gastric inhibitory polypeptide Homo sapiens 68-112 21210936-5 2011 The increased peak glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) response to oral glucose after GBP did not correlate with DPP-4 activity. Glucose 55-62 gastric inhibitory polypeptide Homo sapiens 101-104 21330636-10 2011 Rather, the suppression of glucagon elicited by GLP-1 was antagonized by the addition of GIP (P = 0.008). Glucagon 27-35 gastric inhibitory polypeptide Homo sapiens 89-92 21330636-13 2011 Rather, the suppression of glucagon by GLP-1 is antagonized by GIP. Glucagon 27-35 gastric inhibitory polypeptide Homo sapiens 63-66 21299928-16 2011 GIP in combination with hyperinsulinemia and hyperglycemia increased blood flow, glucose uptake, and FFA re-esterification, resulting in increased TAG deposition in abdominal, subcutaneous adipose tissue. Glucose 81-88 gastric inhibitory polypeptide Homo sapiens 0-3 21738898-1 2011 BACKGROUND: Sitagliptin is a highly selective dipeptidyl peptide-4 (DPP-4) inhibitor that increases blood levels of active glucagon-like peptide (GLP)-1 and glucose-dependent insulinotrophic polypeptide (GIP), resulting in increased insulin secretion. Sitagliptin Phosphate 12-23 gastric inhibitory polypeptide Homo sapiens 157-202 21738898-1 2011 BACKGROUND: Sitagliptin is a highly selective dipeptidyl peptide-4 (DPP-4) inhibitor that increases blood levels of active glucagon-like peptide (GLP)-1 and glucose-dependent insulinotrophic polypeptide (GIP), resulting in increased insulin secretion. Sitagliptin Phosphate 12-23 gastric inhibitory polypeptide Homo sapiens 204-207 21264796-0 2011 Transient efficacy of octreotide and pasireotide (SOM230) treatment in GIP-dependent Cushing"s syndrome. Octreotide 22-32 gastric inhibitory polypeptide Homo sapiens 71-74 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 gastric inhibitory polypeptide Homo sapiens 39-42 22127766-7 2011 Notably, the subjects with a family history of diabetes exert significantly higher GIP response in the early phase of glucose load compared with those without a family history. Glucose 118-125 gastric inhibitory polypeptide Homo sapiens 83-86 21300845-7 2011 After controlling for a GIPR variation, we showed that serum glucose concentrations of patients carrying GIP(-1920A/A) homozygotes are significantly higher than that of those carrying an ancestral GIP(-1920G) haplotype (odds ratio 3.53). Glucose 61-68 gastric inhibitory polypeptide Homo sapiens 24-27 21300845-7 2011 After controlling for a GIPR variation, we showed that serum glucose concentrations of patients carrying GIP(-1920A/A) homozygotes are significantly higher than that of those carrying an ancestral GIP(-1920G) haplotype (odds ratio 3.53). Glucose 61-68 gastric inhibitory polypeptide Homo sapiens 105-108 21300845-8 2011 CONCLUSIONS: Our proof-of-concept study indicates that common regulatory GIP variants impart a difference in GIP and glucose metabolism. Glucose 117-124 gastric inhibitory polypeptide Homo sapiens 73-76 21299928-9 2011 Due to its therapeutic potential in obesity treatment, a rapidly increasing number of functional studies are investigating effects of acute and chronic loss of GIP signaling in glucose and lipid homeostasis. Glucose 177-184 gastric inhibitory polypeptide Homo sapiens 160-163 21510839-1 2011 Dipeptidyl peptidase-IV (DPP-IV), a serine protease that specifically cleaves the N-terminal dipeptide with a preference for L-proline or L-alanine at the penultimate position, is involved in the degradation of incretin hormones, including glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Dipeptides 93-102 gastric inhibitory polypeptide Homo sapiens 276-320 21194578-1 2011 The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagonlike peptide-1 (GLP-1), which are secreted by cells of the gastrointestinal tract in response to meal ingestion, exercise important glucoregulatory effects, including the glucose-dependent potentiation of insulin secretion by pancreatic beta-cells. Glucose 23-30 gastric inhibitory polypeptide Homo sapiens 69-72 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 gastric inhibitory polypeptide Homo sapiens 111-114 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 gastric inhibitory polypeptide Homo sapiens 230-233 21537414-8 2011 The GIP concentration was elevated at 30 minutes and 60 minutes in the pGDM group. 9-hydroxy-11,15-dioxo-2,3,18,19-tetranorprost-5-ene-1,20-dioic acid 71-75 gastric inhibitory polypeptide Homo sapiens 4-7 21441754-5 2011 Incretins (glucose-dependent insulinotropic polypeptide [GIP] and glucagon-like peptide-1 [GLP-1]) are hormones released post-meal from intestinal endocrine cells that stimulate insulin secretion and suppress postprandial glucagon secretion in a glucose-dependent manner. Glucose 11-18 gastric inhibitory polypeptide Homo sapiens 57-60 21510839-1 2011 Dipeptidyl peptidase-IV (DPP-IV), a serine protease that specifically cleaves the N-terminal dipeptide with a preference for L-proline or L-alanine at the penultimate position, is involved in the degradation of incretin hormones, including glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Proline 125-134 gastric inhibitory polypeptide Homo sapiens 276-320 21510839-1 2011 Dipeptidyl peptidase-IV (DPP-IV), a serine protease that specifically cleaves the N-terminal dipeptide with a preference for L-proline or L-alanine at the penultimate position, is involved in the degradation of incretin hormones, including glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Proline 125-134 gastric inhibitory polypeptide Homo sapiens 322-325 21510839-1 2011 Dipeptidyl peptidase-IV (DPP-IV), a serine protease that specifically cleaves the N-terminal dipeptide with a preference for L-proline or L-alanine at the penultimate position, is involved in the degradation of incretin hormones, including glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Alanine 138-147 gastric inhibitory polypeptide Homo sapiens 276-320 21510839-1 2011 Dipeptidyl peptidase-IV (DPP-IV), a serine protease that specifically cleaves the N-terminal dipeptide with a preference for L-proline or L-alanine at the penultimate position, is involved in the degradation of incretin hormones, including glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Dipeptides 93-102 gastric inhibitory polypeptide Homo sapiens 322-325 21510839-1 2011 Dipeptidyl peptidase-IV (DPP-IV), a serine protease that specifically cleaves the N-terminal dipeptide with a preference for L-proline or L-alanine at the penultimate position, is involved in the degradation of incretin hormones, including glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Alanine 138-147 gastric inhibitory polypeptide Homo sapiens 322-325 20868233-5 2010 There were no apparent acute effects of metformin on intracellular Ca2(+) concentrations, but metformin enhanced (p<0.05 to p<0.01) the acute insulinotropic actions of GIP and GLP-1. Metformin 94-103 gastric inhibitory polypeptide Homo sapiens 174-177 21869539-8 2011 The change in total glucose-dependent insulinotropic peptide (GIP) significantly decreased in the MTT at week 12. monooxyethylene trimethylolpropane tristearate 98-101 gastric inhibitory polypeptide Homo sapiens 20-60 21869539-8 2011 The change in total glucose-dependent insulinotropic peptide (GIP) significantly decreased in the MTT at week 12. monooxyethylene trimethylolpropane tristearate 98-101 gastric inhibitory polypeptide Homo sapiens 62-65 21869539-10 2011 MTT findings suggest that this combination therapy improves blood glucose control by delaying carbohydrate absorption and modifying the responses of incretins, GIP, and GLP-1. monooxyethylene trimethylolpropane tristearate 0-3 gastric inhibitory polypeptide Homo sapiens 160-163 20978139-4 2011 Comparative and functional analyses showed that the human GIP gene encodes a cryptic glucose-dependent insulinotropic polypeptide (GIP) isoform (GIP55S or GIP55G) that encompasses the SNP and is resistant to serum degradation relative to the known mature GIP peptide. Glucose 85-92 gastric inhibitory polypeptide Homo sapiens 58-61 20978139-4 2011 Comparative and functional analyses showed that the human GIP gene encodes a cryptic glucose-dependent insulinotropic polypeptide (GIP) isoform (GIP55S or GIP55G) that encompasses the SNP and is resistant to serum degradation relative to the known mature GIP peptide. Glucose 85-92 gastric inhibitory polypeptide Homo sapiens 131-134 20978139-4 2011 Comparative and functional analyses showed that the human GIP gene encodes a cryptic glucose-dependent insulinotropic polypeptide (GIP) isoform (GIP55S or GIP55G) that encompasses the SNP and is resistant to serum degradation relative to the known mature GIP peptide. Glucose 85-92 gastric inhibitory polypeptide Homo sapiens 131-134 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 gastric inhibitory polypeptide Homo sapiens 43-46 21335995-5 2011 Whey proteins are most potent inducers of glucose-dependent insulinotropic polypeptide secreted by enteroendocrine K cells which in concert with hydrolyzed whey protein-derived essential amino acids stimulate insulin secretion of pancreatic beta-cells. Amino Acids, Essential 177-198 gastric inhibitory polypeptide Homo sapiens 42-86 21966329-5 2011 In addition, GIP and GLP-1 act on insulin receptors to facilitate insulin-receptor binding, resulting in optimal glucose metabolism. Glucose 113-120 gastric inhibitory polypeptide Homo sapiens 13-16 20829521-0 2010 Effects of metoclopramide on duodenal motility and flow events, glucose absorption, and incretin hormone release in response to intraduodenal glucose infusion. Glucose 142-149 gastric inhibitory polypeptide Homo sapiens 88-104 20829521-2 2010 A reduction in duodenal flow events after hyoscine butylbromide, despite no change in pressure waves, was associated with reduced secretion of the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) and a delay in glucose absorption. Butylscopolammonium Bromide 42-63 gastric inhibitory polypeptide Homo sapiens 201-245 20829521-9 2010 Metoclopramide was associated with increased plasma concentrations of GLP-1 (P < 0.05) and GIP (P = 0.07) but lower plasma insulin concentrations (P < 0.05). Metoclopramide 0-14 gastric inhibitory polypeptide Homo sapiens 94-97 20829521-11 2010 Furthermore, GLP-1 and GIP release increased with metoclopramide, but insulin release paradoxically decreased. Metoclopramide 50-64 gastric inhibitory polypeptide Homo sapiens 23-26 20708812-2 2010 Since the launch of sitagliptin in 2006, a compelling body of evidence has accumulated showing that dipeptidyl peptidase-4 (DPP-4) inhibitors, which augment endogenous GLP-1 and GIP levels, represent an important advance in the management of T2DM. Sitagliptin Phosphate 20-31 gastric inhibitory polypeptide Homo sapiens 178-181 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 gastric inhibitory polypeptide Homo sapiens 0-44 20693566-8 2010 GIP-induced phospho-CREB and TORC2 were shown to bind to a cAMP-response element (-II) site in the human LPL promoter and GIP increased protein-protein interactions of these two factors. Cyclic AMP 59-63 gastric inhibitory polypeptide Homo sapiens 0-3 30780831-2 2010 By inhibiting dipeptidyl peptidase-4, saxagliptin increases concentrations of the intact forms of the incretin hormones, glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide, prolonging their effects. saxagliptin 38-49 gastric inhibitory polypeptide Homo sapiens 149-193 20954337-1 2010 Incretin, GIP and GLP-1, are blood glucose lowering hormones secreted from K cells and L cells, and are rapidly degenerated by DPP-4 within a few minutes. Glucose 35-42 gastric inhibitory polypeptide Homo sapiens 10-13 20655673-5 2010 The incretin effect results from release of the incretin hormones Glucagon like peptide-1 (GLP-1) and Glucose-dependent insulinotropic polypeptide (GIP) from intestinal cells in response to glucose ingestion. Glucose 190-197 gastric inhibitory polypeptide Homo sapiens 102-146 20655673-5 2010 The incretin effect results from release of the incretin hormones Glucagon like peptide-1 (GLP-1) and Glucose-dependent insulinotropic polypeptide (GIP) from intestinal cells in response to glucose ingestion. Glucose 190-197 gastric inhibitory polypeptide Homo sapiens 148-151 20151941-8 2010 Finally, it was readily demonstrated that GIP conjugated to either fluorescein or doxorubicin (DOX) underwent tumor cell uptake; subsequently, DOX-GIP conjugates induced cytotoxic cell destruction indicating the utility of GIP segments as cancer therapeutic agents. Fluorescein 67-78 gastric inhibitory polypeptide Homo sapiens 42-45 20547981-0 2010 Glucose-dependent insulinotropic polypeptide may enhance fatty acid re-esterification in subcutaneous abdominal adipose tissue in lean humans. Fatty Acids 57-67 gastric inhibitory polypeptide Homo sapiens 0-44 20547981-7 2010 CONCLUSIONS: In conclusion, GIP in combination with hyperinsulinemia and slight hyperglycemia increased adipose tissue blood flow, glucose uptake, and FFA re-esterification, thus resulting in increased TAG deposition in abdominal subcutaneous adipose tissue. Glucose 131-138 gastric inhibitory polypeptide Homo sapiens 28-31 20452407-1 2010 Glucose-dependent insulinotropic polypeptide (GIP), a physiological incretin and enterogastrone, plays a vital role in regulating glucose-dependent insulin release from the pancreas and gastric acid secretion from the stomach. Glucose 130-137 gastric inhibitory polypeptide Homo sapiens 0-44 20452407-1 2010 Glucose-dependent insulinotropic polypeptide (GIP), a physiological incretin and enterogastrone, plays a vital role in regulating glucose-dependent insulin release from the pancreas and gastric acid secretion from the stomach. Glucose 130-137 gastric inhibitory polypeptide Homo sapiens 46-49 20452407-8 2010 Consistent with this finding, we demonstrated the transcriptional regulation of the hGIP promoter by progesterone via the PR-B isoform and that progesterone treatment in both HuTu80 and PANC-1 cells resulted in an increase in hGIP transcript level. Progesterone 101-113 gastric inhibitory polypeptide Homo sapiens 84-88 20151941-8 2010 Finally, it was readily demonstrated that GIP conjugated to either fluorescein or doxorubicin (DOX) underwent tumor cell uptake; subsequently, DOX-GIP conjugates induced cytotoxic cell destruction indicating the utility of GIP segments as cancer therapeutic agents. Doxorubicin 82-93 gastric inhibitory polypeptide Homo sapiens 42-45 20151941-8 2010 Finally, it was readily demonstrated that GIP conjugated to either fluorescein or doxorubicin (DOX) underwent tumor cell uptake; subsequently, DOX-GIP conjugates induced cytotoxic cell destruction indicating the utility of GIP segments as cancer therapeutic agents. Doxorubicin 95-98 gastric inhibitory polypeptide Homo sapiens 42-45 20151941-8 2010 Finally, it was readily demonstrated that GIP conjugated to either fluorescein or doxorubicin (DOX) underwent tumor cell uptake; subsequently, DOX-GIP conjugates induced cytotoxic cell destruction indicating the utility of GIP segments as cancer therapeutic agents. Doxorubicin 95-98 gastric inhibitory polypeptide Homo sapiens 147-150 20151941-8 2010 Finally, it was readily demonstrated that GIP conjugated to either fluorescein or doxorubicin (DOX) underwent tumor cell uptake; subsequently, DOX-GIP conjugates induced cytotoxic cell destruction indicating the utility of GIP segments as cancer therapeutic agents. Doxorubicin 95-98 gastric inhibitory polypeptide Homo sapiens 147-150 20151941-8 2010 Finally, it was readily demonstrated that GIP conjugated to either fluorescein or doxorubicin (DOX) underwent tumor cell uptake; subsequently, DOX-GIP conjugates induced cytotoxic cell destruction indicating the utility of GIP segments as cancer therapeutic agents. Doxorubicin 143-146 gastric inhibitory polypeptide Homo sapiens 42-45 20151941-8 2010 Finally, it was readily demonstrated that GIP conjugated to either fluorescein or doxorubicin (DOX) underwent tumor cell uptake; subsequently, DOX-GIP conjugates induced cytotoxic cell destruction indicating the utility of GIP segments as cancer therapeutic agents. Doxorubicin 143-146 gastric inhibitory polypeptide Homo sapiens 147-150 20151941-8 2010 Finally, it was readily demonstrated that GIP conjugated to either fluorescein or doxorubicin (DOX) underwent tumor cell uptake; subsequently, DOX-GIP conjugates induced cytotoxic cell destruction indicating the utility of GIP segments as cancer therapeutic agents. Doxorubicin 143-146 gastric inhibitory polypeptide Homo sapiens 147-150 20484128-0 2010 Sex steroids affect triglyceride handling, glucose-dependent insulinotropic polypeptide, and insulin sensitivity: a 1-week randomized clinical trial in healthy young men. Steroids 4-12 gastric inhibitory polypeptide Homo sapiens 43-87 20484128-4 2010 RESULTS: Following intervention, the postprandial triglyceride response displayed a diverging response with a decline in group T and an increase in group E; the postprandial glucose-dependent insulinotropic polypeptide (GIP) response increased in group T. Insulin sensitivity increased in group T but remained unaltered in group E. CONCLUSIONS: In healthy young men, short-term changes in sex steroids affect postprandial triglyceride and GIP response and insulin sensitivity. Triglycerides 50-62 gastric inhibitory polypeptide Homo sapiens 220-223 20484128-4 2010 RESULTS: Following intervention, the postprandial triglyceride response displayed a diverging response with a decline in group T and an increase in group E; the postprandial glucose-dependent insulinotropic polypeptide (GIP) response increased in group T. Insulin sensitivity increased in group T but remained unaltered in group E. CONCLUSIONS: In healthy young men, short-term changes in sex steroids affect postprandial triglyceride and GIP response and insulin sensitivity. Steroids 393-401 gastric inhibitory polypeptide Homo sapiens 220-223 20484128-4 2010 RESULTS: Following intervention, the postprandial triglyceride response displayed a diverging response with a decline in group T and an increase in group E; the postprandial glucose-dependent insulinotropic polypeptide (GIP) response increased in group T. Insulin sensitivity increased in group T but remained unaltered in group E. CONCLUSIONS: In healthy young men, short-term changes in sex steroids affect postprandial triglyceride and GIP response and insulin sensitivity. Triglycerides 422-434 gastric inhibitory polypeptide Homo sapiens 220-223 20607844-1 2010 Glucose-dependent insulinotropic polypeptide (gastric inhibitory polypeptide, or GIP), a 42-amino acid incretin hormone, modulates insulin secretion in a glucose-concentration-dependent manner. Glucose 154-161 gastric inhibitory polypeptide Homo sapiens 0-44 20607844-1 2010 Glucose-dependent insulinotropic polypeptide (gastric inhibitory polypeptide, or GIP), a 42-amino acid incretin hormone, modulates insulin secretion in a glucose-concentration-dependent manner. Glucose 154-161 gastric inhibitory polypeptide Homo sapiens 81-84 20200305-8 2010 Changes in insulin secretion were directly related to the GIP responses to oral glucose (r = 0.64, P = 0.005), which were augmented in the obese-type 2 diabetic group and only moderately suppressed in the obese-NGT group. Glucose 80-87 gastric inhibitory polypeptide Homo sapiens 58-61 20501683-11 2010 CONCLUSION: Acute hyperglycemia in the physiological range has no effect on duodenal pressure waves and flow events but is associated with increased GIP secretion and rate of glucose absorption in response to intraduodenal glucose. Glucose 223-230 gastric inhibitory polypeptide Homo sapiens 149-152 20799012-5 2010 A mutated GIP peptide in which Tyr(1), Ile(7), Asp(15), and His(18) were replaced by His, Thr, Glu, and Ala, respectively, was able to activate both GLP1R and GIPR with moderate potency. Tyrosine 31-34 gastric inhibitory polypeptide Homo sapiens 10-13 20799012-5 2010 A mutated GIP peptide in which Tyr(1), Ile(7), Asp(15), and His(18) were replaced by His, Thr, Glu, and Ala, respectively, was able to activate both GLP1R and GIPR with moderate potency. Isoleucine 39-42 gastric inhibitory polypeptide Homo sapiens 10-13 20799012-5 2010 A mutated GIP peptide in which Tyr(1), Ile(7), Asp(15), and His(18) were replaced by His, Thr, Glu, and Ala, respectively, was able to activate both GLP1R and GIPR with moderate potency. Aspartic Acid 47-50 gastric inhibitory polypeptide Homo sapiens 10-13 20799012-5 2010 A mutated GIP peptide in which Tyr(1), Ile(7), Asp(15), and His(18) were replaced by His, Thr, Glu, and Ala, respectively, was able to activate both GLP1R and GIPR with moderate potency. Threonine 90-93 gastric inhibitory polypeptide Homo sapiens 10-13 20799012-5 2010 A mutated GIP peptide in which Tyr(1), Ile(7), Asp(15), and His(18) were replaced by His, Thr, Glu, and Ala, respectively, was able to activate both GLP1R and GIPR with moderate potency. Glutamic Acid 95-98 gastric inhibitory polypeptide Homo sapiens 10-13 20799012-5 2010 A mutated GIP peptide in which Tyr(1), Ile(7), Asp(15), and His(18) were replaced by His, Thr, Glu, and Ala, respectively, was able to activate both GLP1R and GIPR with moderate potency. Alanine 104-107 gastric inhibitory polypeptide Homo sapiens 10-13 20799012-8 2010 These results suggest that Tyr/His(1) and Ile/Thr(7) of GIP/GLP-1 peptides confer differential ligand selectivity toward GIPR and GLP1R. Tyrosine 27-30 gastric inhibitory polypeptide Homo sapiens 56-59 20799012-8 2010 These results suggest that Tyr/His(1) and Ile/Thr(7) of GIP/GLP-1 peptides confer differential ligand selectivity toward GIPR and GLP1R. Histidine 31-34 gastric inhibitory polypeptide Homo sapiens 56-59 20799012-8 2010 These results suggest that Tyr/His(1) and Ile/Thr(7) of GIP/GLP-1 peptides confer differential ligand selectivity toward GIPR and GLP1R. Isoleucine 42-45 gastric inhibitory polypeptide Homo sapiens 56-59 20799012-8 2010 These results suggest that Tyr/His(1) and Ile/Thr(7) of GIP/GLP-1 peptides confer differential ligand selectivity toward GIPR and GLP1R. Threonine 46-49 gastric inhibitory polypeptide Homo sapiens 56-59 20061446-8 2010 Further characterization of these mutants, including tests with alanine-substituted GIP analogs, were in agreement with interaction of Glu3 in GIP with Arg183 in GIPR. Alanine 64-71 gastric inhibitory polypeptide Homo sapiens 84-87 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 gastric inhibitory polypeptide Homo sapiens 105-108 20425582-1 2010 The gastrointestinal hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), termed incretins, are essential regulators of normal glucose homeostasis. Glucose 30-37 gastric inhibitory polypeptide Homo sapiens 76-79 24843404-1 2010 Gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are the two primary incretin hormones secreted from the intestine on ingestion of glucose or nutrients to stimulate insulin secretion from pancreatic beta cells. Glucose 155-162 gastric inhibitory polypeptide Homo sapiens 32-35 20446595-2 2010 GIP and GLP-1 potentiate glucose-induced insulin secretion by binding GIP receptor and GLP-1 receptor, respectively, on pancreatic beta-cell and increasing intracellular cAMP concentration (incretin effect). Cyclic AMP 170-174 gastric inhibitory polypeptide Homo sapiens 0-3 20103744-7 2010 These results suggest that the inappropriate glucagon response to glucose in patients with type 1 diabetes occurs as a consequence of the oral administration way, suggesting a role of the gastrointestinal tract, possibly via glucagonotropic signaling from gut hormones (e.g., glucose-dependent insulinotropic polypeptide), in type 1 diabetic hyperglucagonemia. Glucagon 45-53 gastric inhibitory polypeptide Homo sapiens 276-320 20061446-8 2010 Further characterization of these mutants, including tests with alanine-substituted GIP analogs, were in agreement with interaction of Glu3 in GIP with Arg183 in GIPR. Alanine 64-71 gastric inhibitory polypeptide Homo sapiens 143-146 20061446-9 2010 Furthermore, they strongly supported a binding mode of GIP to GIPR in which the N-terminal moiety of GIP was sited within transmembrane helices (TMH) 2, 3, 5, and 6 with biologically crucial Tyr1 interacting with Gln224 (TMH3), Arg300 (TMH5), and Phe357 (TMH6). tmh3 221-225 gastric inhibitory polypeptide Homo sapiens 55-58 20061446-9 2010 Furthermore, they strongly supported a binding mode of GIP to GIPR in which the N-terminal moiety of GIP was sited within transmembrane helices (TMH) 2, 3, 5, and 6 with biologically crucial Tyr1 interacting with Gln224 (TMH3), Arg300 (TMH5), and Phe357 (TMH6). tmh3 221-225 gastric inhibitory polypeptide Homo sapiens 62-65 20061446-9 2010 Furthermore, they strongly supported a binding mode of GIP to GIPR in which the N-terminal moiety of GIP was sited within transmembrane helices (TMH) 2, 3, 5, and 6 with biologically crucial Tyr1 interacting with Gln224 (TMH3), Arg300 (TMH5), and Phe357 (TMH6). tmh5 236-240 gastric inhibitory polypeptide Homo sapiens 55-58 20061446-9 2010 Furthermore, they strongly supported a binding mode of GIP to GIPR in which the N-terminal moiety of GIP was sited within transmembrane helices (TMH) 2, 3, 5, and 6 with biologically crucial Tyr1 interacting with Gln224 (TMH3), Arg300 (TMH5), and Phe357 (TMH6). tmh5 236-240 gastric inhibitory polypeptide Homo sapiens 62-65 20061446-9 2010 Furthermore, they strongly supported a binding mode of GIP to GIPR in which the N-terminal moiety of GIP was sited within transmembrane helices (TMH) 2, 3, 5, and 6 with biologically crucial Tyr1 interacting with Gln224 (TMH3), Arg300 (TMH5), and Phe357 (TMH6). tmh6 255-259 gastric inhibitory polypeptide Homo sapiens 55-58 20061446-9 2010 Furthermore, they strongly supported a binding mode of GIP to GIPR in which the N-terminal moiety of GIP was sited within transmembrane helices (TMH) 2, 3, 5, and 6 with biologically crucial Tyr1 interacting with Gln224 (TMH3), Arg300 (TMH5), and Phe357 (TMH6). tmh6 255-259 gastric inhibitory polypeptide Homo sapiens 62-65 20532013-6 2010 Incretin hormones, such as glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP), have been shown to lower the postprandial and fasting glucose and the glycated hemoglobin levels, suppress the elevated glucagon level, and stimulate glucose-dependent insulin synthesis and secretion. Glucose 61-68 gastric inhibitory polypeptide Homo sapiens 107-110 19881341-2 2010 RECENT FINDINGS: Both GLP-1 and GIP stimulate insulin secretion in a glucose-dependent manner and are thus classified as incretins. Glucose 69-76 gastric inhibitory polypeptide Homo sapiens 32-35 20460948-3 2010 METHODS: Responses of the GI hormone glucose-dependent insulinotropic polypeptide (GIP) and GLP-2 were measured following an 80-min liquid meal test in 8 patients (6 males) with chronic pancreatitis (CP) and pancreatic exocrine insufficiency (PEI) and 8 healthy control subjects (5 males). Glucose 37-44 gastric inhibitory polypeptide Homo sapiens 83-86 19841474-1 2010 Glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are gut-derived incretin hormones that regulate blood glucose levels. Glucose 36-43 gastric inhibitory polypeptide Homo sapiens 82-85 20519806-2 2010 Dipeptidyl peptidase-4 (DPP-4) inhibitors, such as sitagliptin, increase active GLP-1 and GIP levels and improve hyperglycemia in a glucose-dependent fashion. Sitagliptin Phosphate 51-62 gastric inhibitory polypeptide Homo sapiens 90-93 20115929-4 2009 The incretin hormones glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP) are secreted in the gut upon meal ingestion and lower blood glucose by glucose-dependent stimulation of insulin secretion and production. Glucose 56-63 gastric inhibitory polypeptide Homo sapiens 102-105 21094896-6 2010 Here, we provide an overview of current knowledge relating to the physiological roles of GIP and GLP-1, with specific emphasis on their modes of action on islet hormone secretion, beta-cell proliferation and survival, central and autonomic neuronal function, gastrointestinal motility, and glucose and lipid metabolism. Glucose 290-297 gastric inhibitory polypeptide Homo sapiens 89-92 21094898-12 2010 The application of GIP as a glucose-lowering drug is limited due to reduced efficacy in humans with type 2 diabetes and its potential obesogenic effects demonstrated by rodent studies. Glucose 28-35 gastric inhibitory polypeptide Homo sapiens 19-22 21094898-14 2010 The meal-dependent nature of GIP release makes K-cells a potential target for genetically engineered production of satiety factors or glucose-lowering agents, for example, insulin. Glucose 134-141 gastric inhibitory polypeptide Homo sapiens 29-32 21094901-1 2010 The two incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are key factors in the regulation of islet function and glucose metabolism, and incretin-based therapy for type 2 diabetes has gained considerable interest during recent years. Glucose 26-33 gastric inhibitory polypeptide Homo sapiens 72-75 21094901-3 2010 The main stimulus for incretin hormone secretion is presence of nutrients in the intestinal lumen, and carbohydrate, fat as well as protein all have the capacity to stimulate GIP and GLP-1 secretion. Carbohydrates 103-115 gastric inhibitory polypeptide Homo sapiens 22-38 21094901-3 2010 The main stimulus for incretin hormone secretion is presence of nutrients in the intestinal lumen, and carbohydrate, fat as well as protein all have the capacity to stimulate GIP and GLP-1 secretion. Carbohydrates 103-115 gastric inhibitory polypeptide Homo sapiens 175-178 21094910-3 2010 The activation of GPR119 increases the intracellular accumulation of cAMP, leading to enhanced glucose-dependent insulin secretion from pancreatic beta-cells and increased release of the gut peptides GLP-1 (glucagon-like peptide 1), GIP (glucose-dependent insulinotropic peptide) and PYY (polypeptide YY). Cyclic AMP 69-73 gastric inhibitory polypeptide Homo sapiens 233-236 21094910-3 2010 The activation of GPR119 increases the intracellular accumulation of cAMP, leading to enhanced glucose-dependent insulin secretion from pancreatic beta-cells and increased release of the gut peptides GLP-1 (glucagon-like peptide 1), GIP (glucose-dependent insulinotropic peptide) and PYY (polypeptide YY). Cyclic AMP 69-73 gastric inhibitory polypeptide Homo sapiens 238-278 19952298-1 2009 Nutrient intake stimulates the secretion of the gastrointestinal incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which exert glucose-dependent insulinotropic effects and assist pancreatic insulin and glucagon in maintaining glucose homeostasis. Glucose 120-127 gastric inhibitory polypeptide Homo sapiens 166-169 20115929-4 2009 The incretin hormones glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP) are secreted in the gut upon meal ingestion and lower blood glucose by glucose-dependent stimulation of insulin secretion and production. Glucose 167-174 gastric inhibitory polypeptide Homo sapiens 56-100 20115929-4 2009 The incretin hormones glucagon-like peptide (GLP)-1 and glucose-dependent insulinotropic polypeptide (GIP) are secreted in the gut upon meal ingestion and lower blood glucose by glucose-dependent stimulation of insulin secretion and production. Glucose 167-174 gastric inhibitory polypeptide Homo sapiens 102-105 19625311-10 2009 GIP interacted with hyaluronic acid, a major component of the cumulus matrix. Hyaluronic Acid 20-35 gastric inhibitory polypeptide Homo sapiens 0-3 19755410-7 2009 DPP-IV-mediated degradation of GIP was significantly less in patients receiving nateglinide compared with placebo. Nateglinide 80-91 gastric inhibitory polypeptide Homo sapiens 31-34 19755410-8 2009 Inhibition of DPP-IV activity corresponded with a time- and concentration-dependent inhibitory effect of nateglinide on DPP-IV-mediated truncation of GIP(1-42) to GIP(3-42) in vitro. Nateglinide 105-116 gastric inhibitory polypeptide Homo sapiens 150-153 19755410-8 2009 Inhibition of DPP-IV activity corresponded with a time- and concentration-dependent inhibitory effect of nateglinide on DPP-IV-mediated truncation of GIP(1-42) to GIP(3-42) in vitro. Nateglinide 105-116 gastric inhibitory polypeptide Homo sapiens 163-166 19947814-1 2009 The incretin effect, mediated by glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), plays an important role in the regulation of insulin secretion in response to oral glucose. Glucose 69-76 gastric inhibitory polypeptide Homo sapiens 115-118 19755410-10 2009 CONCLUSIONS: Although considerably less potent than specified DPP-IV inhibitors, the possibility that some of the beneficial actions of nateglinide are indirectly mediated through DPP-IV inhibition and increased bioavailability of GIP and other incretins merits consideration. Nateglinide 136-147 gastric inhibitory polypeptide Homo sapiens 231-234 19625311-11 2009 Glycodelin-C bound to hyaluronic acid-coated agarose beads in the presence of GIP. Hyaluronic Acid 22-37 gastric inhibitory polypeptide Homo sapiens 78-81 19625311-12 2009 Human spermatozoa acquired the hyaluronic acid-GIP-bound glycodelin-C during incubation in vitro. Hyaluronic Acid 31-46 gastric inhibitory polypeptide Homo sapiens 47-50 19625311-13 2009 CONCLUSION: The hyaluronic acid-GIP complex formed in the cumulus matrix retains and concentrates glycodelin-C in the cumulus matrix for displacing sperm-bound glycodelin-A and -F and stimulating the zona binding activity of the spermatozoa traversing through the cumulus mass. Hyaluronic Acid 16-31 gastric inhibitory polypeptide Homo sapiens 32-35 19582394-9 2009 Gip promoter elements mediating WNT/lithium induction were identified (electrophoretic mobility shift assay, co-transfection of deletion mutants, ChIP). Lithium 36-43 gastric inhibitory polypeptide Homo sapiens 0-3 19791828-1 2009 Saxagliptin and its active metabolite M2 are dipeptidyl peptidase-4 inhibitors that improve glycaemic control by preventing the inactivation of the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide. saxagliptin 0-11 gastric inhibitory polypeptide Homo sapiens 202-246 19533083-6 2009 In addition, by causing preferential oxidation of fat, blockade of GIP signalling clears triacylglycerol deposits from liver and muscle, thereby restoring mechanisms for suppression of hepatic glucose output and improving insulin sensitivity. Triglycerides 89-104 gastric inhibitory polypeptide Homo sapiens 67-70 19614945-5 2009 In contrast, the GIP and GLP-1 responses to oral glucose were different between the groups in a dissociated pattern. Glucose 49-56 gastric inhibitory polypeptide Homo sapiens 17-20 20737753-7 2009 Several in vitro studies have demonstrated that these two incretin hormones may increase the proliferation of pancreatic beta cell.There is a decrease of GIP function and GLP-1 amount in type-2 diabetes mellitus; thus the attempt to increase both incretin hormones - in this case by using GLP-1 agonist and DPP-IV inhibitor - is one of treatment modalities to control the glucose blood level, either as a monotherapy or a combination therapy. Glucose 372-379 gastric inhibitory polypeptide Homo sapiens 154-157 19582394-10 2009 RESULTS: Lithium or WNT/beta-catenin signalling enhanced GIP production by entero-endocrine cells through a conserved site in the proximal Gip promoter. Lithium 9-16 gastric inhibitory polypeptide Homo sapiens 57-60 19582394-10 2009 RESULTS: Lithium or WNT/beta-catenin signalling enhanced GIP production by entero-endocrine cells through a conserved site in the proximal Gip promoter. Lithium 9-16 gastric inhibitory polypeptide Homo sapiens 139-142 19582394-11 2009 Lithium favours lymphoid enhancer factor-1/beta-catenin binding to Gip promoter and diminishes ChIP through T cell factor-4 and histone deacetylase 1. Lithium 0-7 gastric inhibitory polypeptide Homo sapiens 67-70 19351807-2 2009 Exercise and diet are known to improve glucose metabolism and the pancreatic insulin response to glucose, and this effect may be mediated through the incretin effect of GIP. Glucose 39-46 gastric inhibitory polypeptide Homo sapiens 169-172 19748067-1 2009 Glucose-dependent insulinotropic polypeptide (GIP or gastric inhibitory polypeptide) is a 42-amino-acid hormone, secreted from the enteroendocrine K cells, which has insulin-releasing and extrapancreatic glucoregulatory actions. amino-acid hormone 93-111 gastric inhibitory polypeptide Homo sapiens 0-44 19748067-1 2009 Glucose-dependent insulinotropic polypeptide (GIP or gastric inhibitory polypeptide) is a 42-amino-acid hormone, secreted from the enteroendocrine K cells, which has insulin-releasing and extrapancreatic glucoregulatory actions. amino-acid hormone 93-111 gastric inhibitory polypeptide Homo sapiens 46-49 19595611-1 2009 The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are produced predominantly by enteroendocrine cells and have multiple blood glucose-lowering effects. Glucose 23-30 gastric inhibitory polypeptide Homo sapiens 69-72 19562648-3 2009 The activation of GPR119 increases the intracellular accumulation of cAMP, leading to enhanced glucose-dependent insulin secretion and increased levels of the incretin hormones GLP-1 (glucagon-like peptide 1) and GIP (glucose-dependent insulinotropic peptide). Cyclic AMP 69-73 gastric inhibitory polypeptide Homo sapiens 213-216 19562648-3 2009 The activation of GPR119 increases the intracellular accumulation of cAMP, leading to enhanced glucose-dependent insulin secretion and increased levels of the incretin hormones GLP-1 (glucagon-like peptide 1) and GIP (glucose-dependent insulinotropic peptide). Cyclic AMP 69-73 gastric inhibitory polypeptide Homo sapiens 218-258 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 89-96 gastric inhibitory polypeptide Homo sapiens 108-111 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 107-114 gastric inhibitory polypeptide Homo sapiens 82-85 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 gastric inhibitory polypeptide Homo sapiens 119-122 19276444-6 2009 Intriguingly, GIP also induced an early postprandial augmentation in glucagon, a significant elevation in late postprandial glucose, and a decrease in late postprandial GLP-1 levels. Glucose 124-131 gastric inhibitory polypeptide Homo sapiens 14-17 19217790-4 2009 DPP-4, a protease that specifically cleaves dipeptides from proteins and oligopeptides after a penultimate N-terminal proline or alanine, is involved in the degradation of a number of neuropeptides, peptide hormones and cytokines, including the incretins GLP-1 and GIP. Dipeptides 44-54 gastric inhibitory polypeptide Homo sapiens 265-268 19375579-0 2009 Incretin hormone secretion in women with polycystic ovary syndrome: roles of obesity, insulin sensitivity, and treatment with metformin. Metformin 126-135 gastric inhibitory polypeptide Homo sapiens 0-16 19375579-10 2009 Metformin increased GIP (AUC) and GLP-1 (AUC) in lean women with PCOS (P < .05), and a similar trend was seen in the obese women (P = .07). Metformin 0-9 gastric inhibitory polypeptide Homo sapiens 20-23 19375579-11 2009 The GIP secretion is attenuated in obese women with PCOS, whereas treatment with metformin increases the levels of both GIP and GLP-1 in women with PCOS. Metformin 81-90 gastric inhibitory polypeptide Homo sapiens 120-123 19221011-5 2009 GLP-1, GIP, and insulin also increased after sucrose (P=0.0001) but not after either load of sucralose or saline. Sucrose 45-52 gastric inhibitory polypeptide Homo sapiens 7-10 19217790-5 2009 As soon as released from the gut in response to food intake, GLP-1 and GIP exert a potent glucose-dependent insulinotropic action, thereby playing a key role in the maintenance of post-meal glycemic control. Glucose 90-97 gastric inhibitory polypeptide Homo sapiens 71-74 19066304-5 2009 A smaller response of aldosterone after GIP infusion was observed in a normal subject. Aldosterone 22-33 gastric inhibitory polypeptide Homo sapiens 40-43 19141695-0 2009 Prolonged saturated fat-induced, glucose-dependent insulinotropic polypeptide elevation is associated with adipokine imbalance and liver injury in nonalcoholic steatohepatitis: dysregulated enteroadipocyte axis as a novel feature of fatty liver. saturated fat 10-23 gastric inhibitory polypeptide Homo sapiens 33-77 19141695-2 2009 Glucose-dependent insulinotropic polypeptide (GIP) was recently linked to adipocyte metabolism and obesity-related metabolic disorders, including NAFLD, induced by an excess of saturated fatty acids (SFAs), but its role in vivo, as well as underlying mechanisms, is unknown. Fatty Acids 177-198 gastric inhibitory polypeptide Homo sapiens 0-44 19141695-2 2009 Glucose-dependent insulinotropic polypeptide (GIP) was recently linked to adipocyte metabolism and obesity-related metabolic disorders, including NAFLD, induced by an excess of saturated fatty acids (SFAs), but its role in vivo, as well as underlying mechanisms, is unknown. Fatty Acids 177-198 gastric inhibitory polypeptide Homo sapiens 46-49 19141695-4 2009 OBJECTIVE: We assessed GIP response to SFA ingestion and its effect on glucose and lipid metabolism and on liver injury in patients with nonalcoholic steatohepatitis (NASH). Fatty Acids 39-42 gastric inhibitory polypeptide Homo sapiens 23-26 19141695-4 2009 OBJECTIVE: We assessed GIP response to SFA ingestion and its effect on glucose and lipid metabolism and on liver injury in patients with nonalcoholic steatohepatitis (NASH). Glucose 71-78 gastric inhibitory polypeptide Homo sapiens 23-26 19141695-9 2009 GIP response correlated directly with hepatic steatosis, postprandial resistin, and free fatty acid (FFA) increase and inversely with beta cell function and incretin effect. Fatty Acids, Nonesterified 84-99 gastric inhibitory polypeptide Homo sapiens 0-3 19141695-9 2009 GIP response correlated directly with hepatic steatosis, postprandial resistin, and free fatty acid (FFA) increase and inversely with beta cell function and incretin effect. Fatty Acids, Nonesterified 101-104 gastric inhibitory polypeptide Homo sapiens 0-3 19141695-12 2009 CONCLUSIONS: GIP response to SFA ingestion is prolonged in nondiabetic patients with NASH and is correlated with liver disease, an unfavorable dynamic adipokine profile, and beta cell dysfunction, which provides a rationale for GIP antagonism in these subjects. Fatty Acids 29-32 gastric inhibitory polypeptide Homo sapiens 13-16 19141695-12 2009 CONCLUSIONS: GIP response to SFA ingestion is prolonged in nondiabetic patients with NASH and is correlated with liver disease, an unfavorable dynamic adipokine profile, and beta cell dysfunction, which provides a rationale for GIP antagonism in these subjects. Fatty Acids 29-32 gastric inhibitory polypeptide Homo sapiens 228-231 18974968-1 2009 AIMS/HYPOTHESIS: The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotrophic peptide (GIP) are released from intestinal endocrine cells in response to luminal glucose. Glucose 75-82 gastric inhibitory polypeptide Homo sapiens 118-121 19037628-0 2009 Four weeks of near-normalisation of blood glucose improves the insulin response to glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide in patients with type 2 diabetes. Blood Glucose 36-49 gastric inhibitory polypeptide Homo sapiens 111-155 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 gastric inhibitory polypeptide Homo sapiens 148-151 19037628-7 2009 The late phase C-peptide response (10-120 min) increased during GIP infusion from 33.0 +/- 8.5 to 103.9 +/- 24.2 (nmol/l) x (110 min)(-1) (p < 0.05) and during GLP-1 infusion from 48.7 +/- 11.8 to 126.6 +/- 32.5 (nmol/l) x (110 min)(-1) (p < 0.05), whereas during saline infusion the late-phase response did not differ before vs after near-normalisation of blood glucose (40.2 +/- 11.2 vs 46.5 +/- 12.7 [nmol/l] x [110 min](-1)). Sodium Chloride 270-276 gastric inhibitory polypeptide Homo sapiens 64-67 19037628-7 2009 The late phase C-peptide response (10-120 min) increased during GIP infusion from 33.0 +/- 8.5 to 103.9 +/- 24.2 (nmol/l) x (110 min)(-1) (p < 0.05) and during GLP-1 infusion from 48.7 +/- 11.8 to 126.6 +/- 32.5 (nmol/l) x (110 min)(-1) (p < 0.05), whereas during saline infusion the late-phase response did not differ before vs after near-normalisation of blood glucose (40.2 +/- 11.2 vs 46.5 +/- 12.7 [nmol/l] x [110 min](-1)). Glucose 369-376 gastric inhibitory polypeptide Homo sapiens 64-67 19037628-8 2009 CONCLUSIONS: Near-normalisation of blood glucose for 4 weeks improves beta cell responsiveness to both GLP-1 and GIP by a factor of three to four. Blood Glucose 35-48 gastric inhibitory polypeptide Homo sapiens 113-116 19149538-2 2009 Inhibition of plasma DPP IV enzyme leads to enhanced endogenous GLP-1 and GIP activity, which ultimately results in the potentiation of insulin secretion by pancreatic beta-cells and subsequent lowering of blood glucose levels, HbA[1(c)], glucagon secretion and liver glucose production. Glucose 212-219 gastric inhibitory polypeptide Homo sapiens 74-77 19149538-2 2009 Inhibition of plasma DPP IV enzyme leads to enhanced endogenous GLP-1 and GIP activity, which ultimately results in the potentiation of insulin secretion by pancreatic beta-cells and subsequent lowering of blood glucose levels, HbA[1(c)], glucagon secretion and liver glucose production. Glucose 268-275 gastric inhibitory polypeptide Homo sapiens 74-77 19218562-1 2009 PURPOSE: Gastric inhibitory peptide (GIP) and glucagon-like peptide-1 (GLP-1) stimulate the secretion of insulin when blood glucose levels are elevated and inhibit the postprandial release of glucagon. Glucose 124-131 gastric inhibitory polypeptide Homo sapiens 9-35 19218562-1 2009 PURPOSE: Gastric inhibitory peptide (GIP) and glucagon-like peptide-1 (GLP-1) stimulate the secretion of insulin when blood glucose levels are elevated and inhibit the postprandial release of glucagon. Glucose 124-131 gastric inhibitory polypeptide Homo sapiens 37-40 19275548-6 2009 The other group comprises the gliptins (e.g. sitagliptin and vildagliptin) which boost endogenous incretin activity by inhibiting the enzyme dipeptidyl peptidase 4 (DPP 4) that degrades both GLP-1 and GIP. Sitagliptin Phosphate 45-56 gastric inhibitory polypeptide Homo sapiens 201-204 19275548-6 2009 The other group comprises the gliptins (e.g. sitagliptin and vildagliptin) which boost endogenous incretin activity by inhibiting the enzyme dipeptidyl peptidase 4 (DPP 4) that degrades both GLP-1 and GIP. Vildagliptin 61-73 gastric inhibitory polypeptide Homo sapiens 201-204 19050053-6 2009 RESULTS: Compared to the results of GIP alone, SU alone, or those results added together, coadministration of GIP and SU resulted in a more-than-additive increase in the peripheral insulin (P = 0.002) and C-peptide (P = 0.028) responses and furthermore, a more-than-additive increase in total (P = 0.01), early (P = 0.02), and late-phase (P = 0.02) insulin secretion. Sulfonylurea Compounds 2-4 gastric inhibitory polypeptide Homo sapiens 110-113 19050053-6 2009 RESULTS: Compared to the results of GIP alone, SU alone, or those results added together, coadministration of GIP and SU resulted in a more-than-additive increase in the peripheral insulin (P = 0.002) and C-peptide (P = 0.028) responses and furthermore, a more-than-additive increase in total (P = 0.01), early (P = 0.02), and late-phase (P = 0.02) insulin secretion. Sulfonylurea Compounds 47-49 gastric inhibitory polypeptide Homo sapiens 110-113 19050053-7 2009 CONCLUSION: We have demonstrated that inhibiting the K(ATP) channels of the diabetic beta-cell acutely using SU significantly increases both the peripheral insulin response to GIP and GIP-induced insulin secretion, indicating an ameliorated insulinotropic effect of GIP. Sulfonylurea Compounds 109-111 gastric inhibitory polypeptide Homo sapiens 176-179 19050053-7 2009 CONCLUSION: We have demonstrated that inhibiting the K(ATP) channels of the diabetic beta-cell acutely using SU significantly increases both the peripheral insulin response to GIP and GIP-induced insulin secretion, indicating an ameliorated insulinotropic effect of GIP. Sulfonylurea Compounds 109-111 gastric inhibitory polypeptide Homo sapiens 184-187 19050053-7 2009 CONCLUSION: We have demonstrated that inhibiting the K(ATP) channels of the diabetic beta-cell acutely using SU significantly increases both the peripheral insulin response to GIP and GIP-induced insulin secretion, indicating an ameliorated insulinotropic effect of GIP. Sulfonylurea Compounds 109-111 gastric inhibitory polypeptide Homo sapiens 184-187 19056578-3 2009 OBJECTIVE: Our objective was to determine whether glutamine increases circulating GLP-1 and GIP concentrations in vivo and, if so, whether this is associated with an increase in plasma insulin. Glutamine 50-59 gastric inhibitory polypeptide Homo sapiens 92-95 19056578-8 2009 Glutamine also increased plasma GIP concentrations but less effectively than glucose. Glutamine 0-9 gastric inhibitory polypeptide Homo sapiens 32-35 19056578-11 2009 CONCLUSION: Glutamine effectively increases circulating GLP-1, GIP, and insulin concentrations in vivo and may represent a novel therapeutic approach to stimulating insulin secretion in obesity and type 2 diabetes. Glutamine 12-21 gastric inhibitory polypeptide Homo sapiens 63-66 19182763-10 2009 DPP-4 inhibitors (e.g. sitagliptin, vindagliptin) prevent the degradation of endogenous GLP-1 and GIP, thereby potentiate their actions and help in glycemic control. Sitagliptin Phosphate 23-34 gastric inhibitory polypeptide Homo sapiens 98-101 19182763-10 2009 DPP-4 inhibitors (e.g. sitagliptin, vindagliptin) prevent the degradation of endogenous GLP-1 and GIP, thereby potentiate their actions and help in glycemic control. vindagliptin 36-48 gastric inhibitory polypeptide Homo sapiens 98-101 19251046-1 2009 Glucose-dependent insulinotropic polypeptide (GIP; gastric inhibitory polypeptide) is a 42 amino acid hormone that is produced by enteroendocrine K-cells and released into the circulation in response to nutrient stimulation. amino acid hormone 91-109 gastric inhibitory polypeptide Homo sapiens 0-44 19251046-1 2009 Glucose-dependent insulinotropic polypeptide (GIP; gastric inhibitory polypeptide) is a 42 amino acid hormone that is produced by enteroendocrine K-cells and released into the circulation in response to nutrient stimulation. amino acid hormone 91-109 gastric inhibitory polypeptide Homo sapiens 46-49 19251046-2 2009 Both GIP and glucagon-like peptide-1 (GLP-1) stimulate insulin secretion in a glucose-dependent manner and are thus classified as incretins. Glucose 78-85 gastric inhibitory polypeptide Homo sapiens 5-8 19036624-4 2008 GIP and GLP-1 stimulate insulin biosynthesis and insulin secretion in a glucose-dependent manner. Glucose 72-79 gastric inhibitory polypeptide Homo sapiens 0-3 18600568-2 2008 The two incretins glucagon-like peptide-1 (7-36) (GLP-1(7-36)) amide and glucose-dependent insulinotropic peptide (GIP) are released from the small intestine in response to the ingestion of nutrients and regulate glucose homeostasis in a glucose-dependent fashion; however, the action of both incretins is terminated by the rapid N-terminal cleavage of two amino acid residues of GLP-1 and GIP by dipeptidyl peptidase-IV (DPP-IV). Amides 63-68 gastric inhibitory polypeptide Homo sapiens 390-393 18779825-2 2008 DESIGN: A combination of semiquantitative real-time PCR and measurement of GIP-stimulated cAMP accumulation was used to establish the expression and functional coupling of GIPRs during in vitro differentiation of human Simpson-Golabi-Behmel syndrome (SGBS) preadipocytes. Cyclic AMP 90-94 gastric inhibitory polypeptide Homo sapiens 75-78 18779825-9 2008 In stark contrast, the 9-day differentiated cells produced a robust concentration-dependent increase in cAMP accumulation following stimulation with GIP, with an EC(50) value of 2.3 nM (n=3). Cyclic AMP 104-108 gastric inhibitory polypeptide Homo sapiens 149-152 18612044-1 2008 Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) regulate islet function after carbohydrate ingestion. Carbohydrates 117-129 gastric inhibitory polypeptide Homo sapiens 36-80 18612044-1 2008 Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) regulate islet function after carbohydrate ingestion. Carbohydrates 117-129 gastric inhibitory polypeptide Homo sapiens 82-85 18690705-3 2008 We report here the overexpression, efficient refolding, single-step purification, and biophysical characterization of recombinant human GIP with three different C-terminal target protein recognition sequence motifs by CD, fluorescence, and high-resolution solution NMR methods. Cadmium 218-220 gastric inhibitory polypeptide Homo sapiens 136-139 18806525-3 2008 Through the action of GLP-1 and GIP, DPP-IV inhibitors improve preprandial and postprandial glucose by enhancing insulin secretion and reducing postprandial concentrations of glucagon. Glucose 92-99 gastric inhibitory polypeptide Homo sapiens 32-35 18806525-3 2008 Through the action of GLP-1 and GIP, DPP-IV inhibitors improve preprandial and postprandial glucose by enhancing insulin secretion and reducing postprandial concentrations of glucagon. Glucagon 175-183 gastric inhibitory polypeptide Homo sapiens 32-35 19194917-2 2008 In our previous study, we have engineered a glucose indicator protein (GIP) that can provide continuous glucose monitoring through a conformation change-induced Forster resonance-energy transfer measurement. Glucose 44-51 gastric inhibitory polypeptide Homo sapiens 71-74 19194917-6 2008 This GIP was constructed by flanking a glucose binding protein with a cyan fluorescent protein and a pH-insensitive yellow fluorescent protein. Glucose 39-46 gastric inhibitory polypeptide Homo sapiens 5-8 19194917-8 2008 The glucose response of this new GIP kept almost unchanged from pH 7.3 to 5.3, suggesting its capability of tolerating to acidic environment. Glucose 4-11 gastric inhibitory polypeptide Homo sapiens 33-36 18511472-2 2008 Disturbances in the secretion of the incretin hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) have been observed in states with impaired glucose regulation. Glucose 55-62 gastric inhibitory polypeptide Homo sapiens 101-104 18511472-3 2008 This paper considers the secretion of GIP and GLP-1 after oral glucose load in a group of lean, glucose-tolerant PCOS women in comparison with age- and body mass index (BMI)-matched healthy women. Glucose 63-70 gastric inhibitory polypeptide Homo sapiens 38-41 18600596-8 2008 Furthermore, the insulinotropic effects of GLP-1 and GIP are glucose-dependent, reducing the risk of hypoglycemia. Glucose 61-68 gastric inhibitory polypeptide Homo sapiens 53-56 18600568-2 2008 The two incretins glucagon-like peptide-1 (7-36) (GLP-1(7-36)) amide and glucose-dependent insulinotropic peptide (GIP) are released from the small intestine in response to the ingestion of nutrients and regulate glucose homeostasis in a glucose-dependent fashion; however, the action of both incretins is terminated by the rapid N-terminal cleavage of two amino acid residues of GLP-1 and GIP by dipeptidyl peptidase-IV (DPP-IV). Glucose 73-80 gastric inhibitory polypeptide Homo sapiens 115-118 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 gastric inhibitory polypeptide Homo sapiens 116-119 18520029-7 2008 The DPP IV in the vesicles was metabolically active in cleaving substance P and glucose-dependent insulinotropic polypeptide to release N-terminal dipeptides. Dipeptides 147-157 gastric inhibitory polypeptide Homo sapiens 80-124 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 gastric inhibitory polypeptide Homo sapiens 64-67 18375745-2 2008 In addition to their effect on insulin secretion and consequent glucose lowering, GIP and GLP-1, especially the latter, have a number of physiological effects such as inhibition of glucagon release, gastric emptying and food intake, as well as a tropic action on pancreatic B-cell mass. Glucagon 181-189 gastric inhibitory polypeptide Homo sapiens 82-85 18376350-7 2008 After the oral glucose load, GIP levels presented a significant increase in normal subjects and patients without AN, whereas GLP-1 levels increased only in normal subjects. Glucose 15-22 gastric inhibitory polypeptide Homo sapiens 29-32 18319497-2 2008 SUMMARY: Sitagliptin is a dipeptidyl-peptidase IV (DPP4) inhibitor that increases insulin release and decreases glucagon levels by preventing the activation of incretin hormones--glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide. Sitagliptin Phosphate 9-20 gastric inhibitory polypeptide Homo sapiens 207-251 18057091-10 2008 GIP responses were 186 +/- 17% higher after mixed meal ingestion than after the oral glucose load (P < 0.0001), whereas GLP-1 levels were similar in both experiments. Glucose 85-92 gastric inhibitory polypeptide Homo sapiens 0-3 18319628-8 2008 Plasma glucagon levels were increased and remained at high levels at 120 min, and glucose-dependent insulinotropic polypeptide (GIP) levels were continuously and remarkably increased after glucose ingestion. Glucose 82-89 gastric inhibitory polypeptide Homo sapiens 128-131 18319628-9 2008 CONCLUSION: We observed a strongly reduced sensitivity in glucagon-induced hepatic glycogenolysis, and significantly elevated fasting and postprandial GIP levels, and a defective GIP-mediated glucagon secretion, in an anorectic patient with severe hypoglycemia. Glucagon 192-200 gastric inhibitory polypeptide Homo sapiens 179-182 18182122-1 2008 BACKGROUND: Dipeptidyl peptidase-4 (DPP-4) inhibitors are a new class of oral antihyperglycemic agents that enhance the body"s ability to regulate blood glucose by increasing the active levels of incretins, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP). Glucose 153-160 gastric inhibitory polypeptide Homo sapiens 243-283 18182122-1 2008 BACKGROUND: Dipeptidyl peptidase-4 (DPP-4) inhibitors are a new class of oral antihyperglycemic agents that enhance the body"s ability to regulate blood glucose by increasing the active levels of incretins, glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP). Glucose 153-160 gastric inhibitory polypeptide Homo sapiens 285-288 18020966-1 2008 Incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are intestinal hormones that are released in response to ingestion of nutrients, especially carbohydrate. Carbohydrates 197-209 gastric inhibitory polypeptide Homo sapiens 18-62 17947341-7 2008 RESULTS: Relative to placebo, vildagliptin increased GLP-1 (DeltaAUC, +6.0 +/- 1.2 pmol x l(-1) x h(-1), P < 0.001) and GIP (DeltaAUC, +46.8 +/- 5.4 pmol . Vildagliptin 30-42 gastric inhibitory polypeptide Homo sapiens 123-126 18269436-1 2008 Vildagliptin is a potent, selective and reversible inhibitor of dipeptidyl peptidase-4 (DPP-4), the enzyme responsible for rapid inactivation of the incretin hormones glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP). Vildagliptin 0-12 gastric inhibitory polypeptide Homo sapiens 235-238 18269436-2 2008 GLP-1 and GIP are important for the maintenance of normal glucose homeostasis as they enhance the sensitivity of insulin (beta-cell) and glucagon (alpha-cell) secretion to glucose. Glucose 58-65 gastric inhibitory polypeptide Homo sapiens 10-13 18269436-2 2008 GLP-1 and GIP are important for the maintenance of normal glucose homeostasis as they enhance the sensitivity of insulin (beta-cell) and glucagon (alpha-cell) secretion to glucose. Glucose 172-179 gastric inhibitory polypeptide Homo sapiens 10-13 18269436-4 2008 Mechanistic studies of vildagliptin performed to characterise the effects of DPP-4 inhibition on pancreatic islet function and glucose metabolism have found that vildagliptin produces dose-dependent reductions in DPP-4; these result in persistent levels of active GLP-1 and GIP in the circulation leading to improved beta-cell sensitivity to glucose and glucose-dependent insulin secretion, and improved alpha-cell sensitivity to glucose and reduction in inappropriate glucagon secretion. Vildagliptin 162-174 gastric inhibitory polypeptide Homo sapiens 274-277 18095923-1 2008 Vildagliptin is a selective inhibitor of dipeptidyl peptidase-4, and prevents the rapid degradation of the incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide. Vildagliptin 0-12 gastric inhibitory polypeptide Homo sapiens 153-197 18020966-1 2008 Incretins such as glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are intestinal hormones that are released in response to ingestion of nutrients, especially carbohydrate. Carbohydrates 197-209 gastric inhibitory polypeptide Homo sapiens 64-67 17692937-0 2007 The insulinotropic effect of GIP is impaired in patients with chronic pancreatitis and secondary diabetes mellitus as compared to patients with chronic pancreatitis and normal glucose tolerance. Glucose 176-183 gastric inhibitory polypeptide Homo sapiens 29-32 19065992-6 2008 Sitagliptin, the first commercially available dipeptidyl peptidase-4 inhibitor, inhibits the metabolism and inactivation of the incretin hormones GLP-1 and GIP. Sitagliptin Phosphate 0-11 gastric inhibitory polypeptide Homo sapiens 156-159 18052940-8 2007 Two missense SNPs in GIP showed significant effects with palmitoleic and stearic fatty-acid concentration. palmitoleic 57-68 gastric inhibitory polypeptide Homo sapiens 21-24 18052940-8 2007 Two missense SNPs in GIP showed significant effects with palmitoleic and stearic fatty-acid concentration. stearic fatty-acid 73-91 gastric inhibitory polypeptide Homo sapiens 21-24 17692937-1 2007 BACKGROUND: The incretin effect is reduced and the insulinotropic effect of the incretin hormone glucose-dependent insulinotropic polypeptide (GIP) is abolished in patients with type 2 diabetes mellitus (T2DM). Glucose 97-104 gastric inhibitory polypeptide Homo sapiens 143-146 17692937-5 2007 During GIP infusion the late-phase insulin response (20-120 min) was 3.1+/-1.0 fold greater than during saline infusion in the group of patients with CP and NGT (P<0.05), whereas there was no significant differences in patients with CP and DM. dm 243-245 gastric inhibitory polypeptide Homo sapiens 7-10 17987221-2 2007 Sitagliptin inhibits the degradation of glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide (GIP), as well as that of other regulatory peptides important for glucose homeostasis. Sitagliptin Phosphate 0-11 gastric inhibitory polypeptide Homo sapiens 108-111 17698900-1 2007 BACKGROUND/AIMS: Inhibition of dipeptidyl peptidase 4 by vildagliptin enhances the concentrations of the active form of the incretin hormones glucagon-like peptide 1 (GLP-1) and gastric inhibitory polypeptide (GIP). Vildagliptin 57-69 gastric inhibitory polypeptide Homo sapiens 210-213 17505054-0 2007 Ubiquitination is involved in glucose-mediated downregulation of GIP receptors in islets. Glucose 30-37 gastric inhibitory polypeptide Homo sapiens 65-68 17676345-1 2007 Dipeptidyl peptidase IV (DPP-IV) deactivates the incretin hormones GLP-1 and GIP by cleaving the penultimate proline or alanine from the N-terminal (P1-position) of the peptide. Proline 109-116 gastric inhibitory polypeptide Homo sapiens 77-80 17676345-1 2007 Dipeptidyl peptidase IV (DPP-IV) deactivates the incretin hormones GLP-1 and GIP by cleaving the penultimate proline or alanine from the N-terminal (P1-position) of the peptide. Alanine 120-127 gastric inhibitory polypeptide Homo sapiens 77-80 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 gastric inhibitory polypeptide Homo sapiens 29-32 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 gastric inhibitory polypeptide Homo sapiens 119-122 17505054-7 2007 Downregulation of GIP-R was rescued by treating isolated islets with proteasomal inhibitors lactacystin and MG-132, and the islets were once again capable of increasing intracellular cAMP levels in response to GIP. lactacystin 92-103 gastric inhibitory polypeptide Homo sapiens 18-21 17698900-9 2007 Similarly, integrated incremental responses of total GIP were reduced by vildagliptin by 26 and 21%, with and without glibenclamide, respectively (vildagliptin: P = 0.017; glibenclamide: P = 0.44; interaction: P = 0.69). Vildagliptin 73-85 gastric inhibitory polypeptide Homo sapiens 53-56 17698900-9 2007 Similarly, integrated incremental responses of total GIP were reduced by vildagliptin by 26 and 21%, with and without glibenclamide, respectively (vildagliptin: P = 0.017; glibenclamide: P = 0.44; interaction: P = 0.69). Glyburide 118-131 gastric inhibitory polypeptide Homo sapiens 53-56 17698900-9 2007 Similarly, integrated incremental responses of total GIP were reduced by vildagliptin by 26 and 21%, with and without glibenclamide, respectively (vildagliptin: P = 0.017; glibenclamide: P = 0.44; interaction: P = 0.69). Vildagliptin 147-159 gastric inhibitory polypeptide Homo sapiens 53-56 17655515-4 2007 Unlike conventional oral antidiabetic agents, these agents promote glucose homeostasis through inhibition of DPP-IV, the enzyme responsible for degradation of two key glucoregulatory hormones: glucagon-like peptide-1 (GLP-1), which extends the action of insulin while also suppressing the release of glucagon, and glucose-dependent insulinotropic peptide (GIP). Glucagon 193-201 gastric inhibitory polypeptide Homo sapiens 314-354 17655515-4 2007 Unlike conventional oral antidiabetic agents, these agents promote glucose homeostasis through inhibition of DPP-IV, the enzyme responsible for degradation of two key glucoregulatory hormones: glucagon-like peptide-1 (GLP-1), which extends the action of insulin while also suppressing the release of glucagon, and glucose-dependent insulinotropic peptide (GIP). Glucagon 193-201 gastric inhibitory polypeptide Homo sapiens 356-359 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 gastric inhibitory polypeptide Homo sapiens 75-78 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 gastric inhibitory polypeptide Homo sapiens 29-73 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 gastric inhibitory polypeptide Homo sapiens 75-78 17505054-7 2007 Downregulation of GIP-R was rescued by treating isolated islets with proteasomal inhibitors lactacystin and MG-132, and the islets were once again capable of increasing intracellular cAMP levels in response to GIP. benzyloxycarbonylleucyl-leucyl-leucine aldehyde 108-114 gastric inhibitory polypeptide Homo sapiens 18-21 17505054-7 2007 Downregulation of GIP-R was rescued by treating isolated islets with proteasomal inhibitors lactacystin and MG-132, and the islets were once again capable of increasing intracellular cAMP levels in response to GIP. Cyclic AMP 183-187 gastric inhibitory polypeptide Homo sapiens 18-21 17505054-1 2007 Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone that has a potent stimulatory effect on insulin release under conditions of normal glucose tolerance. Glucose 164-171 gastric inhibitory polypeptide Homo sapiens 0-44 17505054-1 2007 Glucose-dependent insulinotropic polypeptide (GIP) is a gastrointestinal hormone that has a potent stimulatory effect on insulin release under conditions of normal glucose tolerance. Glucose 164-171 gastric inhibitory polypeptide Homo sapiens 46-49 17505054-4 2007 Culturing rat and human pancreatic islets in >or=11 mM glucose for up to 24 h resulted in prevention of GIP-mediated intracellular cAMP increase compared with culturing in 5 mM glucose. Glucose 58-65 gastric inhibitory polypeptide Homo sapiens 107-110 17505054-4 2007 Culturing rat and human pancreatic islets in >or=11 mM glucose for up to 24 h resulted in prevention of GIP-mediated intracellular cAMP increase compared with culturing in 5 mM glucose. Cyclic AMP 134-138 gastric inhibitory polypeptide Homo sapiens 107-110 17505054-4 2007 Culturing rat and human pancreatic islets in >or=11 mM glucose for up to 24 h resulted in prevention of GIP-mediated intracellular cAMP increase compared with culturing in 5 mM glucose. Glucose 180-187 gastric inhibitory polypeptide Homo sapiens 107-110 17654450-5 2007 Several hypotheses have been proposed to account for this phenomenon, but the most attractive concerns surgical ablation of gastric inhibitory polypetide (GIP)-secreting intestinal K-cells. polypetide 143-153 gastric inhibitory polypeptide Homo sapiens 155-158 17416796-6 2007 One month after RY-GBP, body weight decreased by 9.2 +/- 7.0 kg, oral glucose-stimulated GLP-1 (AUC) and GIP peak levels increased significantly by 24.3 +/- 7.9 pmol x l(-1) x min(-1) (P < 0.0001) and 131 +/- 85 pg/ml (P = 0.007), respectively. Glucose 70-77 gastric inhibitory polypeptide Homo sapiens 105-108 17393464-6 2007 Therefore, the solution structure of GIP in 50% TFE was determined. Trifluoroethanol 48-51 gastric inhibitory polypeptide Homo sapiens 37-40 17535866-2 2007 Gastrointestinal endocrine L- and K-cells are also glucose-sensing cells secreting glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotrophic polypeptide (GIP) respectively. Glucose 51-58 gastric inhibitory polypeptide Homo sapiens 119-164 17535866-2 2007 Gastrointestinal endocrine L- and K-cells are also glucose-sensing cells secreting glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotrophic polypeptide (GIP) respectively. Glucose 51-58 gastric inhibitory polypeptide Homo sapiens 166-169 17407650-7 2007 FINDINGS: Key factors in maintaining the normal balance between insulin and glucagon levels are the incretins--glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP). Glucagon 76-84 gastric inhibitory polypeptide Homo sapiens 147-191 17413098-10 2007 CONCLUSION: A mixture of leucine, isoleucine, valine, lysine, and threonine resulted in glycemic and insulinemic responses closely mimicking those seen after whey ingestion in the absence of an additional effect of GIP and glucagon-like peptide 1. Leucine 25-32 gastric inhibitory polypeptide Homo sapiens 215-218 17413098-10 2007 CONCLUSION: A mixture of leucine, isoleucine, valine, lysine, and threonine resulted in glycemic and insulinemic responses closely mimicking those seen after whey ingestion in the absence of an additional effect of GIP and glucagon-like peptide 1. Lysine 54-60 gastric inhibitory polypeptide Homo sapiens 215-218 17413098-10 2007 CONCLUSION: A mixture of leucine, isoleucine, valine, lysine, and threonine resulted in glycemic and insulinemic responses closely mimicking those seen after whey ingestion in the absence of an additional effect of GIP and glucagon-like peptide 1. Threonine 66-75 gastric inhibitory polypeptide Homo sapiens 215-218 17200910-1 2007 BACKGROUND: This study was designed to assess the relationship between gastric emptying of glucose solution and the ensuing plasma concentrations of glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and glucose-dependent insulinotropic polypeptide (GIP) in patients having undergone fundoplication for gastroesophageal reflux (GERD). Glucose 91-98 gastric inhibitory polypeptide Homo sapiens 204-248 17334652-10 2007 glucose were correlated with the increments in gastric inhibitory polypeptide (GIP) (r = 0.60, p = 0.001) and glucagon-like peptide (GLP)-1 (r = 0.46, p < 0.05). Glucose 0-7 gastric inhibitory polypeptide Homo sapiens 79-82 17334652-12 2007 CONCLUSIONS/INTERPRETATION: Despite the glucagonostatic actions of GLP-1, the suppression of glucagon secretion by glucose is diminished after oral glucose ingestion, possibly due to the glucagonotropic actions of GIP and GLP-2. Glucose 115-122 gastric inhibitory polypeptide Homo sapiens 214-217 17334652-12 2007 CONCLUSIONS/INTERPRETATION: Despite the glucagonostatic actions of GLP-1, the suppression of glucagon secretion by glucose is diminished after oral glucose ingestion, possibly due to the glucagonotropic actions of GIP and GLP-2. Glucose 148-155 gastric inhibitory polypeptide Homo sapiens 214-217 17244606-2 2007 Glucose-dependent insulinotropic polypeptide (GIP) has been mainly studied because of its glucose-dependent insulinotropic action and its ability to regulate beta-cell proliferation and survival. Glucose 90-97 gastric inhibitory polypeptide Homo sapiens 0-44 17244606-2 2007 Glucose-dependent insulinotropic polypeptide (GIP) has been mainly studied because of its glucose-dependent insulinotropic action and its ability to regulate beta-cell proliferation and survival. Glucose 90-97 gastric inhibitory polypeptide Homo sapiens 46-49 17244606-4 2007 In differentiated 3T3-L1 adipocytes, GIP, in the presence of insulin, increased LPL activity and triglyceride accumulation through a pathway involving increased phosphorylation of protein kinase B (PKB) and reductions in phosphorylated LKB1 and AMP-activated protein kinase (AMPK). Triglycerides 97-109 gastric inhibitory polypeptide Homo sapiens 37-40 17263764-2 2007 Together with glucose-dependent insulinotropic polypeptide (GIP), it is responsible for the incretin effect which is the augmentation of insulin secretion following oral administration of glucose. Glucose 14-21 gastric inhibitory polypeptide Homo sapiens 60-63 17627416-2 2007 The 8-amino acid peptide (GIP-8) comprises the carboxy-terminal portion of a 34-amino acid peptide (GIP-34) previously identified as an occult epitopic segment of the full-length human AFP molecule. amino acid peptide 6-24 gastric inhibitory polypeptide Homo sapiens 26-29 17627416-2 2007 The 8-amino acid peptide (GIP-8) comprises the carboxy-terminal portion of a 34-amino acid peptide (GIP-34) previously identified as an occult epitopic segment of the full-length human AFP molecule. amino acid peptide 6-24 gastric inhibitory polypeptide Homo sapiens 100-103 17200910-1 2007 BACKGROUND: This study was designed to assess the relationship between gastric emptying of glucose solution and the ensuing plasma concentrations of glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and glucose-dependent insulinotropic polypeptide (GIP) in patients having undergone fundoplication for gastroesophageal reflux (GERD). Glucose 91-98 gastric inhibitory polypeptide Homo sapiens 250-253 17160910-3 2006 Inhibition of DPP IV prolongs and enhances the activity of endogenous GLP-1 and GIP, which serve as important prandial stimulators of insulin secretion and regulators of blood glucose control. Glucose 176-183 gastric inhibitory polypeptide Homo sapiens 80-83 17352516-1 2007 Sitagliptin, an oral dipeptidyl peptidase-4 (DPP-4) inhibitor, improves glycaemic control by inhibiting DPP-4 inactivation of the incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide. Sitagliptin Phosphate 0-11 gastric inhibitory polypeptide Homo sapiens 176-220 17484514-3 2007 The aim of study was to evaluate whether an impaired secretion of glucagon-like peptide-1 (GLP-1) and/or glucose-dependent insulinotropic polypeptide (GIP) could play a role in the development of carbohydrate disorders during pregnancy. Carbohydrates 196-208 gastric inhibitory polypeptide Homo sapiens 105-149 17484514-3 2007 The aim of study was to evaluate whether an impaired secretion of glucagon-like peptide-1 (GLP-1) and/or glucose-dependent insulinotropic polypeptide (GIP) could play a role in the development of carbohydrate disorders during pregnancy. Carbohydrates 196-208 gastric inhibitory polypeptide Homo sapiens 151-154 17596103-11 2007 CONCLUSION: Vildagliptin is likely to be a useful therapy for patients with type 2 diabetes based on the inhibition of DPP-4 and the subsequent increase in incretin hormones, GLP-1 and GIP, and the decrease in glucose and glucagon levels. Vildagliptin 12-24 gastric inhibitory polypeptide Homo sapiens 185-188 16912128-11 2006 RESULTS: Sitagliptin dose-dependently inhibited plasma DPP-4 activity over 24 h, enhanced active GLP-1 and GIP levels, increased insulin/C-peptide, decreased glucagon, and reduced glycemic excursion after OGTTs administered at 2 and 24 h after single oral 25- or 200-mg doses of sitagliptin. Sitagliptin Phosphate 9-20 gastric inhibitory polypeptide Homo sapiens 107-110 16954157-8 2006 GIP and hCG stimulated cortisol production via activation of cAMP-dependent protein kinase A in H2. Hydrocortisone 23-31 gastric inhibitory polypeptide Homo sapiens 0-3 16954157-10 2006 Activation of 5-HT7 or GIP receptors enhanced T-type calcium current in H1 or H2 and H3, respectively. Calcium 53-60 gastric inhibitory polypeptide Homo sapiens 23-26 16954157-11 2006 In addition, GIP reduced the amplitude of transient and sustained potassium currents in H2. Potassium 66-75 gastric inhibitory polypeptide Homo sapiens 13-16 16954157-11 2006 In addition, GIP reduced the amplitude of transient and sustained potassium currents in H2. Hydrogen 88-90 gastric inhibitory polypeptide Homo sapiens 13-16 16912128-13 2006 CONCLUSIONS: In this study in patients with type 2 diabetes, near maximal glucose-lowering efficacy of sitagliptin after single oral doses was associated with inhibition of plasma DPP-4 activity of 80% or greater, corresponding to a plasma sitagliptin concentration of 100 nm or greater, and an augmentation of active GLP-1 and GIP levels of 2-fold or higher after an OGTT. Sitagliptin Phosphate 103-114 gastric inhibitory polypeptide Homo sapiens 328-331 16608883-5 2006 When incubated together with native GIP, GIP-(3-42) behaved as a weak antagonist (IC(50), 92 and 731 nM for inhibition of cAMP accumulation elicited by 10 pM and 1 nM native GIP, respectively). Cyclic AMP 122-126 gastric inhibitory polypeptide Homo sapiens 41-44 16608883-4 2006 GIP-(1-42) was a potent agonist, stimulating cAMP accumulation (EC(50), 13.5 pM); GIP-(3-42) alone had no effect. Cyclic AMP 45-49 gastric inhibitory polypeptide Homo sapiens 0-3 16939389-2 2006 As an enzyme, DPP IV cleaves the N-terminal dipeptide from the incretin hormones glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide. Dipeptides 44-53 gastric inhibitory polypeptide Homo sapiens 109-153 16886636-2 2006 This peptide, known as the growth-inhibitory peptide (GIP), has two cysteine residues and demonstrates reduced antigrowth activity after long-term storage, presumably due to disulfide bond formation. Cysteine 68-76 gastric inhibitory polypeptide Homo sapiens 27-52 16886636-2 2006 This peptide, known as the growth-inhibitory peptide (GIP), has two cysteine residues and demonstrates reduced antigrowth activity after long-term storage, presumably due to disulfide bond formation. Cysteine 68-76 gastric inhibitory polypeptide Homo sapiens 54-57 16886636-2 2006 This peptide, known as the growth-inhibitory peptide (GIP), has two cysteine residues and demonstrates reduced antigrowth activity after long-term storage, presumably due to disulfide bond formation. Disulfides 174-183 gastric inhibitory polypeptide Homo sapiens 27-52 16886636-2 2006 This peptide, known as the growth-inhibitory peptide (GIP), has two cysteine residues and demonstrates reduced antigrowth activity after long-term storage, presumably due to disulfide bond formation. Disulfides 174-183 gastric inhibitory polypeptide Homo sapiens 54-57 16608883-5 2006 When incubated together with native GIP, GIP-(3-42) behaved as a weak antagonist (IC(50), 92 and 731 nM for inhibition of cAMP accumulation elicited by 10 pM and 1 nM native GIP, respectively). Cyclic AMP 122-126 gastric inhibitory polypeptide Homo sapiens 41-44 16608883-10 2006 We conclude that, although GIP-(3-42) can weakly antagonize cAMP accumulation and insulin output in vitro, it does not behave as a physiological antagonist in vivo. Cyclic AMP 60-64 gastric inhibitory polypeptide Homo sapiens 27-30 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 gastric inhibitory polypeptide Homo sapiens 54-57 16621806-0 2006 NMR and alanine scan studies of glucose-dependent insulinotropic polypeptide in water. Alanine 8-15 gastric inhibitory polypeptide Homo sapiens 32-76 16621806-0 2006 NMR and alanine scan studies of glucose-dependent insulinotropic polypeptide in water. Water 80-85 gastric inhibitory polypeptide Homo sapiens 32-76 16621806-2 2006 GIP also promotes the synthesis of fatty acids in adipose tissue. Fatty Acids 35-46 gastric inhibitory polypeptide Homo sapiens 0-3 16621806-4 2006 In this study, we present the solution structure of GIP in water determined by NMR spectroscopy. Water 59-64 gastric inhibitory polypeptide Homo sapiens 52-55 16621806-7 2006 Six GIP-(1-42)Ala(1-7) analogues were synthesized by replacing individual N-terminal residues with alanine. Alanine 14-17 gastric inhibitory polypeptide Homo sapiens 4-7 16621806-7 2006 Six GIP-(1-42)Ala(1-7) analogues were synthesized by replacing individual N-terminal residues with alanine. Alanine 99-106 gastric inhibitory polypeptide Homo sapiens 4-7 16621806-8 2006 Alanine scan studies of these N-terminal residues showed that the GIP-(1-42)Ala(6) was the only analogue to show insulin-secreting activity similar to that of the native GIP. Alanine 0-7 gastric inhibitory polypeptide Homo sapiens 66-69 16621806-8 2006 Alanine scan studies of these N-terminal residues showed that the GIP-(1-42)Ala(6) was the only analogue to show insulin-secreting activity similar to that of the native GIP. Alanine 0-3 gastric inhibitory polypeptide Homo sapiens 66-69 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 gastric inhibitory polypeptide Homo sapiens 93-96 16702313-0 2006 The rate of intestinal glucose absorption is correlated with plasma glucose-dependent insulinotropic polypeptide concentrations in healthy men. Glucose 23-30 gastric inhibitory polypeptide Homo sapiens 68-112 16702313-3 2006 We analyzed the correlation between the rate of intestinal absorption of (starch-derived) glucose and plasma concentrations of GLP-1 and GIP after ingestion of glucose and starchy foods with a different content of rapidly and slowly available glucose. Glucose 90-97 gastric inhibitory polypeptide Homo sapiens 137-140 16702313-8 2006 A high GIP response in the early postprandial phase (15-90 min) occurred after consumption of glucose. Glucose 94-101 gastric inhibitory polypeptide Homo sapiens 7-10 16902839-3 2006 Recognition of GIP as a rare manifestation of nitrofurantoin toxicity is important because prompt therapy may be associated with a favorable outcome. Nitrofurantoin 46-60 gastric inhibitory polypeptide Homo sapiens 15-18 16522728-4 2006 The stimulatory effect of GLP-1 and GIP was efficiently mimicked by the adenylate cyclase activator, forskolin, at 10 nM (approximately 90% increase) and was additive (approximately 170-250% increase) with the growth response to human growth hormone (hGH), indicating the use of distinct intracellular signalling pathways leading to mitosis by incretins and cytokines, respectively. Colforsin 101-110 gastric inhibitory polypeptide Homo sapiens 36-39 16522728-6 2006 In addition, the phosphoinositol 3-kinase (PI3K) inhibitor wortmannin and the mitogen-activated protein kinase kinase (MEK) inhibitor PD98059, both inhibited GLP-1- and GIP-stimulated proliferation. Wortmannin 59-69 gastric inhibitory polypeptide Homo sapiens 169-172 16522728-6 2006 In addition, the phosphoinositol 3-kinase (PI3K) inhibitor wortmannin and the mitogen-activated protein kinase kinase (MEK) inhibitor PD98059, both inhibited GLP-1- and GIP-stimulated proliferation. 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one 134-141 gastric inhibitory polypeptide Homo sapiens 169-172 17319471-3 2006 Exenatide is the first in a new class of agents termed incretin mimetics, which replicate several glucoregulatory effects of the endogenous incretin hormone, glucagon-like peptide-1 (GLP-1). Exenatide 0-9 gastric inhibitory polypeptide Homo sapiens 140-156 16188911-9 2006 Ghrelin concentrations were only weakly correlated with insulin concentrations (saline r = -0.36; 95% CI = -0.69, 0.09; GLP- 1 r = -0.42; 95% CI = -0.73, 0.03), but strongly inversely correlated with GIP concentrations (saline r = -0.74; 95% CI= -0.89, -0.45; GLP-1 r = -0.63; 95% CI = -0.84, -0.27). Ghrelin 0-7 gastric inhibitory polypeptide Homo sapiens 200-203 16188911-11 2006 Conversely, our data suggest a role of glucose-dependent insulinotropic polypeptide in ghrelin secretion. Ghrelin 87-94 gastric inhibitory polypeptide Homo sapiens 39-83 16469977-8 2006 Ghrelin concentrations were correlated with glucose-dependent insulinotropic polypeptide (r = -0.65; 95% CI: -0.85, -0.29) and glucagon concentrations (r = -0.47; 95% CI: -0.75, -0.03). Ghrelin 0-7 gastric inhibitory polypeptide Homo sapiens 44-88 16469977-12 2006 High associations between ghrelin and glucose-dependent insulinotropic polypeptide and glucagon suggest that stimulation of these peptides may mediate the postprandial ghrelin response. Ghrelin 26-33 gastric inhibitory polypeptide Homo sapiens 38-82 16469977-12 2006 High associations between ghrelin and glucose-dependent insulinotropic polypeptide and glucagon suggest that stimulation of these peptides may mediate the postprandial ghrelin response. Ghrelin 168-175 gastric inhibitory polypeptide Homo sapiens 38-82 16472170-9 2006 Concerning the nuclear compartment, GIP is capable of complexing with the estrogen receptor and binding estradiol, but does not affect estradiol-induced estrogen receptor transcription. Estradiol 104-113 gastric inhibitory polypeptide Homo sapiens 36-39 16046120-1 2005 Dipeptidyl peptidase IV (DPP4) is a multifunctional type II transmembrane serine peptidase which regulates various physiological processes, most notably plasma glucose homeostasis by cleaving peptide hormones glucagon-like peptide-1 and glucose-dependent insulinotropic polypeptide. Glucose 160-167 gastric inhibitory polypeptide Homo sapiens 237-281 15993590-2 2005 N-terminal modification of GIP(1-30) with 40 kDa polyethylene glycol (PEG) abrogates functional activity. Polyethylene Glycols 49-68 gastric inhibitory polypeptide Homo sapiens 27-30 15993590-2 2005 N-terminal modification of GIP(1-30) with 40 kDa polyethylene glycol (PEG) abrogates functional activity. Polyethylene Glycols 70-73 gastric inhibitory polypeptide Homo sapiens 27-30 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 gastric inhibitory polypeptide Homo sapiens 81-84 15383372-5 2005 We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). meat hydrolysate 41-57 gastric inhibitory polypeptide Homo sapiens 126-129 15955806-5 2005 Using mutant forms of K(V)1.4 with Ala-Ser/Thr substitutions in a potential PKA phosphorylation site, C-terminal phosphorylation was shown to be linked to GIP-mediated current amplitude decreases. Alanine 35-38 gastric inhibitory polypeptide Homo sapiens 155-158 15955806-5 2005 Using mutant forms of K(V)1.4 with Ala-Ser/Thr substitutions in a potential PKA phosphorylation site, C-terminal phosphorylation was shown to be linked to GIP-mediated current amplitude decreases. Serine 39-42 gastric inhibitory polypeptide Homo sapiens 155-158 15955806-5 2005 Using mutant forms of K(V)1.4 with Ala-Ser/Thr substitutions in a potential PKA phosphorylation site, C-terminal phosphorylation was shown to be linked to GIP-mediated current amplitude decreases. Threonine 43-46 gastric inhibitory polypeptide Homo sapiens 155-158 15955806-7 2005 Expression of K(V)1.4 protein was also demonstrated in human beta-cells; GIP treatment resulting in similar decreases in A-type potassium current peak amplitude to those in HEK293 cells. Potassium 128-137 gastric inhibitory polypeptide Homo sapiens 73-76 15955806-9 2005 These results strongly support an important novel role for GIP in regulating K(V)1.4 cell surface expression and modulation of A-type potassium currents, which is likely to be critically important for its insulinotropic action. Potassium 134-143 gastric inhibitory polypeptide Homo sapiens 59-62 15787675-10 2005 GIP plasma concentrations (increasing with placebo from approximately 10 to approximately 85 pmol/l and with acarbose to approximately 55 pmol/l (P < 0.0001) and their integrated responses were significantly lowered (by 43%) by acarbose (P = 0.021). Acarbose 109-117 gastric inhibitory polypeptide Homo sapiens 0-3 15787675-10 2005 GIP plasma concentrations (increasing with placebo from approximately 10 to approximately 85 pmol/l and with acarbose to approximately 55 pmol/l (P < 0.0001) and their integrated responses were significantly lowered (by 43%) by acarbose (P = 0.021). Acarbose 231-239 gastric inhibitory polypeptide Homo sapiens 0-3 15807714-1 2005 OBJECTIVES: We investigated whether the incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which are major regulators of glucose tolerance through the stimulation of insulin secretion, contribute to impaired glucose tolerance (IGT) among HIV-infected patients on highly active antiretroviral therapy (HAART). Glucose 94-101 gastric inhibitory polypeptide Homo sapiens 140-143 15807714-6 2005 In pooled study groups, the GIP incrAUC correlated positively with the ISR incrAUC without adjustment (r=0.38, P<0.05) and following adjustment for glucose incrAUC (r=0.49, P<0.01). Glucose 151-158 gastric inhibitory polypeptide Homo sapiens 28-31 15807714-7 2005 CONCLUSIONS: Our data suggest: (1) that glucose-intolerant, HIV-infected male patients may display enhanced GLP-1 responses to oral glucose compared with normal glucose-tolerant HIV-infected male patients, which may represent a compensatory mechanism rather than explain the IGT; (2) that the GIP response may be associated with ISR independently of plasma glucose in nondiabetic HIV-infected males on HAART. Glucose 40-47 gastric inhibitory polypeptide Homo sapiens 293-296 15807714-7 2005 CONCLUSIONS: Our data suggest: (1) that glucose-intolerant, HIV-infected male patients may display enhanced GLP-1 responses to oral glucose compared with normal glucose-tolerant HIV-infected male patients, which may represent a compensatory mechanism rather than explain the IGT; (2) that the GIP response may be associated with ISR independently of plasma glucose in nondiabetic HIV-infected males on HAART. Glucose 132-139 gastric inhibitory polypeptide Homo sapiens 293-296 15705925-9 2005 However, cultures taken from all four ACTH-dependent and the one food-dependent hyperplastic adrenals studied were also responsive to GIP (EC50 for cAMP, 1.3 x 10(-9) M in Cushing"s disease and 4.1 x 10(-10) M in food-dependent disease). Cyclic AMP 148-152 gastric inhibitory polypeptide Homo sapiens 134-137 15383372-5 2005 We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). meat hydrolysate 41-57 gastric inhibitory polypeptide Homo sapiens 154-157 15383372-5 2005 We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). Glyceraldehyde 59-73 gastric inhibitory polypeptide Homo sapiens 126-129 15383372-5 2005 We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). Glyceraldehyde 59-73 gastric inhibitory polypeptide Homo sapiens 154-157 15383372-5 2005 We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). methyl pyruvate 79-93 gastric inhibitory polypeptide Homo sapiens 126-129 15383372-5 2005 We previously showed that PMA, bombesin, meat hydrolysate, glyceraldehyde, and methylpyruvate increase hormone release from a GIP-producing EE cell line (GIP/Ins cells). methyl pyruvate 79-93 gastric inhibitory polypeptide Homo sapiens 154-157 15533777-2 2004 The 42 amino acid polypeptide glucose-dependent insulinotropic polypeptide/gastric inhibitory polypeptide (GIP) is released from intestinal K-cells in response to nutrient ingestion. Glucose 30-37 gastric inhibitory polypeptide Homo sapiens 107-110 16492545-16 2005 The insulinotropic (incretin) gut peptides, GLP-1 and GIP, secreted in response to yet-to-be-absorbed intraluminal nutrients, amplify beta-cell secretion and thereby activate the glucose sourcing switch in a feedforward manner. Glucose 179-186 gastric inhibitory polypeptide Homo sapiens 54-57 15783246-8 2005 In GIP-dependent Cushing syndrome, the most frequent subtype of ACTH-independent macronodular adrenal hyperplasia associated with the presence of aberrant adrenocortical hormone receptors described so far, octreotide administration before each meal showed clinical efficacy only in the first few months, probably because of somatostatin receptor downregulation in GIP-secreting cells. Octreotide 206-216 gastric inhibitory polypeptide Homo sapiens 3-6 15783246-8 2005 In GIP-dependent Cushing syndrome, the most frequent subtype of ACTH-independent macronodular adrenal hyperplasia associated with the presence of aberrant adrenocortical hormone receptors described so far, octreotide administration before each meal showed clinical efficacy only in the first few months, probably because of somatostatin receptor downregulation in GIP-secreting cells. Octreotide 206-216 gastric inhibitory polypeptide Homo sapiens 364-367 15522230-0 2004 NMR structure of the glucose-dependent insulinotropic polypeptide fragment, GIP(1-30)amide. Amides 85-90 gastric inhibitory polypeptide Homo sapiens 21-65 15522230-2 2004 The glucose-dependent action of GIP on pancreatic beta-cells has attracted attention towards its exploitation as a potential drug for type 2 diabetes. Glucose 4-11 gastric inhibitory polypeptide Homo sapiens 32-35 15522230-4 2004 Therefore, to understand the basic structural requirements for the biological activity of GIP, the solution structure of the major biologically active fragment, GIP(1-30)amide, was investigated by proton NMR spectroscopy and molecular modelling. Amides 170-175 gastric inhibitory polypeptide Homo sapiens 90-93 15561910-2 2004 The two hormones responsible for the incretin effect, glucose-dependent insulinotropic hormone (GIP) and glucagon-like peptide-1 (GLP-1), are secreted after oral glucose loads and augment insulin secretion in response to hyperglycemia. Glucose 54-61 gastric inhibitory polypeptide Homo sapiens 96-99 15561911-2 2004 Together with the related hormone glucose-dependent insulinotropic polypeptide (GIP), it is responsible for the incretin effect, the augmentation of insulin secretion after oral as opposed to intravenous administration of glucose. Glucose 34-41 gastric inhibitory polypeptide Homo sapiens 80-83 15563754-7 2004 This could be achieved by the use of GLP-1 or GIP to elevate cAMP in the pancreatic islet beta-cell. Cyclic AMP 61-65 gastric inhibitory polypeptide Homo sapiens 46-49 15491793-1 2004 AIMS/HYPOTHESIS: Since insulin secretion in response to exogenous gastric inhibitory polypeptide (GIP) is diminished not only in patients with type 2 diabetes, but also in their normal glucose-tolerant first-degree relatives, it was the aim to investigate the integrity of the entero-insular axis in such subjects. Glucose 185-192 gastric inhibitory polypeptide Homo sapiens 98-101 15491793-11 2004 Nevertheless, endogenous secretion of GIP and GLP-1 is a major determinant of insulin secretion after oral glucose. Glucose 107-114 gastric inhibitory polypeptide Homo sapiens 38-41 15655703-1 2004 Recent studies have indicated that GIP and GLP-1 are about as important as each other in the incretin effect, being released rapidly after meals and being active already at fasting glucose levels. Glucose 181-188 gastric inhibitory polypeptide Homo sapiens 35-38 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 gastric inhibitory polypeptide Homo sapiens 24-27 15302229-4 2004 The current report examines the N-terminal bioactive domain of GIP residing in residues 1-14 by alanine scanning mutagenesis and N-terminal substitution/modification. Alanine 96-103 gastric inhibitory polypeptide Homo sapiens 63-66 15655715-2 2004 Glucagon-like peptide-1 (GLP1) and, to a lesser extent, glucose-dependent insulinotropic polypeptide (GIP) are potent stimulators of insulin secretion, and consequently have significant effects on the regulation of the glucose metabolism. Glucose 56-63 gastric inhibitory polypeptide Homo sapiens 102-105 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 gastric inhibitory polypeptide Homo sapiens 0-44 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 gastric inhibitory polypeptide Homo sapiens 46-49 15302229-6 2004 The alanine scan of the GIP(1-14) sequence established that the peptide was extremely sensitive to structural perturbations. Alanine 4-11 gastric inhibitory polypeptide Homo sapiens 24-27 15326569-4 2004 Abnormal responses were observed in three patients with Cushing"s syndrome; one patient showed a gastric inhibitory polypeptide (GIP)-dependent cortisol rise after meal, together with responses after GnRH and cisapride; the second patient showed an LH-dependent cortisol response to GnRH, and in the third cortisol rose after cisapride. Luteinizing Hormone 249-251 gastric inhibitory polypeptide Homo sapiens 129-132 15326569-4 2004 Abnormal responses were observed in three patients with Cushing"s syndrome; one patient showed a gastric inhibitory polypeptide (GIP)-dependent cortisol rise after meal, together with responses after GnRH and cisapride; the second patient showed an LH-dependent cortisol response to GnRH, and in the third cortisol rose after cisapride. Hydrocortisone 144-152 gastric inhibitory polypeptide Homo sapiens 129-132 15326569-4 2004 Abnormal responses were observed in three patients with Cushing"s syndrome; one patient showed a gastric inhibitory polypeptide (GIP)-dependent cortisol rise after meal, together with responses after GnRH and cisapride; the second patient showed an LH-dependent cortisol response to GnRH, and in the third cortisol rose after cisapride. Cisapride 326-335 gastric inhibitory polypeptide Homo sapiens 129-132 15318993-4 2004 GIP is a peptide secreted by the duodenal K-cells in response to ingested fat and carbohydrate. Carbohydrates 82-94 gastric inhibitory polypeptide Homo sapiens 0-3 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 gastric inhibitory polypeptide Homo sapiens 117-120 15131768-12 2004 Plasma levels of GLP-1 and GIP increased after oral glucose. Glucose 52-59 gastric inhibitory polypeptide Homo sapiens 27-30 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 gastric inhibitory polypeptide Homo sapiens 239-283 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 gastric inhibitory polypeptide Homo sapiens 285-288 15013938-2 2004 Extensive research during the past three decades has identified two gut hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP, also known as gastric inhibitory polypeptide) that are important in postprandial glucose metabolism. Glucose 118-125 gastric inhibitory polypeptide Homo sapiens 160-163 15384825-12 2004 At the same time, negative relationships were observed between blood ghrelin and GIP (r = -0.42, p < 0.05), insulin (r = -0.4, p < 0.05), leptin (r = -0.45, p < 0.05), and creatinine clearance [r = -0.33, p = 0.08 (nonsignificant)]. Ghrelin 69-76 gastric inhibitory polypeptide Homo sapiens 81-84 14758140-0 2004 Phase I study with dose escalation of gemcitabine and cisplatin in combination with ifosfamide (GIP) in patients with non-small-cell lung carcinoma. Ifosfamide 84-94 gastric inhibitory polypeptide Homo sapiens 96-99 15566961-4 2004 While several amino acid analogs of the cysteines of the GIP retained inhibitory activity, heavy metal binding and pre-incubation of the peptides with a variety of cations and hormone ligands were found to influence the outcomes of growth bioassays. Cysteine 40-49 gastric inhibitory polypeptide Homo sapiens 57-60 15566961-4 2004 While several amino acid analogs of the cysteines of the GIP retained inhibitory activity, heavy metal binding and pre-incubation of the peptides with a variety of cations and hormone ligands were found to influence the outcomes of growth bioassays. Metals 97-102 gastric inhibitory polypeptide Homo sapiens 57-60 14681846-12 2004 Isocaloric amounts of carbohydrate and alcohol suppressed equally the postprandial free fatty acid levels, but carbohydrate increased the postprandial glucose, GIP, and insulin levels the most. Carbohydrates 111-123 gastric inhibitory polypeptide Homo sapiens 160-163 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 gastric inhibitory polypeptide Homo sapiens 116-160 14617798-6 2003 Cysteine-to-alanine analogues of the GIP retain the antigrowth properties, while similar cysteine-to-glycine and cysteine-to-serine analogues demonstrate little, if any, growth regulatory activity. Cysteine 0-8 gastric inhibitory polypeptide Homo sapiens 37-40 14617798-6 2003 Cysteine-to-alanine analogues of the GIP retain the antigrowth properties, while similar cysteine-to-glycine and cysteine-to-serine analogues demonstrate little, if any, growth regulatory activity. Alanine 12-19 gastric inhibitory polypeptide Homo sapiens 37-40 14617798-9 2003 It was further observed that the GIP can bind both Zn(2+) and Co(2+); the Co(2+) peptide complex was shown to have a distorted tetrahedral symmetry, involving coordination of two cysteine and two histidine residues. Zinc 51-57 gastric inhibitory polypeptide Homo sapiens 33-36 14617798-9 2003 It was further observed that the GIP can bind both Zn(2+) and Co(2+); the Co(2+) peptide complex was shown to have a distorted tetrahedral symmetry, involving coordination of two cysteine and two histidine residues. Cobalt(2+) 62-68 gastric inhibitory polypeptide Homo sapiens 33-36 14617798-9 2003 It was further observed that the GIP can bind both Zn(2+) and Co(2+); the Co(2+) peptide complex was shown to have a distorted tetrahedral symmetry, involving coordination of two cysteine and two histidine residues. Cobalt(2+) 74-80 gastric inhibitory polypeptide Homo sapiens 33-36 14617798-9 2003 It was further observed that the GIP can bind both Zn(2+) and Co(2+); the Co(2+) peptide complex was shown to have a distorted tetrahedral symmetry, involving coordination of two cysteine and two histidine residues. Cysteine 179-187 gastric inhibitory polypeptide Homo sapiens 33-36 14617798-9 2003 It was further observed that the GIP can bind both Zn(2+) and Co(2+); the Co(2+) peptide complex was shown to have a distorted tetrahedral symmetry, involving coordination of two cysteine and two histidine residues. Histidine 196-205 gastric inhibitory polypeptide Homo sapiens 33-36 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 gastric inhibitory polypeptide Homo sapiens 33-49 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 gastric inhibitory polypeptide Homo sapiens 23-26 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 gastric inhibitory polypeptide Homo sapiens 0-44 13679012-2 2003 I propose that, in subjects expressing T54, the secretion of gastric inhibitory polypeptide (GIP) evoked by fatty meals is subnormal, such that adipocytes are less efficient in converting chylomicrons to stored triglyceride. Triglycerides 211-223 gastric inhibitory polypeptide Homo sapiens 93-96 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 gastric inhibitory polypeptide Homo sapiens 46-49 12901855-2 2003 It is this glucose-dependency that has attracted attention towards GIP as a potential therapeutic agent for the treatment of type 2 diabetes. Glucose 11-18 gastric inhibitory polypeptide Homo sapiens 67-70 12721154-4 2003 GIP dose-dependently stimulated HUVEC and ECV 304 proliferation as measured by [3H]thymidine incorporation. Tritium 80-82 gastric inhibitory polypeptide Homo sapiens 0-3 12721154-4 2003 GIP dose-dependently stimulated HUVEC and ECV 304 proliferation as measured by [3H]thymidine incorporation. Thymidine 83-92 gastric inhibitory polypeptide Homo sapiens 0-3 12721154-7 2003 These findings suggest that, although GIP increases [3H]thymidine incorporation in both HUVEC and ECV 304, this proliferative response is mediated by ET-1 only in HUVEC. Tritium 53-55 gastric inhibitory polypeptide Homo sapiens 38-41 12902886-1 2003 A phase II study was conducted to evaluate the safety and efficacy of the combination GIP (gemcitabine, ifosfamide, and cisplatin) for the treatment of patients with advanced non-small-cell lung cancer (NSCLC). gemcitabine 91-102 gastric inhibitory polypeptide Homo sapiens 86-89 12902886-1 2003 A phase II study was conducted to evaluate the safety and efficacy of the combination GIP (gemcitabine, ifosfamide, and cisplatin) for the treatment of patients with advanced non-small-cell lung cancer (NSCLC). Ifosfamide 104-114 gastric inhibitory polypeptide Homo sapiens 86-89 12902886-1 2003 A phase II study was conducted to evaluate the safety and efficacy of the combination GIP (gemcitabine, ifosfamide, and cisplatin) for the treatment of patients with advanced non-small-cell lung cancer (NSCLC). Cisplatin 120-129 gastric inhibitory polypeptide Homo sapiens 86-89 12832099-0 2003 Both GLP-1 and GIP are insulinotropic at basal and postprandial glucose levels and contribute nearly equally to the incretin effect of a meal in healthy subjects. Glucose 64-71 gastric inhibitory polypeptide Homo sapiens 15-18 12832099-8 2003 GLP-1 and GIP infusions induced significant and similar increases at fasting glucose levels and at 6 mmol/l. Glucose 77-84 gastric inhibitory polypeptide Homo sapiens 10-13 12525257-3 2003 Therefore, this study examined the plasma stability, biological activity and antidiabetic potential of two novel NH2-terminal Ala2-substituted analogues of GIP, containing glycine (Gly) or serine (Ser). Glycine 172-179 gastric inhibitory polypeptide Homo sapiens 156-159 14630571-1 2003 The incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are important in blood glucose regulation. Glucose 58-65 gastric inhibitory polypeptide Homo sapiens 104-107 14630571-4 2003 VP did not significantly affect levels of intact GLP-1 but increased levels of intact GIP (from 4543 +/- 1880 to 9208 +/- 3267 pM x min; P <.01), thus improving glucose tolerance (area under the curve [AUC] for glucose reduced from 1904 +/- 480 to 1582 +/- 353 mM x min; P =.05). valine-pyrrolidide 0-2 gastric inhibitory polypeptide Homo sapiens 86-89 14630571-4 2003 VP did not significantly affect levels of intact GLP-1 but increased levels of intact GIP (from 4543 +/- 1880 to 9208 +/- 3267 pM x min; P <.01), thus improving glucose tolerance (area under the curve [AUC] for glucose reduced from 1904 +/- 480 to 1582 +/- 353 mM x min; P =.05). Glucose 164-171 gastric inhibitory polypeptide Homo sapiens 86-89 12675251-0 2003 Glucose-dependent insulinotropic polypeptide (GIP): development of DP IV-resistant analogues with therapeutic potential. dp 67-69 gastric inhibitory polypeptide Homo sapiens 0-44 12675251-0 2003 Glucose-dependent insulinotropic polypeptide (GIP): development of DP IV-resistant analogues with therapeutic potential. dp 67-69 gastric inhibitory polypeptide Homo sapiens 46-49 12525257-5 2003 In Chinese hamster lung fibroblasts stably transfected with the human GIP receptor, GIP, (Gly2)GIP and (Ser2)GIP stimulated cAMP production with EC(50) values of 18.2, 14.9 and 15.0 nM respectively. Cyclic AMP 124-128 gastric inhibitory polypeptide Homo sapiens 84-87 12525257-5 2003 In Chinese hamster lung fibroblasts stably transfected with the human GIP receptor, GIP, (Gly2)GIP and (Ser2)GIP stimulated cAMP production with EC(50) values of 18.2, 14.9 and 15.0 nM respectively. Cyclic AMP 124-128 gastric inhibitory polypeptide Homo sapiens 84-87 12525257-5 2003 In Chinese hamster lung fibroblasts stably transfected with the human GIP receptor, GIP, (Gly2)GIP and (Ser2)GIP stimulated cAMP production with EC(50) values of 18.2, 14.9 and 15.0 nM respectively. Cyclic AMP 124-128 gastric inhibitory polypeptide Homo sapiens 84-87 12525257-10 2003 These data indicate that substitution of the penultimate Ala2 in GIP by Gly or Ser confers resistance to plasma DPP IV degradation, resulting in enhanced biological activity, therefore raising the possibility of their use in the treatment of type 2 diabetes. Glycine 72-75 gastric inhibitory polypeptide Homo sapiens 65-68 12525257-10 2003 These data indicate that substitution of the penultimate Ala2 in GIP by Gly or Ser confers resistance to plasma DPP IV degradation, resulting in enhanced biological activity, therefore raising the possibility of their use in the treatment of type 2 diabetes. Serine 79-82 gastric inhibitory polypeptide Homo sapiens 65-68 12764578-1 2003 AIMS/HYPOTHESIS: In the isolated perfused pancreas, gastric inhibitory polypeptide (GIP) has been shown to enhance glucagon secretion at basal glucose concentrations, but in healthy humans no glucagonotropic effect of GIP has yet been reported. Glucose 143-150 gastric inhibitory polypeptide Homo sapiens 52-82 12764578-1 2003 AIMS/HYPOTHESIS: In the isolated perfused pancreas, gastric inhibitory polypeptide (GIP) has been shown to enhance glucagon secretion at basal glucose concentrations, but in healthy humans no glucagonotropic effect of GIP has yet been reported. Glucose 143-150 gastric inhibitory polypeptide Homo sapiens 84-87 12764578-2 2003 Therefore, we studied the effect of GIP on glucagon secretion under normoglycaemic conditions. Glucagon 43-51 gastric inhibitory polypeptide Homo sapiens 36-39 12764578-11 2003 CONCLUSIONS/INTERPRETATION: Glucagon secretion is dose-dependently stimulated by GIP at basal glucose concentrations. Glucose 94-101 gastric inhibitory polypeptide Homo sapiens 81-84 12788877-11 2003 We conclude: 1) that a decreased GLP-1 secretion may contribute to impaired insulin secretion in type 2 diabetes mellitus, whereas GIP and GLP-1 secretion is normal in type 1 diabetic patients; and 2) that it is possible to modulate the beta-cell sensitivity to glucose in obese healthy subjects, and possibly also in type 2 diabetic patients, by giving them a large meal, compared with a small meal. Glucose 262-269 gastric inhibitory polypeptide Homo sapiens 131-134 12800091-1 2003 Glucose-dependent insulinotropic polypeptide (GIP) has significant potential in diabetes therapy due to its ability to serve as a glucose-dependent activator of insulin secretion. Glucose 130-137 gastric inhibitory polypeptide Homo sapiens 0-44 12800091-1 2003 Glucose-dependent insulinotropic polypeptide (GIP) has significant potential in diabetes therapy due to its ability to serve as a glucose-dependent activator of insulin secretion. Glucose 130-137 gastric inhibitory polypeptide Homo sapiens 46-49 12800091-2 2003 However, its biological activity is severely compromised by the ubiquitous enzyme dipeptidylpeptidase IV (DPP IV), which removes the N-terminal Tyr(1)-Ala(2) dipeptide from GIP. Tyrosine 144-147 gastric inhibitory polypeptide Homo sapiens 173-176 12800091-2 2003 However, its biological activity is severely compromised by the ubiquitous enzyme dipeptidylpeptidase IV (DPP IV), which removes the N-terminal Tyr(1)-Ala(2) dipeptide from GIP. Alanine 151-154 gastric inhibitory polypeptide Homo sapiens 173-176 12800091-2 2003 However, its biological activity is severely compromised by the ubiquitous enzyme dipeptidylpeptidase IV (DPP IV), which removes the N-terminal Tyr(1)-Ala(2) dipeptide from GIP. Dipeptides 158-167 gastric inhibitory polypeptide Homo sapiens 173-176 12800091-3 2003 Therefore, 2 novel N-terminal Ala(2)-substituted analogs of GIP, with Ala substituted by 2-aminobutyric acid (Abu) or sarcosine (Sar), were synthesized and tested for metabolic stability and biological activity both in vitro and in vivo. ala(2) 30-36 gastric inhibitory polypeptide Homo sapiens 60-63 12800091-3 2003 Therefore, 2 novel N-terminal Ala(2)-substituted analogs of GIP, with Ala substituted by 2-aminobutyric acid (Abu) or sarcosine (Sar), were synthesized and tested for metabolic stability and biological activity both in vitro and in vivo. Alanine 30-33 gastric inhibitory polypeptide Homo sapiens 60-63 12800091-3 2003 Therefore, 2 novel N-terminal Ala(2)-substituted analogs of GIP, with Ala substituted by 2-aminobutyric acid (Abu) or sarcosine (Sar), were synthesized and tested for metabolic stability and biological activity both in vitro and in vivo. alpha-aminobutyric acid 89-108 gastric inhibitory polypeptide Homo sapiens 60-63 12800091-3 2003 Therefore, 2 novel N-terminal Ala(2)-substituted analogs of GIP, with Ala substituted by 2-aminobutyric acid (Abu) or sarcosine (Sar), were synthesized and tested for metabolic stability and biological activity both in vitro and in vivo. alpha-aminobutyric acid 110-113 gastric inhibitory polypeptide Homo sapiens 60-63 12800091-3 2003 Therefore, 2 novel N-terminal Ala(2)-substituted analogs of GIP, with Ala substituted by 2-aminobutyric acid (Abu) or sarcosine (Sar), were synthesized and tested for metabolic stability and biological activity both in vitro and in vivo. Sarcosine 118-127 gastric inhibitory polypeptide Homo sapiens 60-63 12800091-5 2003 In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, native GIP, (Abu(2))GIP, and (Sar(2))GIP dose-dependently stimulated cyclic adenosine monophosphate (camp) production with EC(50) values of 18.2, 38.5, and 54.6 nmol/L, respectively. Cyclic AMP 147-177 gastric inhibitory polypeptide Homo sapiens 64-67 12800091-5 2003 In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, native GIP, (Abu(2))GIP, and (Sar(2))GIP dose-dependently stimulated cyclic adenosine monophosphate (camp) production with EC(50) values of 18.2, 38.5, and 54.6 nmol/L, respectively. Cyclic AMP 147-177 gastric inhibitory polypeptide Homo sapiens 85-88 12800091-5 2003 In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, native GIP, (Abu(2))GIP, and (Sar(2))GIP dose-dependently stimulated cyclic adenosine monophosphate (camp) production with EC(50) values of 18.2, 38.5, and 54.6 nmol/L, respectively. Cyclic AMP 147-177 gastric inhibitory polypeptide Homo sapiens 85-88 12800091-5 2003 In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, native GIP, (Abu(2))GIP, and (Sar(2))GIP dose-dependently stimulated cyclic adenosine monophosphate (camp) production with EC(50) values of 18.2, 38.5, and 54.6 nmol/L, respectively. Cyclic AMP 147-177 gastric inhibitory polypeptide Homo sapiens 85-88 12800091-5 2003 In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, native GIP, (Abu(2))GIP, and (Sar(2))GIP dose-dependently stimulated cyclic adenosine monophosphate (camp) production with EC(50) values of 18.2, 38.5, and 54.6 nmol/L, respectively. Cyclic AMP 179-183 gastric inhibitory polypeptide Homo sapiens 64-67 12800091-5 2003 In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, native GIP, (Abu(2))GIP, and (Sar(2))GIP dose-dependently stimulated cyclic adenosine monophosphate (camp) production with EC(50) values of 18.2, 38.5, and 54.6 nmol/L, respectively. Cyclic AMP 179-183 gastric inhibitory polypeptide Homo sapiens 85-88 12800091-5 2003 In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, native GIP, (Abu(2))GIP, and (Sar(2))GIP dose-dependently stimulated cyclic adenosine monophosphate (camp) production with EC(50) values of 18.2, 38.5, and 54.6 nmol/L, respectively. Cyclic AMP 179-183 gastric inhibitory polypeptide Homo sapiens 85-88 12800091-5 2003 In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, native GIP, (Abu(2))GIP, and (Sar(2))GIP dose-dependently stimulated cyclic adenosine monophosphate (camp) production with EC(50) values of 18.2, 38.5, and 54.6 nmol/L, respectively. Cyclic AMP 179-183 gastric inhibitory polypeptide Homo sapiens 85-88 12800091-6 2003 In BRIN-BD11 cells, both (Abu(2))GIP and (Sar(2))GIP (10(-13) to 10(-8) mol/L) dose-dependently stimulated insulin secretion with significantly enhanced effects at 16.7 mmol/L compared with 5.6 mmol/L glucose. Glucose 201-208 gastric inhibitory polypeptide Homo sapiens 33-36 12800091-6 2003 In BRIN-BD11 cells, both (Abu(2))GIP and (Sar(2))GIP (10(-13) to 10(-8) mol/L) dose-dependently stimulated insulin secretion with significantly enhanced effects at 16.7 mmol/L compared with 5.6 mmol/L glucose. Glucose 201-208 gastric inhibitory polypeptide Homo sapiens 49-52 12800091-9 2003 The present data show that substitution of the penultimate N-terminal Ala(2) in GIP by Abu or Sar results in analogs with moderately reduced metabolic stability and biological activity in vitro, but with preserved biological activity in vivo. ala(2) 70-76 gastric inhibitory polypeptide Homo sapiens 80-83 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 gastric inhibitory polypeptide Homo sapiens 96-126 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 gastric inhibitory polypeptide Homo sapiens 128-131 12860206-3 2003 We report that GIP dose dependently stimulated 3H-thymidine incorporation in the osteoblastic-like cell line MG-63. Tritium 47-49 gastric inhibitory polypeptide Homo sapiens 15-18 12860206-3 2003 We report that GIP dose dependently stimulated 3H-thymidine incorporation in the osteoblastic-like cell line MG-63. Thymidine 50-59 gastric inhibitory polypeptide Homo sapiens 15-18 12627321-2 2003 METHODS: Cyclic AMP production was assessed in Chinese hamster lung fibroblasts transfected with human GIP or GLP-1 receptors, respectively. Cyclic AMP 9-19 gastric inhibitory polypeptide Homo sapiens 103-106 12150711-0 2002 Enhanced cAMP generation and insulin-releasing potency of two novel Tyr1-modified enzyme-resistant forms of glucose-dependent insulinotropic polypeptide is associated with significant antihyperglycaemic activity in spontaneous obesity-diabetes. Cyclic AMP 9-13 gastric inhibitory polypeptide Homo sapiens 108-152 12150711-4 2002 Therefore two novel Tyr(1)-modified analogues of GIP, N-Fmoc-GIP (where Fmoc is 9-fluorenylmethoxycarbonyl) and N-palmitate-GIP, were synthesized and tested for metabolic stability and biological activity. tyr(1) 20-26 gastric inhibitory polypeptide Homo sapiens 49-52 12150711-4 2002 Therefore two novel Tyr(1)-modified analogues of GIP, N-Fmoc-GIP (where Fmoc is 9-fluorenylmethoxycarbonyl) and N-palmitate-GIP, were synthesized and tested for metabolic stability and biological activity. tyr(1) 20-26 gastric inhibitory polypeptide Homo sapiens 61-64 12150711-4 2002 Therefore two novel Tyr(1)-modified analogues of GIP, N-Fmoc-GIP (where Fmoc is 9-fluorenylmethoxycarbonyl) and N-palmitate-GIP, were synthesized and tested for metabolic stability and biological activity. tyr(1) 20-26 gastric inhibitory polypeptide Homo sapiens 61-64 12150711-4 2002 Therefore two novel Tyr(1)-modified analogues of GIP, N-Fmoc-GIP (where Fmoc is 9-fluorenylmethoxycarbonyl) and N-palmitate-GIP, were synthesized and tested for metabolic stability and biological activity. n-fmoc 54-60 gastric inhibitory polypeptide Homo sapiens 49-52 12150711-4 2002 Therefore two novel Tyr(1)-modified analogues of GIP, N-Fmoc-GIP (where Fmoc is 9-fluorenylmethoxycarbonyl) and N-palmitate-GIP, were synthesized and tested for metabolic stability and biological activity. n-fmoc 54-60 gastric inhibitory polypeptide Homo sapiens 61-64 12150711-4 2002 Therefore two novel Tyr(1)-modified analogues of GIP, N-Fmoc-GIP (where Fmoc is 9-fluorenylmethoxycarbonyl) and N-palmitate-GIP, were synthesized and tested for metabolic stability and biological activity. n-fmoc 54-60 gastric inhibitory polypeptide Homo sapiens 61-64 12150711-4 2002 Therefore two novel Tyr(1)-modified analogues of GIP, N-Fmoc-GIP (where Fmoc is 9-fluorenylmethoxycarbonyl) and N-palmitate-GIP, were synthesized and tested for metabolic stability and biological activity. 9-fluorenylmethoxycarbonyl 80-106 gastric inhibitory polypeptide Homo sapiens 49-52 12150711-6 2002 In Chinese hamster lung (CHL) cells expressing the cloned human GIP receptor, both analogues exhibited a 2-fold increase in cAMP-generating potency compared with native GIP (EC(50) values of 9.4, 10.0 and 18.2 nM respectively). Cyclic AMP 124-128 gastric inhibitory polypeptide Homo sapiens 64-67 12150711-8 2002 In obese diabetic ( ob / ob ) mice, administration of N-Fmoc-GIP or N-palmitate-GIP (25 nmol/kg) together with glucose (18 mmol/kg) significantly reduced the peak 15 min glucose excursion (1.4- and 1.5-fold respectively; P <0.05 to P <0.01) compared with glucose alone. Glucose 170-177 gastric inhibitory polypeptide Homo sapiens 80-83 12150711-8 2002 In obese diabetic ( ob / ob ) mice, administration of N-Fmoc-GIP or N-palmitate-GIP (25 nmol/kg) together with glucose (18 mmol/kg) significantly reduced the peak 15 min glucose excursion (1.4- and 1.5-fold respectively; P <0.05 to P <0.01) compared with glucose alone. Glucose 170-177 gastric inhibitory polypeptide Homo sapiens 80-83 12150711-9 2002 The area under the curve (AUC) for glucose was significantly lower after administration of either analogue compared with glucose administered alone or in combination with native GIP (1.5-fold; P <0.05). Glucose 35-42 gastric inhibitory polypeptide Homo sapiens 178-181 12150711-9 2002 The area under the curve (AUC) for glucose was significantly lower after administration of either analogue compared with glucose administered alone or in combination with native GIP (1.5-fold; P <0.05). Glucose 121-128 gastric inhibitory polypeptide Homo sapiens 178-181 12150711-12 2002 These data indicate that novel N-terminal Tyr(1) modification of GIP with an Fmoc or palmitate group confers resistance to degradation by DPP IV in plasma, which is reflected by increased in vitro potency and greater insulinotropic and antihyperglycaemic activities in an animal model of Type II diabetes mellitus. Tyrosine 42-45 gastric inhibitory polypeptide Homo sapiens 65-68 12525257-3 2003 Therefore, this study examined the plasma stability, biological activity and antidiabetic potential of two novel NH2-terminal Ala2-substituted analogues of GIP, containing glycine (Gly) or serine (Ser). Serine 197-200 gastric inhibitory polypeptide Homo sapiens 156-159 12635849-0 2002 Cyclic AMP production and insulin releasing activity of synthetic fragment peptides of glucose-dependent insulinotropic polypeptide. Cyclic AMP 0-10 gastric inhibitory polypeptide Homo sapiens 87-131 12635849-1 2002 Synthetic fragment peptides of glucose-dependent insulinotropic polypeptide (GIP) were evaluated for their ability to elevate cellular cAMP production and stimulate insulin secretion. Cyclic AMP 135-139 gastric inhibitory polypeptide Homo sapiens 31-75 12635849-1 2002 Synthetic fragment peptides of glucose-dependent insulinotropic polypeptide (GIP) were evaluated for their ability to elevate cellular cAMP production and stimulate insulin secretion. Cyclic AMP 135-139 gastric inhibitory polypeptide Homo sapiens 77-80 12635849-2 2002 In GIP receptor transfected CHL cells, GIP(4-42) and GIP(17-30) dose-dependently inhibited GIP-stimulated cAMP production (40 +/- 8%; p<0.01 and 15 +/- 6%; p<0.05, respectively), while GIP(1-16) exerted very weak agonist effects on cAMP production. Cyclic AMP 106-110 gastric inhibitory polypeptide Homo sapiens 39-42 12635849-2 2002 In GIP receptor transfected CHL cells, GIP(4-42) and GIP(17-30) dose-dependently inhibited GIP-stimulated cAMP production (40 +/- 8%; p<0.01 and 15 +/- 6%; p<0.05, respectively), while GIP(1-16) exerted very weak agonist effects on cAMP production. Cyclic AMP 106-110 gastric inhibitory polypeptide Homo sapiens 39-42 12635849-2 2002 In GIP receptor transfected CHL cells, GIP(4-42) and GIP(17-30) dose-dependently inhibited GIP-stimulated cAMP production (40 +/- 8%; p<0.01 and 15 +/- 6%; p<0.05, respectively), while GIP(1-16) exerted very weak agonist effects on cAMP production. Cyclic AMP 106-110 gastric inhibitory polypeptide Homo sapiens 39-42 12635849-2 2002 In GIP receptor transfected CHL cells, GIP(4-42) and GIP(17-30) dose-dependently inhibited GIP-stimulated cAMP production (40 +/- 8%; p<0.01 and 15 +/- 6%; p<0.05, respectively), while GIP(1-16) exerted very weak agonist effects on cAMP production. Cyclic AMP 106-110 gastric inhibitory polypeptide Homo sapiens 39-42 12635849-2 2002 In GIP receptor transfected CHL cells, GIP(4-42) and GIP(17-30) dose-dependently inhibited GIP-stimulated cAMP production (40 +/- 8%; p<0.01 and 15 +/- 6%; p<0.05, respectively), while GIP(1-16) exerted very weak agonist effects on cAMP production. Cyclic AMP 238-242 gastric inhibitory polypeptide Homo sapiens 39-42 12635849-2 2002 In GIP receptor transfected CHL cells, GIP(4-42) and GIP(17-30) dose-dependently inhibited GIP-stimulated cAMP production (40 +/- 8%; p<0.01 and 15 +/- 6%; p<0.05, respectively), while GIP(1-16) exerted very weak agonist effects on cAMP production. Cyclic AMP 238-242 gastric inhibitory polypeptide Homo sapiens 39-42 12635849-2 2002 In GIP receptor transfected CHL cells, GIP(4-42) and GIP(17-30) dose-dependently inhibited GIP-stimulated cAMP production (40 +/- 8%; p<0.01 and 15 +/- 6%; p<0.05, respectively), while GIP(1-16) exerted very weak agonist effects on cAMP production. Cyclic AMP 238-242 gastric inhibitory polypeptide Homo sapiens 39-42 12635849-2 2002 In GIP receptor transfected CHL cells, GIP(4-42) and GIP(17-30) dose-dependently inhibited GIP-stimulated cAMP production (40 +/- 8%; p<0.01 and 15 +/- 6%; p<0.05, respectively), while GIP(1-16) exerted very weak agonist effects on cAMP production. Cyclic AMP 238-242 gastric inhibitory polypeptide Homo sapiens 39-42 12242461-0 2002 Improved stability, insulin-releasing activity and antidiabetic potential of two novel N-terminal analogues of gastric inhibitory polypeptide: N-acetyl-GIP and pGlu-GIP. Pyrrolidonecarboxylic Acid 160-164 gastric inhibitory polypeptide Homo sapiens 165-168 12242461-9 2002 This antihyperglycaemic effect was coupled to a raised ( p<0.001) and more prolonged insulin response after administration of Ac-GIP and pGlu-GIP (AUC, 644+/-54 and 576+/-51 ng.ml(-1) x min, respectively) compared with native GIP (AUC, 257+/-29 ng.ml(-1) x min). Actinium 129-131 gastric inhibitory polypeptide Homo sapiens 132-135 12124779-8 2002 Like K-cells in vivo, the GIP/insulin-producing cells express the critical glucose sensing enzyme, glucokinase. Glucose 75-82 gastric inhibitory polypeptide Homo sapiens 26-29 12189441-0 2002 Defective amplification of the late phase insulin response to glucose by GIP in obese Type II diabetic patients. Glucose 62-69 gastric inhibitory polypeptide Homo sapiens 73-76 12189441-4 2002 bolus injections of GLP-1(2.5 nmol) or GIP(7.5 nmol) concomitant with an increase of plasma glucose to 15 mmol/l. Glucose 92-99 gastric inhibitory polypeptide Homo sapiens 39-42 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 gastric inhibitory polypeptide Homo sapiens 35-38 12242461-3 2002 Cyclic adenosine 3"5" monophosphate (cAMP) production was assessed in Chinese hamster lung fibroblast cells transfected with the human GIP receptor. Cyclic AMP 0-35 gastric inhibitory polypeptide Homo sapiens 135-138 12242461-3 2002 Cyclic adenosine 3"5" monophosphate (cAMP) production was assessed in Chinese hamster lung fibroblast cells transfected with the human GIP receptor. Cyclic AMP 37-41 gastric inhibitory polypeptide Homo sapiens 135-138 12242461-5 2002 RESULTS: GIP was rapidly degraded by dipeptidylpeptidase IV and plasma (t(1/2) 2.3 and 6.2 h, respectively) whereas Ac-GIP and pGlu-GIP remained intact even after 24 h. Both Ac-GIP and pGlu-GIP were extremely potent ( p<0.001) at stimulating cAMP production (EC(50) values 1.9 and 2.7 nmol/l, respectively), almost a tenfold increase compared to native GIP (18.2 nmol/l). Cyclic AMP 245-249 gastric inhibitory polypeptide Homo sapiens 9-12 12099397-7 2002 Hourly measurements of plasma cortisol and GIP levels during a day with and a day without meals showed meal- and GIP-related cortisol secretion. Hydrocortisone 30-38 gastric inhibitory polypeptide Homo sapiens 113-116 12145765-6 2002 Glucose, but not FRUC, increased GIP concentrations, which were not different between type 2 diabetics and nondiabetics (P >.05). Glucose 0-7 gastric inhibitory polypeptide Homo sapiens 33-36 11994328-6 2002 In vitro study of the GIP-R-expressing AA showed stimulation of cortisol secretion and cAMP production by GIP. Cyclic AMP 87-91 gastric inhibitory polypeptide Homo sapiens 22-25 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. Hydrocortisone 55-63 gastric inhibitory polypeptide Homo sapiens 180-183 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 gastric inhibitory polypeptide Homo sapiens 180-183 11820780-1 2002 A novel N-terminally substituted Pro(3) analogue of glucose-dependent insulinotropic polypeptide (GIP) was synthesized and tested for plasma stability and biological activity both in vitro and in vivo. pro(3) 33-39 gastric inhibitory polypeptide Homo sapiens 52-96 11820780-1 2002 A novel N-terminally substituted Pro(3) analogue of glucose-dependent insulinotropic polypeptide (GIP) was synthesized and tested for plasma stability and biological activity both in vitro and in vivo. pro(3) 33-39 gastric inhibitory polypeptide Homo sapiens 98-101 11820780-4 2002 In obese diabetic (ob/ob) mice, intraperitoneal administration of (Pro(3))GIP (25 nmol/kg body wt) countered the ability of native GIP to stimulate plasma insulin (2.4-fold decrease; P < 0.001) and lower the glycemic excursion (1.5-fold decrease; P < 0.001) induced by a glucose load (18 mmol/kg body wt). Glucose 277-284 gastric inhibitory polypeptide Homo sapiens 74-77 11820780-5 2002 Collectively these data demonstrate that (Pro(3))GIP is a novel and potent enzyme-resistant GIP receptor antagonist capable of blocking the ability of native GIP to increase cAMP, stimulate insulin secretion, and improve glucose homeostasis in a commonly employed animal model of type 2 diabetes. Cyclic AMP 174-178 gastric inhibitory polypeptide Homo sapiens 49-52 11820780-5 2002 Collectively these data demonstrate that (Pro(3))GIP is a novel and potent enzyme-resistant GIP receptor antagonist capable of blocking the ability of native GIP to increase cAMP, stimulate insulin secretion, and improve glucose homeostasis in a commonly employed animal model of type 2 diabetes. Cyclic AMP 174-178 gastric inhibitory polypeptide Homo sapiens 92-95 11820780-5 2002 Collectively these data demonstrate that (Pro(3))GIP is a novel and potent enzyme-resistant GIP receptor antagonist capable of blocking the ability of native GIP to increase cAMP, stimulate insulin secretion, and improve glucose homeostasis in a commonly employed animal model of type 2 diabetes. Cyclic AMP 174-178 gastric inhibitory polypeptide Homo sapiens 92-95 11769775-9 2001 CONCLUSION: The close correlation between the use of pyrazinamide as measured by the GIP and NTR provides strong evidence that in the Netherlands tuberculosis is reported in conformity with the guidelines for notifiable diseases. Pyrazinamide 53-65 gastric inhibitory polypeptide Homo sapiens 85-88 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 gastric inhibitory polypeptide Homo sapiens 147-150 11522498-0 2001 Secretion of GIP in responders to acarbose in obese Type 2(NIDDM) patients. Acarbose 34-42 gastric inhibitory polypeptide Homo sapiens 13-16 11518688-4 2001 In meal groups with carbohydrates, acarbose attenuated responses of plasma insulin and glucose-dependent insulinotropic polypeptide (GIP) while augmenting responses of CCK, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY). Acarbose 35-43 gastric inhibitory polypeptide Homo sapiens 87-131 11518688-4 2001 In meal groups with carbohydrates, acarbose attenuated responses of plasma insulin and glucose-dependent insulinotropic polypeptide (GIP) while augmenting responses of CCK, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY). Acarbose 35-43 gastric inhibitory polypeptide Homo sapiens 133-136 11518688-6 2001 With the carbohydrate-free meal after sucrose and acarbose ingestion, AUC of gastric emptying was negatively correlated with integrated plasma response of GIP, implying that prior alteration of carbohydrate absorption modifies gastric emptying of a meal. Carbohydrates 9-21 gastric inhibitory polypeptide Homo sapiens 155-158 11518688-6 2001 With the carbohydrate-free meal after sucrose and acarbose ingestion, AUC of gastric emptying was negatively correlated with integrated plasma response of GIP, implying that prior alteration of carbohydrate absorption modifies gastric emptying of a meal. Acarbose 50-58 gastric inhibitory polypeptide Homo sapiens 155-158 11518688-6 2001 With the carbohydrate-free meal after sucrose and acarbose ingestion, AUC of gastric emptying was negatively correlated with integrated plasma response of GIP, implying that prior alteration of carbohydrate absorption modifies gastric emptying of a meal. Carbohydrates 194-206 gastric inhibitory polypeptide Homo sapiens 155-158 11377818-1 2001 Glucose-dependent insulinotropic peptide (GIP) is a gut-derived hormone known to be important in modulating glucose-induced insulin secretion. Glucose 108-115 gastric inhibitory polypeptide Homo sapiens 0-40 11415859-8 2001 Moreover, multivariate linear regression analysis showed that the presence of acromegalic status was associated with higher fasting and postprandial GIP levels independently of sex, age, fasting and postprandial plasma glucose and insulin levels, and the occurrence of normal or impaired glucose tolerance. Glucose 219-226 gastric inhibitory polypeptide Homo sapiens 149-152 11373257-11 2001 A slightly significant increase (P = 0.02) in the numbers of glucagon and GIP cells was seen in the alcohol group. Alcohols 100-107 gastric inhibitory polypeptide Homo sapiens 74-77 11344200-0 2001 Glucose-dependent insulinotropic hormone potentiates the hypoglycemic effect of glibenclamide in healthy volunteers: evidence for an effect on insulin extraction. Glyburide 80-93 gastric inhibitory polypeptide Homo sapiens 0-40 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 gastric inhibitory polypeptide Homo sapiens 0-40 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 gastric inhibitory polypeptide Homo sapiens 42-45 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 gastric inhibitory polypeptide Homo sapiens 0-40 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 gastric inhibitory polypeptide Homo sapiens 42-45 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 gastric inhibitory polypeptide Homo sapiens 49-52 11344200-4 2001 We now show that an infusion of GIP in healthy volunteers in whom blood glucose levels were maintained at 5 mmol/L, increased glibenclamide-stimulated levels of plasma insulin without significantly changing the C peptide profile. Blood Glucose 66-79 gastric inhibitory polypeptide Homo sapiens 32-35 11344200-4 2001 We now show that an infusion of GIP in healthy volunteers in whom blood glucose levels were maintained at 5 mmol/L, increased glibenclamide-stimulated levels of plasma insulin without significantly changing the C peptide profile. Glyburide 126-139 gastric inhibitory polypeptide Homo sapiens 32-35 11344200-7 2001 Hence, our results show that at a blood glucose concentration of 5 mmol/L, GIP augments the increase in plasma insulin levels stimulated by glibenclamide, possibly acting through a mechanism involving decreased insulin extraction in the liver or peripheral tissues, thus increasing insulin availability. Glucose 40-47 gastric inhibitory polypeptide Homo sapiens 75-78 11344200-7 2001 Hence, our results show that at a blood glucose concentration of 5 mmol/L, GIP augments the increase in plasma insulin levels stimulated by glibenclamide, possibly acting through a mechanism involving decreased insulin extraction in the liver or peripheral tissues, thus increasing insulin availability. Glyburide 140-153 gastric inhibitory polypeptide Homo sapiens 75-78 11377818-1 2001 Glucose-dependent insulinotropic peptide (GIP) is a gut-derived hormone known to be important in modulating glucose-induced insulin secretion. Glucose 108-115 gastric inhibitory polypeptide Homo sapiens 42-45 11158012-12 2001 The in vitro secretory response to GIP was higher for the adrenal androgen DHEA, compared with cortisol. Dehydroepiandrosterone 75-79 gastric inhibitory polypeptide Homo sapiens 35-38 11158012-12 2001 The in vitro secretory response to GIP was higher for the adrenal androgen DHEA, compared with cortisol. Hydrocortisone 95-103 gastric inhibitory polypeptide Homo sapiens 35-38 11158012-13 2001 The expression of the GIP receptor in tumor cells, but not in the adjacent normal adrenal, was demonstrated by RT-PCR), using specific oligonucleotide probes for this receptor. Oligonucleotides 135-150 gastric inhibitory polypeptide Homo sapiens 22-25 11280717-6 2001 GIP secretion was similar in lean and obese subjects both during oral fat and carbohydrate ingestion. Carbohydrates 78-90 gastric inhibitory polypeptide Homo sapiens 0-3 11199448-11 2000 Subcutaneous injection of octreotide completely inhibited the plasma cortisol and GIP response to oral glucose. Octreotide 26-36 gastric inhibitory polypeptide Homo sapiens 82-85 11116211-8 2000 GIP(1-151)/GLP-1R, but not GIP(1-222)/GLP-1R, exhibited specific GLP-1 binding and GLP-1-induced cAMP production, suggesting that the region encompassing transmembrane (TM) domain 1 through to TM3 was required for binding. Cyclic AMP 97-101 gastric inhibitory polypeptide Homo sapiens 0-3 11199448-11 2000 Subcutaneous injection of octreotide completely inhibited the plasma cortisol and GIP response to oral glucose. Glucose 103-110 gastric inhibitory polypeptide Homo sapiens 82-85 11072131-5 2000 Furthermore, stimulation of these cells with GIP led to cell type dependent differences in activation of the calcium and cAMP signaling pathways. Calcium 109-116 gastric inhibitory polypeptide Homo sapiens 45-48 11072131-5 2000 Furthermore, stimulation of these cells with GIP led to cell type dependent differences in activation of the calcium and cAMP signaling pathways. Cyclic AMP 121-125 gastric inhibitory polypeptide Homo sapiens 45-48 10990079-7 2000 This glucose effect was amplified by 10 nmol/l GLP-1, GIP or glucagon. Glucose 5-12 gastric inhibitory polypeptide Homo sapiens 54-57 10813588-2 2000 This augmented beta-cell secretory response to an oral glucose load results from the release of mainly two gut hormones: gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1, which potentiate glucose-induced insulin secretion. Glucose 55-62 gastric inhibitory polypeptide Homo sapiens 153-156 10792342-10 2000 glucose administration and GIP infusion led to comparable glucose values within the groups. Glucose 58-65 gastric inhibitory polypeptide Homo sapiens 27-30 10975043-4 2000 Blood glucose peak following a meal is modulated by gut hormones incretin effect, essentially GIP and GLP1. Blood Glucose 0-13 gastric inhibitory polypeptide Homo sapiens 94-97 10872532-3 2000 The current studies were designed to examine the effect of ageing, obesity and diabetes on GIP and DPP-IV responses to oral glucose. Glucose 124-131 gastric inhibitory polypeptide Homo sapiens 91-94 10872532-8 2000 CONCLUSIONS: It was concluded that ageing in obese subjects is associated with enhanced GIP responses to oral glucose. Glucose 110-117 gastric inhibitory polypeptide Homo sapiens 88-91 10813588-2 2000 This augmented beta-cell secretory response to an oral glucose load results from the release of mainly two gut hormones: gastric inhibitory polypeptide (GIP) and glucagon-like peptide-1, which potentiate glucose-induced insulin secretion. Glucose 204-211 gastric inhibitory polypeptide Homo sapiens 153-156 10813588-13 2000 After oral glucose, plasma GIP concentrations rose sharply in all groups (p < 0.002). Glucose 11-18 gastric inhibitory polypeptide Homo sapiens 27-30 10813588-15 2000 In conclusion, under conditions of stable hyperglycemia, the ingestion of a small amount of glucose elicited equivalent GIP responses in both lean and obese children. Glucose 92-99 gastric inhibitory polypeptide Homo sapiens 120-123 10698169-5 2000 Beta-arrestin-1 transfection also induced a significantly decrease in GIP-stimulated cAMP production, and this effect was greater with cotransfection of both GRK2 and beta-arrestin-1 than with either alone. Cyclic AMP 85-89 gastric inhibitory polypeptide Homo sapiens 70-73 10698169-4 2000 GIP dose dependently increased intracellular cAMP levels in L293-GIPR cells, but this response was abolished (65%) by cotransfection with G protein-coupled receptor kinase 2 (GRK2), but not with GRK5 or GRK6. Cyclic AMP 45-49 gastric inhibitory polypeptide Homo sapiens 0-3 10698200-4 2000 When applied to osteoblast-like cells (SaOS2), GIP stimulated increases in cellular cAMP content and intracellular calcium, with both responses being dose dependent. Cyclic AMP 84-88 gastric inhibitory polypeptide Homo sapiens 47-50 10698200-4 2000 When applied to osteoblast-like cells (SaOS2), GIP stimulated increases in cellular cAMP content and intracellular calcium, with both responses being dose dependent. Calcium 115-122 gastric inhibitory polypeptide Homo sapiens 47-50 10617941-8 2000 CONCLUSION: The significantly higher GIP and insulin responses and HL activities in southern Europeans may provide an explanation for our previous report of attenuated postprandial triacylglycerol and apolipoprotein B-48 responses in them. Triglycerides 181-196 gastric inhibitory polypeptide Homo sapiens 37-40 10666005-12 2000 In adipose tissue, GIP has been reported to (1) stimulate fatty acid synthesis, (2) enhance insulin-stimulated incorporation of fatty acids into triglycerides, (3) increase insulin receptor affinity, and (4) increase sensitivity of insulin-stimulated glucose transport. Fatty Acids 58-68 gastric inhibitory polypeptide Homo sapiens 19-22 10666005-12 2000 In adipose tissue, GIP has been reported to (1) stimulate fatty acid synthesis, (2) enhance insulin-stimulated incorporation of fatty acids into triglycerides, (3) increase insulin receptor affinity, and (4) increase sensitivity of insulin-stimulated glucose transport. Fatty Acids 128-139 gastric inhibitory polypeptide Homo sapiens 19-22 10666005-12 2000 In adipose tissue, GIP has been reported to (1) stimulate fatty acid synthesis, (2) enhance insulin-stimulated incorporation of fatty acids into triglycerides, (3) increase insulin receptor affinity, and (4) increase sensitivity of insulin-stimulated glucose transport. Triglycerides 145-158 gastric inhibitory polypeptide Homo sapiens 19-22 10666005-12 2000 In adipose tissue, GIP has been reported to (1) stimulate fatty acid synthesis, (2) enhance insulin-stimulated incorporation of fatty acids into triglycerides, (3) increase insulin receptor affinity, and (4) increase sensitivity of insulin-stimulated glucose transport. Glucose 251-258 gastric inhibitory polypeptide Homo sapiens 19-22 10634963-8 1999 Integrated responses for GIP and GLP-1 were markedly reduced following glucagon infusion. Glucagon 71-79 gastric inhibitory polypeptide Homo sapiens 25-28 10634963-9 1999 CONCLUSIONS: Exogenous glucagon in addition to its well-documented action of increasing glucose and insulin concentrations and delaying gastric emptying also markedly reduces GIP and GLP-1 secretion. Glucagon 23-31 gastric inhibitory polypeptide Homo sapiens 175-178 10443649-6 1999 Plasma cortisol and GIP levels were positively correlated (r = 0.95; P = 0.0001); cortisol was stimulated by the administration of human GIP iv (225%), but not by GLP-1, insulin, TRH, GnRH, glucagon, arginine vasopressin, upright posture, or cisapride orally. Cisapride 242-251 gastric inhibitory polypeptide Homo sapiens 137-140 10634963-0 1999 Effect of glucagon on carbohydrate-mediated secretion of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-36 amide) (GLP-1). Glucagon 10-18 gastric inhibitory polypeptide Homo sapiens 57-101 10634963-0 1999 Effect of glucagon on carbohydrate-mediated secretion of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-36 amide) (GLP-1). Carbohydrates 22-34 gastric inhibitory polypeptide Homo sapiens 57-101 10634963-0 1999 Effect of glucagon on carbohydrate-mediated secretion of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (7-36 amide) (GLP-1). Carbohydrates 22-34 gastric inhibitory polypeptide Homo sapiens 103-106 10523036-3 1999 In this patient we were able to confirm a paradoxical stimulation of cortisol secretion by GIP in vivo as well as in vitro on dispersed tumor adrenal cells obtained at surgery. Hydrocortisone 69-77 gastric inhibitory polypeptide Homo sapiens 91-94 10443649-9 1999 Three months after surgery, fasting plasma ACTH and cortisol were suppressed, but cortisol increased 3.6-fold after oral glucose, whereas ACTH remained suppressed; this was inhibited by octreotide pretreatment, suggesting that cortisol secretion by the left adrenal is also GIP dependent. Octreotide 186-196 gastric inhibitory polypeptide Homo sapiens 274-277 10102692-1 1999 Gastric inhibitory polypeptide (GIP) is an important insulin-releasing hormone of the enteroinsular axis that, like glucagon-like peptide 1(7-36) amide (tGLP-1), has a functional profile of possible therapeutic value for type 2 diabetes. Amides 146-151 gastric inhibitory polypeptide Homo sapiens 32-35 10333081-0 1999 Inhibition of insulin, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) secretion by octreotide has no effect on post-heparin plasma lipoprotein lipase activity. Octreotide 123-133 gastric inhibitory polypeptide Homo sapiens 23-67 10102692-6 1999 Tyr1-glucitol GIP was similarly resistant to serum degradation. tyr1-glucitol 0-13 gastric inhibitory polypeptide Homo sapiens 14-17 10333081-6 1999 Insulin, GIP and GLP-1 secretion post-carbohydrate was markedly reduced by octreotide in lean and obese subjects. Octreotide 75-85 gastric inhibitory polypeptide Homo sapiens 9-12 10102692-7 1999 The formation of GIP(3-42) was almost completely abolished by inhibition of plasma DPP IV with diprotin A. diprotin A 95-105 gastric inhibitory polypeptide Homo sapiens 17-20 10102692-10 1999 More importantly, individual glucose values at 15 and 30 min together with the areas under the curve (AUCs) for glucose were significantly lower after administration of Tyr1-glucitol GIP compared with GIP (AUC 255 +/- 33 vs. 368 +/- 8 mmol x l(-1) x min(-1), respectively; P < 0.01). Glucose 29-36 gastric inhibitory polypeptide Homo sapiens 183-186 10102692-10 1999 More importantly, individual glucose values at 15 and 30 min together with the areas under the curve (AUCs) for glucose were significantly lower after administration of Tyr1-glucitol GIP compared with GIP (AUC 255 +/- 33 vs. 368 +/- 8 mmol x l(-1) x min(-1), respectively; P < 0.01). Glucose 29-36 gastric inhibitory polypeptide Homo sapiens 201-204 10102692-10 1999 More importantly, individual glucose values at 15 and 30 min together with the areas under the curve (AUCs) for glucose were significantly lower after administration of Tyr1-glucitol GIP compared with GIP (AUC 255 +/- 33 vs. 368 +/- 8 mmol x l(-1) x min(-1), respectively; P < 0.01). Glucose 112-119 gastric inhibitory polypeptide Homo sapiens 183-186 10102692-10 1999 More importantly, individual glucose values at 15 and 30 min together with the areas under the curve (AUCs) for glucose were significantly lower after administration of Tyr1-glucitol GIP compared with GIP (AUC 255 +/- 33 vs. 368 +/- 8 mmol x l(-1) x min(-1), respectively; P < 0.01). tyr1-glucitol 169-182 gastric inhibitory polypeptide Homo sapiens 183-186 10102692-11 1999 This was associated with a significantly greater and more protracted insulin response after Tyr1-glucitol GIP than GIP (AUC 773 +/- 41 vs. 639 +/- 39 ng x ml(-1) x min(-1); P < 0.05). tyr1-glucitol 92-105 gastric inhibitory polypeptide Homo sapiens 106-109 10102692-12 1999 These data demonstrate that Tyr1-glucitol GIP displays resistance to plasma DPP IV degradation and exhibits enhanced antihyperglycemic activity and insulin-releasing action in vivo. Sorbitol 33-41 gastric inhibitory polypeptide Homo sapiens 42-45 9924262-4 1998 The higher-carbohydrate meal induced significantly higher insulin and glucose-dependent insulinotropic polypeptide responses (P = 0.0009 and P = 0.0041 respectively). Carbohydrates 11-23 gastric inhibitory polypeptide Homo sapiens 70-114 10092985-6 1999 Total integrated GIP (P < 0.05) and glucose (P < 0.01) responses were higher post heparin than after acipimox in obese subjects only. Heparin 88-95 gastric inhibitory polypeptide Homo sapiens 17-20 10092985-6 1999 Total integrated GIP (P < 0.05) and glucose (P < 0.01) responses were higher post heparin than after acipimox in obese subjects only. acipimox 107-115 gastric inhibitory polypeptide Homo sapiens 17-20 9833938-7 1998 We hypothesise that an age-related impairment of insulin secretion to insulinotropic hormones, GIP and GLP-1, contributes to a reduction in glucose tolerance in this age group. Glucose 140-147 gastric inhibitory polypeptide Homo sapiens 95-98 9794105-12 1998 glucose the lowest glucose concentrations were 4.5 (3.7-4.9) (median, range) for glucose alone; 2.4 (1.9-2.8) mmol/l with GLP-1; 3.7 (2.6-4.0) with low GIP and 3.3 (2.1-4.2) with high GIP. Glucose 0-7 gastric inhibitory polypeptide Homo sapiens 152-155 9794105-12 1998 glucose the lowest glucose concentrations were 4.5 (3.7-4.9) (median, range) for glucose alone; 2.4 (1.9-2.8) mmol/l with GLP-1; 3.7 (2.6-4.0) with low GIP and 3.3 (2.1-4.2) with high GIP. Glucose 0-7 gastric inhibitory polypeptide Homo sapiens 184-187 9794107-1 1998 The two incretins, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), are insulinotropic factors released from the small intestine to the blood stream in response to oral glucose ingestion. Glucose 19-26 gastric inhibitory polypeptide Homo sapiens 65-68 9632123-7 1998 Initially (0-150 min), glucose (p = 0.001), insulin (p = 0.001), and GIP (p < 0.001) were suppressed by acarbose, whereas later there were no significant differences. Acarbose 107-115 gastric inhibitory polypeptide Homo sapiens 69-72 9794105-1 1998 The plasma concentrations of the insulinotropic incretin hormone, glucagon-like peptide-1 (GLP-1) are abnormally high after oral glucose in partially gastrectomised subjects with reactive hypoglycaemia, suggesting a causal relationship. Glucose 129-136 gastric inhibitory polypeptide Homo sapiens 48-64 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. Octreotide 12-22 gastric inhibitory polypeptide Homo sapiens 107-110 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 gastric inhibitory polypeptide Homo sapiens 107-110 9745416-7 1998 In quiescent cells, GIP and ACTH stimulated [3H]thymidine incorporation and p42-p44 mitogen-activated protein kinase activity. Tritium 45-47 gastric inhibitory polypeptide Homo sapiens 20-23 9745416-7 1998 In quiescent cells, GIP and ACTH stimulated [3H]thymidine incorporation and p42-p44 mitogen-activated protein kinase activity. Thymidine 48-57 gastric inhibitory polypeptide Homo sapiens 20-23 9745416-11 1998 We conclude that abnormal expression of the GIP receptor allows adrenocortical cells to respond to food intake with an increase in cAMP that may participate in the stimulation of both cortisol secretion and proliferation of the tumor cells. Cyclic AMP 131-135 gastric inhibitory polypeptide Homo sapiens 44-47 9888586-0 1998 Gastric inhibitory polypeptide (GIP) stimulates cortisol secretion, cAMP production and DNA synthesis in an adrenal adenoma responsible for food-dependent Cushing"s syndrome. Hydrocortisone 48-56 gastric inhibitory polypeptide Homo sapiens 0-30 9888586-0 1998 Gastric inhibitory polypeptide (GIP) stimulates cortisol secretion, cAMP production and DNA synthesis in an adrenal adenoma responsible for food-dependent Cushing"s syndrome. Hydrocortisone 48-56 gastric inhibitory polypeptide Homo sapiens 32-35 9888586-0 1998 Gastric inhibitory polypeptide (GIP) stimulates cortisol secretion, cAMP production and DNA synthesis in an adrenal adenoma responsible for food-dependent Cushing"s syndrome. Cyclic AMP 68-72 gastric inhibitory polypeptide Homo sapiens 0-30 9888586-0 1998 Gastric inhibitory polypeptide (GIP) stimulates cortisol secretion, cAMP production and DNA synthesis in an adrenal adenoma responsible for food-dependent Cushing"s syndrome. Cyclic AMP 68-72 gastric inhibitory polypeptide Homo sapiens 32-35 9888586-3 1998 Both GIP and ACTH stimulated production of cAMP but not inositol 1,4,5-trisphosphate IP3). Cyclic AMP 43-47 gastric inhibitory polypeptide Homo sapiens 5-8 9888586-4 1998 In quiescent tumor cells, GIP and ACTH stimulated [3H]-thymidine incorporation and p42-p44 MAP kinase activity. Tritium 51-53 gastric inhibitory polypeptide Homo sapiens 26-29 9888586-4 1998 In quiescent tumor cells, GIP and ACTH stimulated [3H]-thymidine incorporation and p42-p44 MAP kinase activity. Thymidine 55-64 gastric inhibitory polypeptide Homo sapiens 26-29 9888586-8 1998 We conclude that abnormal expression of the GIP receptor allows adrenocortical cells to respond to food intake with an increase of cAMP that may participate in stimulation of both cortisol secretion and proliferation of the tumor cells. Cyclic AMP 131-135 gastric inhibitory polypeptide Homo sapiens 44-47 9734735-0 1998 Interaction of insulin, glucagon-like peptide 1, gastric inhibitory polypeptide, and appetite in response to intraduodenal carbohydrate. Carbohydrates 123-135 gastric inhibitory polypeptide Homo sapiens 49-79 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 gastric inhibitory polypeptide Homo sapiens 152-155 9678192-2 1998 Gastric inhibitory peptide/glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide-1 (GLP-1) have been found to have a profound incretin effect in humans. Glucose 27-34 gastric inhibitory polypeptide Homo sapiens 69-72 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 gastric inhibitory polypeptide Homo sapiens 174-177 9272099-1 1997 OBJECTIVE: The gastrointestinal hormones, gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 (GLP-1), are both released from the gut after oral glucose ingestion and stimulate insulin secretion. Glucose 158-165 gastric inhibitory polypeptide Homo sapiens 74-77 9404226-5 1997 Integrated post-prandial GIP concentrations were greater than in controls (P < 0.05) and correlated positively with both fasting and integrated post-prandial triglyceride concentrations (P < 0.05 for both). Triglycerides 161-173 gastric inhibitory polypeptide Homo sapiens 25-28 9404226-12 1997 There is, however, clear evidence for an association between post-prandial GIP concentrations and triglyceride levels. Triglycerides 98-110 gastric inhibitory polypeptide Homo sapiens 75-78 9404226-13 1997 We suggest that this association may depend on changes in lipoprotein lipase activity and that there may be a feedback loop between GIP and triglyceride lipolysis. Triglycerides 140-152 gastric inhibitory polypeptide Homo sapiens 132-135 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 gastric inhibitory polypeptide Homo sapiens 10-36 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 gastric inhibitory polypeptide Homo sapiens 38-41 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 gastric inhibitory polypeptide Homo sapiens 10-36 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 gastric inhibitory polypeptide Homo sapiens 38-41 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 gastric inhibitory polypeptide Homo sapiens 19-22 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 gastric inhibitory polypeptide Homo sapiens 87-90 9820111-2 1998 Numerous experimental trials provide evidence that GIP can participate in the regulation of the postprandial glucose and lipid metabolism and circulation in the splancnic area. Glucose 109-116 gastric inhibitory polypeptide Homo sapiens 51-54 9507911-4 1998 Peak plasma glucose, insulin, and glucose-dependent insulinotropic polypeptide (GIP) responses were reduced when sucrose was given with acarbose. Sucrose 113-120 gastric inhibitory polypeptide Homo sapiens 34-78 9507911-4 1998 Peak plasma glucose, insulin, and glucose-dependent insulinotropic polypeptide (GIP) responses were reduced when sucrose was given with acarbose. Sucrose 113-120 gastric inhibitory polypeptide Homo sapiens 80-83 9507911-4 1998 Peak plasma glucose, insulin, and glucose-dependent insulinotropic polypeptide (GIP) responses were reduced when sucrose was given with acarbose. Acarbose 136-144 gastric inhibitory polypeptide Homo sapiens 34-78 9507911-4 1998 Peak plasma glucose, insulin, and glucose-dependent insulinotropic polypeptide (GIP) responses were reduced when sucrose was given with acarbose. Acarbose 136-144 gastric inhibitory polypeptide Homo sapiens 80-83 9272099-5 1997 In response to the oral glucose ingestion, plasma levels of both GIP and GLP-1 increased in both groups. Glucose 24-31 gastric inhibitory polypeptide Homo sapiens 65-68 9272099-6 1997 The plasma GIP increase after glucose ingestion was, however, reduced in women with IGT. Glucose 30-37 gastric inhibitory polypeptide Homo sapiens 11-14 9272099-7 1997 Thus, the GIP response as determined as the area under the curve for the 60 min after oral glucose was 34.8 +/- 3.2 pmol/l per min in women with IGT versus 56.4 +/- 7.8 pmol/l per min in those with NGT (P = 0.021). Glucose 91-98 gastric inhibitory polypeptide Homo sapiens 10-13 9272099-10 1997 CONCLUSIONS: The GIP response to oral glucose is impaired in postmenopausal women with IGT, whereas the plasma GLP-1 response is not affected. Glucose 38-45 gastric inhibitory polypeptide Homo sapiens 17-20 9226399-0 1997 GIP(6-30amide) contains the high affinity binding region of GIP and is a potent inhibitor of GIP1-42 action in vitro. 6-30amide 4-13 gastric inhibitory polypeptide Homo sapiens 0-3 9226399-0 1997 GIP(6-30amide) contains the high affinity binding region of GIP and is a potent inhibitor of GIP1-42 action in vitro. 6-30amide 4-13 gastric inhibitory polypeptide Homo sapiens 60-63 9226399-3 1997 All three peptides were found to be receptor antagonists, however GIP(6-30amide) exhibited receptor binding affinity equivalent to that of GIP(1-42) in competitive binding studies (IC50 = 3.08+/-0.57 nM). 6-30amide 70-79 gastric inhibitory polypeptide Homo sapiens 66-69 9226399-4 1997 GIP(6-30amide) inhibited GIP(1-42)-induced cAMP production by 58% at a concentration of 100 nM, whereas GIP(10-30) and GIP(7-30), inhibited only in the microM range. 6-30amide 4-13 gastric inhibitory polypeptide Homo sapiens 0-3 9226399-4 1997 GIP(6-30amide) inhibited GIP(1-42)-induced cAMP production by 58% at a concentration of 100 nM, whereas GIP(10-30) and GIP(7-30), inhibited only in the microM range. 6-30amide 4-13 gastric inhibitory polypeptide Homo sapiens 25-28 9226399-4 1997 GIP(6-30amide) inhibited GIP(1-42)-induced cAMP production by 58% at a concentration of 100 nM, whereas GIP(10-30) and GIP(7-30), inhibited only in the microM range. 6-30amide 4-13 gastric inhibitory polypeptide Homo sapiens 25-28 9226399-4 1997 GIP(6-30amide) inhibited GIP(1-42)-induced cAMP production by 58% at a concentration of 100 nM, whereas GIP(10-30) and GIP(7-30), inhibited only in the microM range. 6-30amide 4-13 gastric inhibitory polypeptide Homo sapiens 25-28 9226399-4 1997 GIP(6-30amide) inhibited GIP(1-42)-induced cAMP production by 58% at a concentration of 100 nM, whereas GIP(10-30) and GIP(7-30), inhibited only in the microM range. Cyclic AMP 43-47 gastric inhibitory polypeptide Homo sapiens 0-3 9226399-4 1997 GIP(6-30amide) inhibited GIP(1-42)-induced cAMP production by 58% at a concentration of 100 nM, whereas GIP(10-30) and GIP(7-30), inhibited only in the microM range. Cyclic AMP 43-47 gastric inhibitory polypeptide Homo sapiens 25-28 9226399-4 1997 GIP(6-30amide) inhibited GIP(1-42)-induced cAMP production by 58% at a concentration of 100 nM, whereas GIP(10-30) and GIP(7-30), inhibited only in the microM range. Cyclic AMP 43-47 gastric inhibitory polypeptide Homo sapiens 25-28 9226399-4 1997 GIP(6-30amide) inhibited GIP(1-42)-induced cAMP production by 58% at a concentration of 100 nM, whereas GIP(10-30) and GIP(7-30), inhibited only in the microM range. Cyclic AMP 43-47 gastric inhibitory polypeptide Homo sapiens 25-28 9226399-5 1997 GIP(6-30amide) therefore contains the high affinity binding region of GIP and is a potent inhibitor of GIP(1-42) action in vitro. 6-30amide 4-13 gastric inhibitory polypeptide Homo sapiens 0-3 9226399-5 1997 GIP(6-30amide) therefore contains the high affinity binding region of GIP and is a potent inhibitor of GIP(1-42) action in vitro. 6-30amide 4-13 gastric inhibitory polypeptide Homo sapiens 70-73 9226399-5 1997 GIP(6-30amide) therefore contains the high affinity binding region of GIP and is a potent inhibitor of GIP(1-42) action in vitro. 6-30amide 4-13 gastric inhibitory polypeptide Homo sapiens 70-73 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 gastric inhibitory polypeptide Homo sapiens 57-87 9125160-4 1997 Single amino acid substitutions in the GIP receptor were made by site-directed mutagenesis and receptor binding and cAMP levels were measured in transfected human embryonal kidney cell line (L293). Cyclic AMP 116-120 gastric inhibitory polypeptide Homo sapiens 39-42 9125160-7 1997 Despite its high basal cAMP level, the T340P mutant could be further stimulated by GIP, with maximal cAMP generation comparable to the wild-type receptor. Cyclic AMP 101-105 gastric inhibitory polypeptide Homo sapiens 83-86 9078536-0 1997 Acute incretin response to oral glucose is associated with stimulation of gastric inhibitory polypeptide, not glucagon-like peptide in young subjects. Glucose 32-39 gastric inhibitory polypeptide Homo sapiens 74-104 9078536-10 1997 Plasma gastric inhibitory polypeptide (GIP) levels increased significantly in response to oral glucose, whereas plasma levels of glucagon-like peptide-1 (7-37) were not affected. Glucose 95-102 gastric inhibitory polypeptide Homo sapiens 7-37 9078536-10 1997 Plasma gastric inhibitory polypeptide (GIP) levels increased significantly in response to oral glucose, whereas plasma levels of glucagon-like peptide-1 (7-37) were not affected. Glucose 95-102 gastric inhibitory polypeptide Homo sapiens 39-42 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 gastric inhibitory polypeptide Homo sapiens 21-24 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 gastric inhibitory polypeptide Homo sapiens 21-24 8784063-3 1996 There was a close correlation between circulating gastric inhibitory polypeptide (GIP) and cortisol levels during normal food intake (r = 0.92; P < 0.0002). Hydrocortisone 91-99 gastric inhibitory polypeptide Homo sapiens 82-85 8784063-7 1996 The infusion of GIP increased plasma cortisol levels to 7.8 times above baseline. Hydrocortisone 37-45 gastric inhibitory polypeptide Homo sapiens 16-19 8784063-9 1996 Treatment with octreotide initially prevented the meal-induced increases in cortisol and GIP levels and decreased urinary cortisol excretion. Octreotide 15-25 gastric inhibitory polypeptide Homo sapiens 89-92 8784063-11 1996 Cortisol production by cultured adrenal adenoma cells from the patient was stimulated by GIP and ACTH. Hydrocortisone 0-8 gastric inhibitory polypeptide Homo sapiens 89-92 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 gastric inhibitory polypeptide Homo sapiens 89-92 7762650-5 1995 GIP and GLP-I-(7--36) amide further stimulated insulin (1.8-fold, P = 0.0001 and 0.004, respectively) and C-peptide (1.3-fold, P = 0.0003 and 0.013, respectively), with a subsequent slight reduction in plasma glucose (P < 0.0001). Glucose 209-216 gastric inhibitory polypeptide Homo sapiens 0-3 8586147-5 1995 The secretion of GIP, a 42 amino acid polypeptide secreted by duodenal K cells, is triggered by fat and glucose. Glucose 104-111 gastric inhibitory polypeptide Homo sapiens 17-20 8586147-6 1995 GIP stimulation of insulin secretion depends on the presence of specific beta-cell receptors and requires glucose at a concentration at least equal to or higher than the normoglycaemic level of approximately 5 mM. Glucose 106-113 gastric inhibitory polypeptide Homo sapiens 0-3 8586147-9 1995 As with GIP, its stimulatory action requires a specific membrane receptor and normal or elevated glucose concentrations. Glucose 97-104 gastric inhibitory polypeptide Homo sapiens 8-11 7589426-5 1995 When transfected stably into fibroblast CHL-cells a high affinity receptor was expressed which coupled to the adenylate cyclase with normal basal cAMP and increasing intracellular cAMP levels under stimulation with human GIP-1-42 (EC50 = 1.29 x 10(-13) M). Cyclic AMP 146-150 gastric inhibitory polypeptide Homo sapiens 221-224 7589426-5 1995 When transfected stably into fibroblast CHL-cells a high affinity receptor was expressed which coupled to the adenylate cyclase with normal basal cAMP and increasing intracellular cAMP levels under stimulation with human GIP-1-42 (EC50 = 1.29 x 10(-13) M). Cyclic AMP 180-184 gastric inhibitory polypeptide Homo sapiens 221-224 7589426-7 1995 At 1 microM, exendin-4 and (9-39)amide weakly reduced GIP-binding (25%) whereas secretin, glucagon, glucagon-like peptide-1, vasoactive intestinal polypeptide, peptide histidine-isoleucine, and pituitary adenylyl cyclase activating peptide were without effect. Amides 33-38 gastric inhibitory polypeptide Homo sapiens 54-57 7669127-8 1995 These results suggest that meal timing and sleep/wake cycles are more important factors than insulin and glucose-dependent insulinotropic polypeptide in controlling the rhythms of whole body cholesterol synthesis. Cholesterol 191-202 gastric inhibitory polypeptide Homo sapiens 105-149 7556958-1 1995 Glucose-dependent insulinotropic polypeptide (GIP) is a hormone secreted by the endocrine K-cells from the duodenum that stimulates glucose-induced insulin secretion. Glucose 132-139 gastric inhibitory polypeptide Homo sapiens 0-44 7556958-1 1995 Glucose-dependent insulinotropic polypeptide (GIP) is a hormone secreted by the endocrine K-cells from the duodenum that stimulates glucose-induced insulin secretion. Glucose 132-139 gastric inhibitory polypeptide Homo sapiens 46-49 7556958-7 1995 GIP binding was displaced by < 20% by 1 mumol/l glucagon, glucagon-like peptide (GLP-I)(7-36) amide, vasoactive intestinal peptide, and secretin. Amides 97-102 gastric inhibitory polypeptide Homo sapiens 0-3 7556958-9 1995 GIP binding to both forms of the receptor induced a dose-dependent increase in intracellular cAMP levels (EC50 values of 0.6-0.8 nmol/l) but no elevation of cytoplasmic calcium concentrations. Cyclic AMP 93-97 gastric inhibitory polypeptide Homo sapiens 0-3 7556958-10 1995 Interestingly, both exendin-4 and exendin-(9-39) were antagonists of the receptor, inhibiting GIP-induced cAMP formation by up to 60% when present at a concentration of 10 mumol/l. Cyclic AMP 106-110 gastric inhibitory polypeptide Homo sapiens 94-97 7664683-4 1995 GIP-R1, when expressed transiently in monkey kidney (COS-7) or stably in Chinese hamster ovary (CHO-K1) cells, demonstrated comparable high affinity binding for either synthetic porcine (sp) GIP or synthetic human (sh) GIP. carbonyl sulfide 53-56 gastric inhibitory polypeptide Homo sapiens 0-3 7664683-13 1995 GIP-R1 receptor binding correlated with activation of the adenylyl cyclase system, whereby spGIP and shGIP evoked concentration-dependent increases in cAMP accumulation with EC50 values of 8.7 +/- 1.5 x 10(-10)M and 8.1 +/- 1.6 x 10(-10)M for spGIP and shGIP, respectively. Cyclic AMP 151-155 gastric inhibitory polypeptide Homo sapiens 0-3 8578189-6 1995 The sucrose-related increments in glucose, insulin, C-peptide, and gastric inhibitory polypeptide (GIP) and the suppression of glucagon were only marginally affected by acarbose administration. Sucrose 4-11 gastric inhibitory polypeptide Homo sapiens 99-102 7762650-8 1995 In conclusion, GIP and GLP-I-(7--36) amide are not only able to interact with elevated plasma glucose but are insulinotropic also with physiologically raised amino acid concentrations. Glucose 94-101 gastric inhibitory polypeptide Homo sapiens 15-18 9279024-0 1995 Effect of glucose-dependent insulinotropic polypeptide (GIP) on insulin response to glucose in acromegalics. Glucose 10-17 gastric inhibitory polypeptide Homo sapiens 56-59 7733263-7 1995 The data indicate that GLP-I-(7-36) and porcine GIP are equally insulinotropic and share the same glucose threshold for activity, whereas shGIP is less active. Glucose 98-105 gastric inhibitory polypeptide Homo sapiens 48-51 7705803-2 1995 Oral glucose is a better stimulant to insulin secretion than intravenous (IV) glucose in part because of release of gut peptides, notably glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 [7-36 amide] (GLP-1 [7-36 amide]). Glucose 5-12 gastric inhibitory polypeptide Homo sapiens 138-178 7705803-2 1995 Oral glucose is a better stimulant to insulin secretion than intravenous (IV) glucose in part because of release of gut peptides, notably glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 [7-36 amide] (GLP-1 [7-36 amide]). Glucose 5-12 gastric inhibitory polypeptide Homo sapiens 180-183 7852887-6 1993 Ingestion of both carbohydrate and fat induced substantial rises in GIP secretion, but the protein meal had no effect. Carbohydrates 18-30 gastric inhibitory polypeptide Homo sapiens 68-71 8054322-4 1994 Mean integrated insulin, gastric inhibitory polypeptide (GIP) and glucose concentrations were higher after the C diets compared with the F diets, TRP supplementation globally augmented ks linearly in the liver, ST, skin and whole body, while it had quadratic effects in the LD (ks highest in the TRP-adequate diet groups) and jejunal mucosa (ks lowest in the TRP-adequate diet groups). Tryptophan 146-149 gastric inhibitory polypeptide Homo sapiens 57-60 8169563-6 1994 The serum glucose and plasma GIP responses to oral glucose were similar in the euthyroid and hypothyroid states. Glucose 51-58 gastric inhibitory polypeptide Homo sapiens 29-32 8243312-1 1993 Gastric inhibitory polypeptide (GIP), or glucose-dependent insulinotropic peptide, is released from endocrine cells in the small intestine after meals. Glucose 41-48 gastric inhibitory polypeptide Homo sapiens 32-35 8345813-7 1993 Plasma levels of immunoreactive gastric inhibitory polypeptide (GIP) increased substantially after ingestion of 75 g glucose, but did not change during isoglycemic IV glucose infusions or during IV infusions of glucose plus arginine. Glucose 117-124 gastric inhibitory polypeptide Homo sapiens 64-67 8022751-0 1994 Regulation of polyunsaturated fatty acid-stimulated insulin release by GIP in isolated perifused islets. Fatty Acids, Unsaturated 14-40 gastric inhibitory polypeptide Homo sapiens 71-74 8022751-1 1994 It has recently been suggested that gastric inhibitory polypeptide (GIP) may block the risk factors associated with both hypo- and hyperglycemia by either suppressing or enhancing (depending on the prevailing glucose conditions) insulin release. Glucose 209-216 gastric inhibitory polypeptide Homo sapiens 36-66 8022751-1 1994 It has recently been suggested that gastric inhibitory polypeptide (GIP) may block the risk factors associated with both hypo- and hyperglycemia by either suppressing or enhancing (depending on the prevailing glucose conditions) insulin release. Glucose 209-216 gastric inhibitory polypeptide Homo sapiens 68-71 8022751-7 1994 When GIP concentrations of either 1 x 10(-9) or 1 x 10(-8) M were added to the fatty acid perifusate, insulin secretion stimulated by PUFA was significantly attenuated in a dose-dependent manner, but was completely restored after withdrawal of GIP. Fatty Acids 79-89 gastric inhibitory polypeptide Homo sapiens 5-8 7852887-11 1993 The increases in circulating GLP-1(7-36)amide and GIP levels following carbohydrate or a mixed meal are consistent with their role as incretins. Carbohydrates 71-83 gastric inhibitory polypeptide Homo sapiens 50-53 8100523-3 1993 Growth-hormone-releasing factor (1-29)amide and gastric inhibitory peptide/glucose-dependent insulinotropic peptide (GIP) with terminal Tyr-Ala as well as glucagon-like peptide-1(7-36)amide/insulinotropin [GLP-1(7-36)amide] and peptide histidine methionine (PHM) with terminal His-Ala were hydrolysed to their des-Xaa-Ala derivatives by dipeptidyl-peptidase IV purified from human placenta. Glucose 75-82 gastric inhibitory polypeptide Homo sapiens 117-120 8100523-7 1993 When human serum was incubated with GIP or GLP-1(7-36)amide the same fragments as with the purified dipeptidyl-peptidase IV, namely the des-Xaa-Ala peptides and Tyr-Ala in the case of GIP or His-Ala in the case of GLP-1(7-36)amide, were identified as the main degradation products of these peptide hormones. Alanine 144-147 gastric inhibitory polypeptide Homo sapiens 36-39 8100523-3 1993 Growth-hormone-releasing factor (1-29)amide and gastric inhibitory peptide/glucose-dependent insulinotropic peptide (GIP) with terminal Tyr-Ala as well as glucagon-like peptide-1(7-36)amide/insulinotropin [GLP-1(7-36)amide] and peptide histidine methionine (PHM) with terminal His-Ala were hydrolysed to their des-Xaa-Ala derivatives by dipeptidyl-peptidase IV purified from human placenta. Tyrosine 136-139 gastric inhibitory polypeptide Homo sapiens 117-120 8100523-7 1993 When human serum was incubated with GIP or GLP-1(7-36)amide the same fragments as with the purified dipeptidyl-peptidase IV, namely the des-Xaa-Ala peptides and Tyr-Ala in the case of GIP or His-Ala in the case of GLP-1(7-36)amide, were identified as the main degradation products of these peptide hormones. Tyr-Ala 161-168 gastric inhibitory polypeptide Homo sapiens 36-39 8100523-7 1993 When human serum was incubated with GIP or GLP-1(7-36)amide the same fragments as with the purified dipeptidyl-peptidase IV, namely the des-Xaa-Ala peptides and Tyr-Ala in the case of GIP or His-Ala in the case of GLP-1(7-36)amide, were identified as the main degradation products of these peptide hormones. Histidine 191-194 gastric inhibitory polypeptide Homo sapiens 36-39 8100523-7 1993 When human serum was incubated with GIP or GLP-1(7-36)amide the same fragments as with the purified dipeptidyl-peptidase IV, namely the des-Xaa-Ala peptides and Tyr-Ala in the case of GIP or His-Ala in the case of GLP-1(7-36)amide, were identified as the main degradation products of these peptide hormones. Alanine 165-168 gastric inhibitory polypeptide Homo sapiens 36-39 8100523-7 1993 When human serum was incubated with GIP or GLP-1(7-36)amide the same fragments as with the purified dipeptidyl-peptidase IV, namely the des-Xaa-Ala peptides and Tyr-Ala in the case of GIP or His-Ala in the case of GLP-1(7-36)amide, were identified as the main degradation products of these peptide hormones. Amides 225-230 gastric inhibitory polypeptide Homo sapiens 36-39 8292862-4 1993 Moreover, the early and total postcibal secretions of GIP after gastrectomy were less in the DM-group than in the N-group. dm 93-95 gastric inhibitory polypeptide Homo sapiens 54-57 8396579-3 1993 Mutations in another alpha-subunit of a GTP-binding protein, Gi2 alpha (gip mutations) have been described in other endocrine tumors. Guanosine Triphosphate 40-43 gastric inhibitory polypeptide Homo sapiens 72-75 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 gastric inhibitory polypeptide Homo sapiens 32-35 8473405-5 1993 After the administration of 50 g oral glucose, immunoreactive GIP rose several-fold to 337 +/- 43 pmol/L, while there was only a transient (10-30 min) and moderate increment in immunoreactive GLP-1 (from basal, 25-30, to 41 +/- 4 pmol/L). Glucose 38-45 gastric inhibitory polypeptide Homo sapiens 62-65 8473405-14 1993 Therefore, in conclusion, circulating GIP seems to make a major contribution to the incretin effect after oral glucose, and GLP-1 appears to mediate a smaller proportion. Glucose 111-118 gastric inhibitory polypeptide Homo sapiens 38-41 8428636-0 1993 Two 3",5"-cyclic-adenosine monophosphate response elements in the promoter region of the human gastric inhibitory polypeptide gene. 3",5"-cyclic-adenosine monophosphate 4-40 gastric inhibitory polypeptide Homo sapiens 95-125 8435987-7 1993 These results suggest that the combined augmentation of plasma GIP and tGLP-1 responses were involved in the delayed and considerable increases in plasma insulin after glucose ingestion in obese diabetic patients. Glucose 168-175 gastric inhibitory polypeptide Homo sapiens 63-66 8422763-0 1993 The effect of glyburide on beta-cell sensitivity to glucose-dependent insulinotropic polypeptide. Glyburide 14-23 gastric inhibitory polypeptide Homo sapiens 52-96 8422763-1 1993 OBJECTIVE: To assess whether treatment with glyburide alters beta-cell sensitivity to GIP in NIDDM patients. Glyburide 44-53 gastric inhibitory polypeptide Homo sapiens 86-89 8422763-10 1993 CONCLUSIONS: We conclude that glyburide enhances beta-cell sensitivity to GIP. Glyburide 30-39 gastric inhibitory polypeptide Homo sapiens 74-77 8423228-8 1993 Glucagon was lowered during hyperglycemic clamps in normal subjects, but not in type-2 diabetic patients, and further by GLP-1 [7-36 amide] in both groups (P < 0.05), but not by GIP. Glucagon 0-8 gastric inhibitory polypeptide Homo sapiens 181-184 8292862-4 1993 Moreover, the early and total postcibal secretions of GIP after gastrectomy were less in the DM-group than in the N-group. Nitrogen 114-115 gastric inhibitory polypeptide Homo sapiens 54-57 1589696-5 1992 The IR GIP in samples of human plasma was then assayed with 125I-labelled synthetic human or porcine GIP using natural porcine GIP as standard. Iodine-125 60-64 gastric inhibitory polypeptide Homo sapiens 101-104 1325608-8 1992 Cell suspensions of adrenal tissue from the patient produced more cortisol when stimulated by GIP than when stimulated by corticotropin. Hydrocortisone 66-74 gastric inhibitory polypeptide Homo sapiens 94-97 1325609-11 1992 The infusion of gastric inhibitory polypeptide (GIP) increased the patient"s plasma cortisol concentration to 3.7 times the base-line value, but had no effect in normal subjects. Hydrocortisone 84-92 gastric inhibitory polypeptide Homo sapiens 48-51 1325609-12 1992 The patient"s fasting plasma GIP concentrations were normal both before and after a meal, and there was a close correlation between her plasma cortisol and GIP concentrations. Hydrocortisone 143-151 gastric inhibitory polypeptide Homo sapiens 156-159 1643802-2 1992 However, circulating levels of GIP in diabetes have been reported to be exaggerated, normal or decreased following glucose ingestion, which may be due to the presence of variable crossreacting immunoreactive GIP forms in the circulation. Glucose 115-122 gastric inhibitory polypeptide Homo sapiens 31-34 1643802-2 1992 However, circulating levels of GIP in diabetes have been reported to be exaggerated, normal or decreased following glucose ingestion, which may be due to the presence of variable crossreacting immunoreactive GIP forms in the circulation. Glucose 115-122 gastric inhibitory polypeptide Homo sapiens 208-211 18407095-0 1992 Insulinotropic glucagonlike peptide-I(7-37)/(7-36)amide A new incretin hormone. Amides 50-55 gastric inhibitory polypeptide Homo sapiens 62-78 1589696-5 1992 The IR GIP in samples of human plasma was then assayed with 125I-labelled synthetic human or porcine GIP using natural porcine GIP as standard. Iodine-125 60-64 gastric inhibitory polypeptide Homo sapiens 101-104 1576919-0 1992 Differences in glucagon-like peptide-1 and GIP responses following sucrose ingestion. Sucrose 67-74 gastric inhibitory polypeptide Homo sapiens 43-46 1576919-1 1992 To investigate the mechanism of oral carbohydrate-stimulated secretion of the two most potent incretin candidates, gastric inhibitory polypeptide (GIP) and truncated glucagon-like peptide-1 (tGLP-1), we studied the changes in the plasma levels of these peptides in five healthy men after sucrose ingestion with or without pretreatment with an alpha-D-glucosidase inhibitor (AO-128). Carbohydrates 37-49 gastric inhibitory polypeptide Homo sapiens 147-150 1576919-2 1992 After sucrose ingestion, plasma levels of GIP peaked at 15 min and remained high up to 120 min. Sucrose 6-13 gastric inhibitory polypeptide Homo sapiens 42-45 1576919-5 1992 After treatment with AO-128 (0.6 mg/day) for 1 week, increases in plasma glucose and insulin levels were attenuated and the increase in plasma GIP levels was diminished, while the increase in tGLP-1 levels was sustained much longer. AO 128 21-27 gastric inhibitory polypeptide Homo sapiens 143-146 1459356-1 1992 Gastric inhibitory polypeptide (GIP) and glucagon-like peptide 1 [7-36 amide] (GLP-1) are glucose-dependent insulinotropic gut hormones. Glucose 90-97 gastric inhibitory polypeptide Homo sapiens 32-35 1600330-7 1992 GIP was raised after glucose and triglyceride more than after protein (P = 0.0003). Glucose 21-28 gastric inhibitory polypeptide Homo sapiens 0-3 1600330-7 1992 GIP was raised after glucose and triglyceride more than after protein (P = 0.0003). Triglycerides 33-45 gastric inhibitory polypeptide Homo sapiens 0-3 1459356-4 1992 At 0 min, a glucose infusion was started that mimicked the glycemic profile after an oral glucose load of 50 g/400 ml and allowed for the glucose-dependent insulinotropic action of GIP and GLP-1 [7-36 amide]. Glucose 12-19 gastric inhibitory polypeptide Homo sapiens 181-184 1767243-4 1991 The release of GIP and GLP-1 (7-36 amide) was suppressed in the hyperglycaemic hyperinsulinaemic state. Amides 35-40 gastric inhibitory polypeptide Homo sapiens 15-18 1576919-6 1992 It is concluded that GIP secretion is stimulated by glucose absorption and tGLP-1 secretion by the presence of sucrose in the gut. Glucose 52-59 gastric inhibitory polypeptide Homo sapiens 21-24 1576919-6 1992 It is concluded that GIP secretion is stimulated by glucose absorption and tGLP-1 secretion by the presence of sucrose in the gut. Sucrose 111-118 gastric inhibitory polypeptide Homo sapiens 21-24 1884880-0 1991 Effect of Miglitol (Bay m1099), a new alpha-glucosidase inhibitor, on glucose, insulin, C-peptide and GIP responses to an oral sucrose load in patients with post-prandial hypoglycaemic symptoms. miglitol 10-18 gastric inhibitory polypeptide Homo sapiens 102-105 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 gastric inhibitory polypeptide Homo sapiens 113-116 2192849-7 1990 Remarkably, high glucose leads to an increase in the same intracellular signals, as does a combination of acetylcholine and GIP. Glucose 17-24 gastric inhibitory polypeptide Homo sapiens 124-127 1899823-12 1991 Plasma GIP levels were significantly higher with the enteral feeding solution than with saline solution during most of the infusion. Sodium Chloride 88-94 gastric inhibitory polypeptide Homo sapiens 7-10 1986010-5 1991 Ingestion of triglyceride (60 g) in hyperglucagonemic cirrhotic patients with porta-caval anastomoses also resulted in elevation of plasma immunoreactive GIP, and this was again associated with significant elevation of the plasma IRG level. Triglycerides 13-25 gastric inhibitory polypeptide Homo sapiens 154-157 2124984-4 1990 When glucose was administered intravenously plasma GIP levels did not rise significantly over basal. Glucose 5-12 gastric inhibitory polypeptide Homo sapiens 51-54 2124984-5 1990 The infusion of hGIP mimicked the physiological plasma GIP response after oral glucose during the first 60 min of the study. Glucose 79-86 gastric inhibitory polypeptide Homo sapiens 16-20 2124984-5 1990 The infusion of hGIP mimicked the physiological plasma GIP response after oral glucose during the first 60 min of the study. Glucose 79-86 gastric inhibitory polypeptide Homo sapiens 17-20 2124984-8 1990 Thus, in the presence of mild physiological hyperglycaemia, human GIP is able to enhance the initial insulin response almost equivalently to the stimulus provided by oral glucose. Glucose 171-178 gastric inhibitory polypeptide Homo sapiens 66-69 2087431-1 1990 Glucose-dependent insulinotropic polypeptide (GIP) is a forty-two amino acid hormone that stimulates the secretion of insulin from the pancreatic B-cells in the presence of elevated glucose concentrations. Glucose 182-189 gastric inhibitory polypeptide Homo sapiens 0-44 2087431-1 1990 Glucose-dependent insulinotropic polypeptide (GIP) is a forty-two amino acid hormone that stimulates the secretion of insulin from the pancreatic B-cells in the presence of elevated glucose concentrations. Glucose 182-189 gastric inhibitory polypeptide Homo sapiens 46-49 2087431-5 1990 The identity of the recombinant human GIP was confirmed by SDS-PAGE, ELISA, HPLC and amino-terminal amino acid sequence analysis. Sodium Dodecyl Sulfate 59-62 gastric inhibitory polypeptide Homo sapiens 38-41 26120808-5 2015 The main results showed lower serum levels of Glucagon, GLP-1, Ghrelin, and higher levels of GIP in BD patients as compared to controls (p = 0.018 for Ghrelin; p < 0.0001 for Glucagon; p < 0.0001 for GLP-1; p < 0.0001 for GIP). Glucagon 178-186 gastric inhibitory polypeptide Homo sapiens 93-96 2108729-2 1990 Gip, a 41 kDa protein from washed microvilli, was ADP ribosylated by pertussis toxin in the presence of GDP in the dark. Guanosine Diphosphate 104-107 gastric inhibitory polypeptide Homo sapiens 0-3 33791428-1 2021 The gut-derived incretin hormone, glucagon-like peptide-1 (GLP1), plays an important physiological role in attenuating post-prandial blood glucose excursions in part by amplifying pancreatic insulin secretion. Glucose 139-146 gastric inhibitory polypeptide Homo sapiens 16-32 33236115-1 2021 CONTEXT: Novel dual GIP and GLP-1 receptor agonist (RA) tirzepatide demonstrated substantially greater glucose control and weight loss (WL) compared with selective GLP-1RA dulaglutide. Glucose 103-110 gastric inhibitory polypeptide Homo sapiens 20-23 34953208-1 2022 Glucagon like peptide-1 (GLP-1) is one of incretin hormone and is secreted when enteroendocrine L cells sense saccharides, amino acids, and fatty acids. Carbohydrates 110-121 gastric inhibitory polypeptide Homo sapiens 42-58 19410576-1 2009 BACKGROUND & AIMS: Ablation of gastric inlet patches (GIP) in the cervical esophagus by argon plasma coagulation (APC) can alleviate chronic globus sensations in the throat. Adenosine Monophosphate 12-15 gastric inhibitory polypeptide Homo sapiens 58-61 34915297-4 2022 The bioaccessible metal fractions in the gastric (GP) and gastrointestinal (GIP) phases were 0 (Cr) - 91.39% (Cd)) and 0 (Cr) - 47.80% (Ni). Metals 18-23 gastric inhibitory polypeptide Homo sapiens 76-79 34915297-6 2022 The Pearson correlation analysis showed that the carbonate bound phases of heavy metals were responsible for their bioaccessibility in GP and GIP. Carbonates 49-58 gastric inhibitory polypeptide Homo sapiens 142-145 34953208-1 2022 Glucagon like peptide-1 (GLP-1) is one of incretin hormone and is secreted when enteroendocrine L cells sense saccharides, amino acids, and fatty acids. Fatty Acids 140-151 gastric inhibitory polypeptide Homo sapiens 42-58 34932984-2 2022 We developed SAR441255, a synthetic peptide agonist of the GLP-1, GCG, and GIP receptors, structurally based on the exendin-4 sequence. sar441255 13-22 gastric inhibitory polypeptide Homo sapiens 75-78 34932984-6 2022 In healthy subjects, SAR441255 improved glycemic control during a mixed-meal tolerance test and impacted biomarkers for GCG and GIP receptor activation. sar441255 21-30 gastric inhibitory polypeptide Homo sapiens 128-131 34490741-1 2022 INTRODUCTION: Glucose-dependent insulinotropic polypeptide (GIP) contributes importantly to glucose and lipid metabolism. Glucose 92-99 gastric inhibitory polypeptide Homo sapiens 14-58 34490741-1 2022 INTRODUCTION: Glucose-dependent insulinotropic polypeptide (GIP) contributes importantly to glucose and lipid metabolism. Glucose 92-99 gastric inhibitory polypeptide Homo sapiens 60-63 34490741-4 2022 RESULTS: Plasma glycerol concentrations increased from baseline during GIP infusion and decreased during placebo infusion (baseline-subtracted area under the curve (bsAUC): 703 +- 407 vs. -262 +- 240 mumol/L x min, respectively, p < 0.001). Glycerol 16-24 gastric inhibitory polypeptide Homo sapiens 71-74 34490741-5 2022 Free fatty acids (FFA) increased during GIP infusions (bsAUC: 5505 +- 2170 muEq/L x min) and remained unchanged during placebo infusion (bsAUC: -74 +- 2363 muEq/L x min) resulting in a significant difference between GIP and placebo infusions (p < 0.001). Fatty Acids, Nonesterified 0-16 gastric inhibitory polypeptide Homo sapiens 40-43 34490741-5 2022 Free fatty acids (FFA) increased during GIP infusions (bsAUC: 5505 +- 2170 muEq/L x min) and remained unchanged during placebo infusion (bsAUC: -74 +- 2363 muEq/L x min) resulting in a significant difference between GIP and placebo infusions (p < 0.001). Fatty Acids, Nonesterified 0-16 gastric inhibitory polypeptide Homo sapiens 216-219 34490741-7 2022 CONCLUSIONS: GIP increased plasma glycerol and FFA in patients with type 1 diabetes during hyperglycemia and stable basal insulin levels. Glycerol 34-42 gastric inhibitory polypeptide Homo sapiens 13-16 34490741-8 2022 This supports a direct lipolytic effect of GIP at high glucose and low levels of plasma insulin. Glucose 55-62 gastric inhibitory polypeptide Homo sapiens 43-46 34672967-1 2021 BACKGROUND: We aimed to assess efficacy and safety, with a special focus on cardiovascular safety, of the novel dual GIP and GLP-1 receptor agonist tirzepatide versus insulin glargine in adults with type 2 diabetes and high cardiovascular risk inadequately controlled on oral glucose-lowering medications. Glucose 276-283 gastric inhibitory polypeptide Homo sapiens 117-120 34932984-0 2022 Effects on weight loss and glycemic control with SAR441255, a potent unimolecular peptide GLP-1/GIP/GCG receptor triagonist. sar441255 49-58 gastric inhibitory polypeptide Homo sapiens 96-99 34932984-1 2022 Unimolecular triple incretins, combining the activity of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and glucagon (GCG), have demonstrated reduction in body weight and improved glucose control in rodent models. Glucose 218-225 gastric inhibitory polypeptide Homo sapiens 90-134 34932984-1 2022 Unimolecular triple incretins, combining the activity of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and glucagon (GCG), have demonstrated reduction in body weight and improved glucose control in rodent models. Glucose 218-225 gastric inhibitory polypeptide Homo sapiens 136-139 34265066-8 2021 RESULTS: In humans, melatonin treatment resulted in reduced GIP secretion compared with placebo (ANOVA p=0.003), an effect also observed in the perfused rat intestines (ANOVA p=0.003) in which GLP-1 secretion also was impaired by arterial melatonin infusion (ANOVA p<0.001). Melatonin 20-29 gastric inhibitory polypeptide Homo sapiens 60-63 34265066-10 2021 CONCLUSION: Melatonin reduced GIP secretion during an oral glucose challenge in healthy young men but did not affect insulin secretion. Melatonin 12-21 gastric inhibitory polypeptide Homo sapiens 30-33 34916733-4 2022 Glucagon like peptide-1 (GLP-1) is well known as an incretin hormone responsible for regulation of blood glucose through its receptor. Glucose 105-112 gastric inhibitory polypeptide Homo sapiens 52-68 34687727-10 2022 Post-prandially, LuCI group had increased GLP-1 and GIP secretion following a glucose challenge. Glucose 78-85 gastric inhibitory polypeptide Homo sapiens 52-55 34913553-2 2022 OBJECTIVE: To assess incretin hormone dynamics during an oral glucose tolerance test (OGTT) and incretin effect in obese children with prediabetes in comparison with those with normal glucose tolerance (NGT) METHODS: Overweight and obese children were enrolled and classified according to OGTT results as NGT and prediabetes. Glucose 62-69 gastric inhibitory polypeptide Homo sapiens 21-37 34913553-2 2022 OBJECTIVE: To assess incretin hormone dynamics during an oral glucose tolerance test (OGTT) and incretin effect in obese children with prediabetes in comparison with those with normal glucose tolerance (NGT) METHODS: Overweight and obese children were enrolled and classified according to OGTT results as NGT and prediabetes. Glucose 184-191 gastric inhibitory polypeptide Homo sapiens 21-37 34889083-4 2022 This model (4GI model) incorporates known feedback mechanisms between glucose, GLP-1, glucagon, glucose-dependent insulinotropic peptide (GIP) and insulin after glucose provocation (i.e. food intake) and drug intervention utilizing published non-pharmacological and pharmacological (liraglutide, a GLP-1RA) data. Glucose 161-168 gastric inhibitory polypeptide Homo sapiens 96-136 34405256-3 2021 Here we investigate the effect of a 6-day s.c. GIP infusion on time in glycaemic range as assessed by continuous glucose monitoring (CGM) in individuals with type 1 diabetes. Glucose 113-120 gastric inhibitory polypeptide Homo sapiens 47-50 34620002-1 2021 Glucagon-like peptide-1 (GLP-1), an incretin hormone, is known to lower glucose levels, suppress glucagon secretion, and slow gastric emptying. Glucose 72-79 gastric inhibitory polypeptide Homo sapiens 36-52 34426508-7 2021 We demonstrate that associations with GIP, anthropometric and glycaemic traits are driven by distinct genetic signals from those driving CAD and lipid traits in the GIPR region, and higher E354-mediated fasting GIP levels are not associated with CAD risk. tartaric acid 189-193 gastric inhibitory polypeptide Homo sapiens 211-214 34503597-8 2021 However, plasma GIP concentrations were markedly increased after WR ingesting versus after RR ingestion. Arg-arg 91-93 gastric inhibitory polypeptide Homo sapiens 16-19 34321316-5 2021 Single and repeated doses of SCO-267 stimulated the secretion of insulin, glucagon, glucagon-like peptide 1, glucose-dependent insulinotropic polypeptide, and peptide YY in healthy adults. SCO-267 29-36 gastric inhibitory polypeptide Homo sapiens 109-153 34503597-10 2021 Plasma GIP concentrations are likely related to differences in GER and carbohydrate absorption. Carbohydrates 71-83 gastric inhibitory polypeptide Homo sapiens 7-10 34310013-6 2021 GLP-1 suppresses, and GIP increases glucagon secretion, both in a glucose-dependent manner. Glucose 66-73 gastric inhibitory polypeptide Homo sapiens 22-25 34310013-12 2021 GIP, but not GLP-1 increases triglyceride storage in white adipose tissue not only through stimulating insulin secretion, but by interacting with regional blood vessels and GIP receptors. Triglycerides 29-41 gastric inhibitory polypeptide Homo sapiens 0-3 34296449-1 2021 Dipeptidyl peptidase-IV (DPP-IV) inhibitors can reduce the blood sugar levels of diabetic patients by preventing the rapid decomposition of incretin hormone and prolonging its physiological effects. Blood Glucose 59-70 gastric inhibitory polypeptide Homo sapiens 140-156 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 gastric inhibitory polypeptide Homo sapiens 298-342 34310013-12 2021 GIP, but not GLP-1 increases triglyceride storage in white adipose tissue not only through stimulating insulin secretion, but by interacting with regional blood vessels and GIP receptors. Triglycerides 29-41 gastric inhibitory polypeptide Homo sapiens 173-176 34260853-7 2021 The GIPR-specific binding of 211At-MeATE-SPN-GIP combined with effective inhibition of tumor growth and fewer side effects compared to control suggests that 211At-MeATE-SPN-GIP TRT holds great potential as a novel nanoengineered TRT strategy for patients with GIPR-positive cancer. meate-spn 35-44 gastric inhibitory polypeptide Homo sapiens 45-48 34406395-5 2021 RESULTS: Following 6-months of sitagliptin vs placebo, MMTT intact GLP-1 and GIP responses increased (P < 0.001), ISR dynamics improved (P < 0.05), and glucagon suppression was modestly enhanced (P < 0.05) while GPA test responses for glucagon were lower. Sitagliptin Phosphate 31-42 gastric inhibitory polypeptide Homo sapiens 77-80 34446852-1 2021 Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are regarded as "incretins" working closely to regulate glucose homeostasis. Glucose 143-150 gastric inhibitory polypeptide Homo sapiens 36-80 34446852-1 2021 Glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) are regarded as "incretins" working closely to regulate glucose homeostasis. Glucose 143-150 gastric inhibitory polypeptide Homo sapiens 82-85 34446852-5 2021 We show that when the two receptors were co-expressed in HEK 293T cells with comparable receptor ratio to pancreatic cancer cells, GIP predominately induced cAMP accumulation while GLP-1 was biased towards beta-arrestin 2 recruitment. Cyclic AMP 157-161 gastric inhibitory polypeptide Homo sapiens 131-134 34334589-1 2021 Objective Glucose-dependent insulinotropic polypeptide (GIP) is speculated to worsen growth hormone (GH) hypersecretion in acromegaly and to be a cause of paradoxical increases in GH (PI-GH) during 75-g oral glucose tolerance testing (75-g OGTT). Glucose 208-215 gastric inhibitory polypeptide Homo sapiens 10-54 34334589-1 2021 Objective Glucose-dependent insulinotropic polypeptide (GIP) is speculated to worsen growth hormone (GH) hypersecretion in acromegaly and to be a cause of paradoxical increases in GH (PI-GH) during 75-g oral glucose tolerance testing (75-g OGTT). Glucose 208-215 gastric inhibitory polypeptide Homo sapiens 56-59 34334589-9 2021 The increase in plasma glucose was reduced during DPP4i-OGTT compared to during 75-g OGTT, suggesting that the increase in GH during DPP4i-OGTT was due not to high glucose concentrations but instead increased GIP caused by the administration of DPP4i. Glucose 23-30 gastric inhibitory polypeptide Homo sapiens 209-212 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 gastric inhibitory polypeptide Homo sapiens 344-347 35593668-0 2022 Tirzepatide - a dual GIP/GLP-1 receptor agonist - a new antidiabetic drug with potential metabolic activity in the treatment of type 2 diabetes. tirzepatide - a 0-15 gastric inhibitory polypeptide Homo sapiens 21-24 35232225-9 2022 CONCLUSIONS: The glucose-induced worsening orthostatic tachycardia in POTS was associated with a decline in SV; these changes occurred while GIP, a splanchnic vasodilator, was maximally elevated. Glucose 17-24 gastric inhibitory polypeptide Homo sapiens 141-144 35521766-4 2022 DESIGN AND METHODS: A group of 22 overweight/obese men was studied to determine associations between plasma levels of glucagon-like peptides 1 and 2 (GLP-1, GLP-2), and glucose-dependent insulinotropic polypeptide (GIP) after a fat rich meal and the production and clearance rates of apoB48- and apoB100-containing triglyceride rich lipoproteins. Triglycerides 315-327 gastric inhibitory polypeptide Homo sapiens 169-213 35452190-1 2022 A glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretins that play an important role in glucose metabolism, by increasing glucose-induced insulin secretion (GIIS) from pancreatic beta cells and help regulate body weight. Glucose 134-141 gastric inhibitory polypeptide Homo sapiens 48-51 35452190-1 2022 A glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) are incretins that play an important role in glucose metabolism, by increasing glucose-induced insulin secretion (GIIS) from pancreatic beta cells and help regulate body weight. Glucose 168-175 gastric inhibitory polypeptide Homo sapiens 48-51 35452190-4 2022 The mechanism of GIP secretion induced by nutrients, especially carbohydrates, is different from that of GLP-1 secretion. Carbohydrates 64-77 gastric inhibitory polypeptide Homo sapiens 17-20 35458186-2 2022 Such potency of human milk might be modulated either by incretins (glucagon-like polypeptide-1,GLP-1); glucose-inhibitory-polypeptide, GIP), and/or by milk casein content. Glucose 103-110 gastric inhibitory polypeptide Homo sapiens 135-138 35587193-11 2022 CONCLUSIONS: Glucose, protein and fat all stimulate GIP secretion in humans and mice. Glucose 13-20 gastric inhibitory polypeptide Homo sapiens 52-55 34984794-0 2022 Acute effects of linagliptin on intact and total GLP-1 and GIP levels in insulin-dependent type 2 diabetic patients with and without moderate renal impairment. Linagliptin 17-28 gastric inhibitory polypeptide Homo sapiens 59-62 34984794-9 2022 Treatment with linagliptin resulted in a significant increase in intact GLP-1 and GIP levels in patients with normal (p=0.048 and p=0.0001, respectively) and impaired (p=0.040 and p=0.0011, respectively) renal function during OGTT. Linagliptin 15-26 gastric inhibitory polypeptide Homo sapiens 82-85 35193160-0 2022 Gastric inhibitory polypeptide as the new candidate for the interaction of skeletal muscle blood flow and glucose disposal. Glucose 106-113 gastric inhibitory polypeptide Homo sapiens 0-30 35299971-4 2022 Interest in GIPR agonism for the treatment of obesity and diabetes was recently propelled by the clinical success of unimolecular dual-agonists targeting the receptors for GIP and GLP-1, with reported significantly improved body weight and glucose control in patients with obesity and type II diabetes. Glucose 240-247 gastric inhibitory polypeptide Homo sapiens 172-175 35217653-0 2022 Structural insights into multiplexed pharmacological actions of tirzepatide and peptide 20 at the GIP, GLP-1 or glucagon receptors. peptide 20 80-90 gastric inhibitory polypeptide Homo sapiens 98-101 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 gastric inhibitory polypeptide Homo sapiens 74-77 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 gastric inhibitory polypeptide Homo sapiens 79-119 35082201-6 2022 Plasma levels of both glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) were increased at the postprandial state, but only the GIP levels post-MTT were significantly higher than those post-OGTT. monooxyethylene trimethylolpropane tristearate 176-179 gastric inhibitory polypeptide Homo sapiens 58-98 35082201-6 2022 Plasma levels of both glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) were increased at the postprandial state, but only the GIP levels post-MTT were significantly higher than those post-OGTT. monooxyethylene trimethylolpropane tristearate 176-179 gastric inhibitory polypeptide Homo sapiens 160-163 35082201-7 2022 The enhancement of glucose disposal rates in patients with NGT or IGT after the MTT was associated with increased GIP levels. Glucose 19-26 gastric inhibitory polypeptide Homo sapiens 114-117 35082201-7 2022 The enhancement of glucose disposal rates in patients with NGT or IGT after the MTT was associated with increased GIP levels. monooxyethylene trimethylolpropane tristearate 80-83 gastric inhibitory polypeptide Homo sapiens 114-117 2533043-1 1989 To study the role of hormonal and neural factors in the control of the entero-insular axis the insulin, C-peptide, and glucose-dependent insulinotropic peptide (GIP) responses to oral and intravenous glucose were investigated in 5 patients who had received a combined kidney and paratopic pancreas transplant, with physiological portal venous drainage. Glucose 119-126 gastric inhibitory polypeptide Homo sapiens 161-164 35053889-7 2022 For all three drinks, adding L-arabinose increased glucagon-like peptide 1 (GLP-1) responses and lowered Glucose-dependent insulinotropic polypeptide (GIP) responses. Arabinose 29-40 gastric inhibitory polypeptide Homo sapiens 105-149 35053889-7 2022 For all three drinks, adding L-arabinose increased glucagon-like peptide 1 (GLP-1) responses and lowered Glucose-dependent insulinotropic polypeptide (GIP) responses. Arabinose 29-40 gastric inhibitory polypeptide Homo sapiens 151-154 35355921-0 2021 Efficacy and safety of novel twincretin tirzepatide a dual GIP and GLP-1 receptor agonist in the management of type-2 diabetes: A Cochrane meta-analysis. twincretin tirzepatide 29-51 gastric inhibitory polypeptide Homo sapiens 59-62 35017529-4 2022 We observed marked induction of EE cell differentiation and gut-derived expression and secretion of SST, 5HT, GIP, CCK, GLP-1 and PYY upon treatment with various combinations of three small molecules: rimonabant, SP600125 and AS1842856. pyrazolanthrone 213-221 gastric inhibitory polypeptide Homo sapiens 110-113 2693029-0 1989 A supplementary infusion of glucose-dependent insulinotropic polypeptide (GIP) with a meal does not significantly improve the beta cell response or glucose tolerance in type 2 diabetes mellitus. Glucose 28-35 gastric inhibitory polypeptide Homo sapiens 74-77 2695982-10 1989 The threshold for plasma glucose at which GIP would exert an incretin effect only reached at one time point, 30 min after ingestion of the meal. Glucose 25-32 gastric inhibitory polypeptide Homo sapiens 42-45 2693029-6 1989 Following the meal infusion of CS GIP increased from a fasting level of 10.3 +/- 1.2 pmol/1 to a significantly lower peak of 58.0 +/- 8.3 pmol/1 at 60 min. Cesium 31-33 gastric inhibitory polypeptide Homo sapiens 34-37 2509214-4 1989 Misoprostol and rioprostil reduced integrated incremental responses of GIP by 57% (P less than or equal to 0.001) and 45% (P less than or equal to 0.01), respectively, and both gave rise to an initial (approximately 10 min) delay of insulin and C-peptide responses, without a significant overall reduction in integrated incremental responses. Misoprostol 0-11 gastric inhibitory polypeptide Homo sapiens 71-74 2512938-1 1989 Oral administration of Gardrin (enprostil), a synthetic prostaglandin E2 structural analogue, is associated with a rapid reduction in serum lipoproteins as well as a reduction in meal-stimulated increments for glucose, insulin, and glucose-dependent insulinotropic peptide (GIP). Enprostil 23-30 gastric inhibitory polypeptide Homo sapiens 232-272 2512938-1 1989 Oral administration of Gardrin (enprostil), a synthetic prostaglandin E2 structural analogue, is associated with a rapid reduction in serum lipoproteins as well as a reduction in meal-stimulated increments for glucose, insulin, and glucose-dependent insulinotropic peptide (GIP). Enprostil 23-30 gastric inhibitory polypeptide Homo sapiens 274-277 2512938-1 1989 Oral administration of Gardrin (enprostil), a synthetic prostaglandin E2 structural analogue, is associated with a rapid reduction in serum lipoproteins as well as a reduction in meal-stimulated increments for glucose, insulin, and glucose-dependent insulinotropic peptide (GIP). Enprostil 32-41 gastric inhibitory polypeptide Homo sapiens 232-272 2512938-1 1989 Oral administration of Gardrin (enprostil), a synthetic prostaglandin E2 structural analogue, is associated with a rapid reduction in serum lipoproteins as well as a reduction in meal-stimulated increments for glucose, insulin, and glucose-dependent insulinotropic peptide (GIP). Enprostil 32-41 gastric inhibitory polypeptide Homo sapiens 274-277 2676668-3 1989 The tests were performed in random order after overnight fasts and blood samples were taken at 30 min intervals for 4 h. During the oral glucose tolerance test plasma glucose dependent insulinotropic polypeptide levels increased in the normal subjects from a fasting value of 20 +/- 3 pmol/l to a peak of 68 +/- 5 pmol/l at 30 min and in the Type 2 diabetic patients from a similar fasting level of 27 +/- 3 pmol/l to a higher peak value of 104 +/- 6 pmol/l at 30 min (p less than 0.001). Glucose 137-144 gastric inhibitory polypeptide Homo sapiens 167-211 2676668-4 1989 Glucose dependent insulinotropic polypeptide levels were significantly higher in the diabetic patients compared with the normal subjects from 30-90 min (p less than 0.01-0.001) following oral glucose. Glucose 192-199 gastric inhibitory polypeptide Homo sapiens 0-44 2668324-0 1989 Insulinotropic properties of synthetic human gastric inhibitory polypeptide in man: interactions with glucose, phenylalanine, and cholecystokinin-8. Glucose 102-109 gastric inhibitory polypeptide Homo sapiens 45-75 2668324-0 1989 Insulinotropic properties of synthetic human gastric inhibitory polypeptide in man: interactions with glucose, phenylalanine, and cholecystokinin-8. Phenylalanine 111-124 gastric inhibitory polypeptide Homo sapiens 45-75 2668324-0 1989 Insulinotropic properties of synthetic human gastric inhibitory polypeptide in man: interactions with glucose, phenylalanine, and cholecystokinin-8. cholecystokinin 8 130-147 gastric inhibitory polypeptide Homo sapiens 45-75 2668324-1 1989 The quantitative contribution of glucose-dependent insulinotropic polypeptide [gastric inhibitory polypeptide (GIP)] to the incretin effect after oral glucose (augmentation of insulin secretion over the degree that is explained by the glycemic rise) is not known. Glucose 33-40 gastric inhibitory polypeptide Homo sapiens 79-109 2668324-1 1989 The quantitative contribution of glucose-dependent insulinotropic polypeptide [gastric inhibitory polypeptide (GIP)] to the incretin effect after oral glucose (augmentation of insulin secretion over the degree that is explained by the glycemic rise) is not known. Glucose 33-40 gastric inhibitory polypeptide Homo sapiens 111-114 2668324-9 1989 It is concluded that human synthetic GIP is insulinotropic in man and that this activity may well explain a substantial part of the incretin effect after oral glucose. Glucose 159-166 gastric inhibitory polypeptide Homo sapiens 37-40 2658536-6 1989 Glucose suppressed motilin and stimulated GIP secretion; xylitol stimulated motilin secretion but had no effect on GIP, which is currently the main candidate for the role of enterogastrone. Glucose 0-7 gastric inhibitory polypeptide Homo sapiens 42-45 2509214-4 1989 Misoprostol and rioprostil reduced integrated incremental responses of GIP by 57% (P less than or equal to 0.001) and 45% (P less than or equal to 0.01), respectively, and both gave rise to an initial (approximately 10 min) delay of insulin and C-peptide responses, without a significant overall reduction in integrated incremental responses. Rioprostil 16-26 gastric inhibitory polypeptide Homo sapiens 71-74 2509214-7 1989 In conclusion, prostaglandin E analogues which caused a reduction in GIP responses, and thereby disrupting the enteroinsular axis to varying degrees, delayed the time-course of insulin secretion without a significant impact on glucose tolerance. Prostaglandins E 15-30 gastric inhibitory polypeptide Homo sapiens 69-72 2822518-2 1987 Specific gastric inhibitory polypeptide (GIP) receptors were characterized in human benign insulinoma plasma membranes employing [mono-[125I]iodo-Tyr10]-GIP (125I-GIP) as the radioligand. mono-[125i]iodo-tyr10 130-151 gastric inhibitory polypeptide Homo sapiens 41-44 2662384-0 1989 The influence of body weight, age and glucose tolerance on the relationship between GIP secretion and beta-cell function in man. Glucose 38-45 gastric inhibitory polypeptide Homo sapiens 84-87 2665779-1 1989 The gastrointestinal hormone, gastric inhibitory polypeptide (GIP), has been isolated and characterized because of its enterogastrone-type effects. enterogastrone 119-133 gastric inhibitory polypeptide Homo sapiens 62-65 2497435-7 1989 Plasma GIP concentration increased significantly with enteral glucose administration in all infants but remained unchanged with parenteral glucose infusion. Glucose 62-69 gastric inhibitory polypeptide Homo sapiens 7-10 2497435-9 1989 However, when glucose was infused orogastrically at a lower rate (8 mg/kg/min), plasma GIP concentrations rose, but no enhancement of insulin response was detected, suggesting the importance of the role of circulating glucose in the "enteroinsular axis". Glucose 14-21 gastric inhibitory polypeptide Homo sapiens 87-90 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 122-129 gastric inhibitory polypeptide Homo sapiens 154-157 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 gastric inhibitory polypeptide Homo sapiens 154-157 3146539-0 1988 Suppression of postprandial glucose, insulin, C-peptide, and glucose-dependent insulinotropic peptide (GIP) in man by oral administration of a prostaglandin analogue (enprostil). Prostaglandins 143-156 gastric inhibitory polypeptide Homo sapiens 61-101 3146539-0 1988 Suppression of postprandial glucose, insulin, C-peptide, and glucose-dependent insulinotropic peptide (GIP) in man by oral administration of a prostaglandin analogue (enprostil). Prostaglandins 143-156 gastric inhibitory polypeptide Homo sapiens 103-106 3408703-6 1988 The gastric inhibitory polypeptide (GIP) response to oral fat was significantly attenuated by IV glucose whilst subjects were consuming their normal diets and the GIP response to fat alone was significantly diminished during the low-fat diet. Glucose 97-104 gastric inhibitory polypeptide Homo sapiens 4-34 3408703-6 1988 The gastric inhibitory polypeptide (GIP) response to oral fat was significantly attenuated by IV glucose whilst subjects were consuming their normal diets and the GIP response to fat alone was significantly diminished during the low-fat diet. Glucose 97-104 gastric inhibitory polypeptide Homo sapiens 36-39 3408703-7 1988 Post-prandial plasma triglycerides, light scattering indices (LSI; an index of post-prandial chylomicronaemia) and paracetamol levels paralleled the integrated GIP responses on both normal and low-fat diets. Acetaminophen 115-126 gastric inhibitory polypeptide Homo sapiens 160-163 3392357-1 1988 Gastric Inhibitory Polypeptide (GIP) is secreted in response to oral glucose, amino acid, and fats. Glucose 69-76 gastric inhibitory polypeptide Homo sapiens 0-30 3075897-1 1988 A physiological role for GIP as an insulinotropic hormone involved in the enteroinsular axis has been established and ingestion of glucose, fatty acids and certain amino acids will produce an increase in circulating IR-GIP levels. Glucose 131-138 gastric inhibitory polypeptide Homo sapiens 219-222 3075897-1 1988 A physiological role for GIP as an insulinotropic hormone involved in the enteroinsular axis has been established and ingestion of glucose, fatty acids and certain amino acids will produce an increase in circulating IR-GIP levels. Fatty Acids 140-151 gastric inhibitory polypeptide Homo sapiens 219-222 3075897-2 1988 The insulinotropic action of GIP is glucose concentration dependent in normal animals. Glucose 36-43 gastric inhibitory polypeptide Homo sapiens 29-32 3075897-4 1988 Animal models have indicated a disturbance of GIP receptor function associated with hyperinsulinaemia, i.e. lowering of the minimum glucose concentration at which GIP is insulinotropic. Glucose 132-139 gastric inhibitory polypeptide Homo sapiens 46-49 3075897-4 1988 Animal models have indicated a disturbance of GIP receptor function associated with hyperinsulinaemia, i.e. lowering of the minimum glucose concentration at which GIP is insulinotropic. Glucose 132-139 gastric inhibitory polypeptide Homo sapiens 163-166 3293660-9 1988 Plasma GIP levels were higher following oral glucose after the HFD (area under plasma GIP curve 0-180 min 1660 (SE 592) v. 2642 (SE 750) ng/l.h for control and HFD respectively; P less than 0.05). Glucose 45-52 gastric inhibitory polypeptide Homo sapiens 7-10 3293660-9 1988 Plasma GIP levels were higher following oral glucose after the HFD (area under plasma GIP curve 0-180 min 1660 (SE 592) v. 2642 (SE 750) ng/l.h for control and HFD respectively; P less than 0.05). Glucose 45-52 gastric inhibitory polypeptide Homo sapiens 86-89 3293660-13 1988 Glucose-stimulated GIP secretion was thus enhanced by the HFD. Glucose 0-7 gastric inhibitory polypeptide Homo sapiens 19-22 3293660-16 1988 The improvement in glucose tolerance post-HFD could possibly be due to a GIP-mediated inhibition of hepatic glycogenolysis, or a decreased rate of glucose uptake from the small intestine. Glucose 19-26 gastric inhibitory polypeptide Homo sapiens 73-76 3057329-6 1988 Increasing doses of Bay 1099 were found to decrease the postprandial rise in serum glucose concentration, delay the time to peak insulin concentration, and decrease the output of GIP after the meal. MIGLITOL 20-28 gastric inhibitory polypeptide Homo sapiens 179-182 3276722-1 1988 Previous studies suggest that the rate of rise of the plasma glucose-dependent insulinotropic peptide (GIP) concentration, rather than the steady state level achieved, may be the stimulus of the increased insulin secretion that occurs when fat is ingested with carbohydrate. Carbohydrates 261-273 gastric inhibitory polypeptide Homo sapiens 61-101 3276722-1 1988 Previous studies suggest that the rate of rise of the plasma glucose-dependent insulinotropic peptide (GIP) concentration, rather than the steady state level achieved, may be the stimulus of the increased insulin secretion that occurs when fat is ingested with carbohydrate. Carbohydrates 261-273 gastric inhibitory polypeptide Homo sapiens 103-106 3276722-3 1988 At the time of the iv glucose injection after the fat-containing meal, the rate of rise of plasma GIP was maximum, but the level was only 40% of the achieved by 30 min. Glucose 22-29 gastric inhibitory polypeptide Homo sapiens 98-101 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 gastric inhibitory polypeptide Homo sapiens 120-123 2890159-1 1987 Gastric inhibitory polypeptide (GIP) is a 42-amino acid hormone that stimulates insulin secretion in the presence of glucose. Glucose 117-124 gastric inhibitory polypeptide Homo sapiens 0-30 2890159-1 1987 Gastric inhibitory polypeptide (GIP) is a 42-amino acid hormone that stimulates insulin secretion in the presence of glucose. Glucose 117-124 gastric inhibitory polypeptide Homo sapiens 32-35 2890159-4 1987 The GIP moiety is flanked by polypeptide segments of 51 and 60 amino acids at its NH2 and COOH termini, respectively. Carbonic Acid 90-94 gastric inhibitory polypeptide Homo sapiens 4-7 2890159-6 1987 GIP is released from the precursor by processing at single arginine residues. Arginine 59-67 gastric inhibitory polypeptide Homo sapiens 0-3 2890159-7 1987 There is a region of nine amino acids in the COOH-terminal propeptide of the GIP precursor that has partial homology with a portion of chromogranin A as well as pancreastatin. propeptide 59-69 gastric inhibitory polypeptide Homo sapiens 77-80 3525048-0 1986 Lack of a direct effect of the autonomic nervous system on glucose-stimulated gastric inhibitory polypeptide (GIP) secretion in man. Glucose 59-66 gastric inhibitory polypeptide Homo sapiens 110-113 3310195-4 1987 In contrast, the GIP response to the test meal was blunted after dexamethasone (126 +/- 17 vs. 177 +/- 23 pmol/l; p less than 0.001). Dexamethasone 65-78 gastric inhibitory polypeptide Homo sapiens 17-20 3310195-6 1987 The mechanism(s) for the decreased GIP response after dexamethasone could involve (1) a direct inhibitory effect on GIP secretion by dexamethasone, and/or (2) a negative feedback of elevated glucose and insulin levels on GIP secretion. Dexamethasone 54-67 gastric inhibitory polypeptide Homo sapiens 35-38 3310195-6 1987 The mechanism(s) for the decreased GIP response after dexamethasone could involve (1) a direct inhibitory effect on GIP secretion by dexamethasone, and/or (2) a negative feedback of elevated glucose and insulin levels on GIP secretion. Dexamethasone 54-67 gastric inhibitory polypeptide Homo sapiens 116-119 3310195-6 1987 The mechanism(s) for the decreased GIP response after dexamethasone could involve (1) a direct inhibitory effect on GIP secretion by dexamethasone, and/or (2) a negative feedback of elevated glucose and insulin levels on GIP secretion. Dexamethasone 54-67 gastric inhibitory polypeptide Homo sapiens 116-119 3310195-6 1987 The mechanism(s) for the decreased GIP response after dexamethasone could involve (1) a direct inhibitory effect on GIP secretion by dexamethasone, and/or (2) a negative feedback of elevated glucose and insulin levels on GIP secretion. Dexamethasone 133-146 gastric inhibitory polypeptide Homo sapiens 35-38 3310195-6 1987 The mechanism(s) for the decreased GIP response after dexamethasone could involve (1) a direct inhibitory effect on GIP secretion by dexamethasone, and/or (2) a negative feedback of elevated glucose and insulin levels on GIP secretion. Dexamethasone 133-146 gastric inhibitory polypeptide Homo sapiens 116-119 3310195-6 1987 The mechanism(s) for the decreased GIP response after dexamethasone could involve (1) a direct inhibitory effect on GIP secretion by dexamethasone, and/or (2) a negative feedback of elevated glucose and insulin levels on GIP secretion. Dexamethasone 133-146 gastric inhibitory polypeptide Homo sapiens 116-119 3310195-6 1987 The mechanism(s) for the decreased GIP response after dexamethasone could involve (1) a direct inhibitory effect on GIP secretion by dexamethasone, and/or (2) a negative feedback of elevated glucose and insulin levels on GIP secretion. Glucose 191-198 gastric inhibitory polypeptide Homo sapiens 35-38 3434081-0 1987 Solid phase synthesis of a 31-residue fragment of human glucose-dependent insulinotropic polypeptide (GIP) by the continuous flow polyamide method. Nylons 130-139 gastric inhibitory polypeptide Homo sapiens 56-100 3434081-0 1987 Solid phase synthesis of a 31-residue fragment of human glucose-dependent insulinotropic polypeptide (GIP) by the continuous flow polyamide method. Nylons 130-139 gastric inhibitory polypeptide Homo sapiens 102-105 3434081-1 1987 A fragment, GIP1-31, of the human Glucose-dependent Insulinotropic Polypeptide (GIP1-42) Tyr-Ala-Glu-Gly-Thr-Phe-Ile-Ser-Asp-Tyr-Ser-Ile-Ala-Met-Asp-Lys-Ile-His- Gln-Gln-Asp-Phe-Val-Asn-Trp-Leu-Leu-Ala-Gln-Lys-Gly has been synthesized by solid phase methodology under continuous flow conditions. Tyrosine 89-92 gastric inhibitory polypeptide Homo sapiens 34-78 3595384-2 1987 The aim of the present study was to investigate if physiologic changes of noradrenaline would evoke any alterations in gastric acid secretion or in the plasma concentration of some gastrointestinal hormones (gastrin, secretin, PP, PYY, and GIP) known to affect gastric physiology. Norepinephrine 74-87 gastric inhibitory polypeptide Homo sapiens 240-243 3298936-7 1987 In all subjects plasma, C-peptide increased more after 10 minutes of GIP infusion (IDD, 0.48 +/- 0.05; NIDD, 0.79 +/- 0.11; normal subjects, 2.27 +/- 0.29 nmol/L) than on the corresponding day with NaCl infusion (IDD, 0.35 +/- 0.03; NIDD, 0.62 +/- 0.08; normal subjects, 1.22 +/- 0.13 nmol/L, P less than .05 for all). Sodium Chloride 198-202 gastric inhibitory polypeptide Homo sapiens 69-72 3298936-10 1987 In the presence of a plasma glucose concentration of 8 mmol/L, physiologic concentrations of porcine GIP caused an immediate but impaired beta-cell response in IDD and NIDD patients. Glucose 28-35 gastric inhibitory polypeptide Homo sapiens 101-104 3568934-3 1987 The long-chain triglyceride meal evoked a brisk and sustained gallbladder contraction, higher levels of CCK, and a significant increase in plasma PP and GIP levels. Triglycerides 15-27 gastric inhibitory polypeptide Homo sapiens 153-156 3546047-1 1986 The effect of cholinomimetic stimulation by infusion of edrophonium chloride or muscarinic blockade by infusion of atropine sulfate on insulin and GIP secretion was studied in normal lean subjects during eu- and hyperglycemia. Atropine 115-131 gastric inhibitory polypeptide Homo sapiens 147-150 3546047-4 1986 The effect of atropine infusion on fasting plasma insulin and GIP was subsequently studied in 11 obese patients and 10 lean subjects. Atropine 14-22 gastric inhibitory polypeptide Homo sapiens 62-65 3546047-5 1986 Muscarinic antagonism by atropine led to a transient non-significant suppression of GIP and insulin in lean subjects, but to a significant, sustained suppression of these hormones in obese patients. Atropine 25-33 gastric inhibitory polypeptide Homo sapiens 84-87 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 gastric inhibitory polypeptide Homo sapiens 73-76 3529782-0 1986 Effects of acarbose on the relationship between changes in GIP and insulin responses to meals in normal subjects. Acarbose 11-19 gastric inhibitory polypeptide Homo sapiens 59-62 3514334-12 1986 Exercise-induced improvement in glucose utilization in these obese children was associated with an increase in GIP secretion. Glucose 32-39 gastric inhibitory polypeptide Homo sapiens 111-114 3526084-8 1986 Also the peak and integrated IR-GIP response increased in a dose-dependent manner by increasing the size of the glucose load. Glucose 112-119 gastric inhibitory polypeptide Homo sapiens 32-35 3526084-9 1986 Larger amounts of glucose mainly prolong the GIP response. Glucose 18-25 gastric inhibitory polypeptide Homo sapiens 45-48 3526084-10 1986 Significantly greater amounts of IR-GIP were released with 60 and 90 g glucose when given in 600 mL instead of 300 mL water. Glucose 71-78 gastric inhibitory polypeptide Homo sapiens 36-39 3526084-10 1986 Significantly greater amounts of IR-GIP were released with 60 and 90 g glucose when given in 600 mL instead of 300 mL water. Water 118-123 gastric inhibitory polypeptide Homo sapiens 36-39 3520915-9 1986 It is also assumed that the glucose-dependent insulinotropic action of GIP would be impaired by the procedure. Glucose 28-35 gastric inhibitory polypeptide Homo sapiens 71-74 3529782-2 1986 Acarbose caused a significant reduction of GIP and insulin responses (P less than 0.05). Acarbose 0-8 gastric inhibitory polypeptide Homo sapiens 43-46 3529782-5 1986 The changes in GIP response after Acarbose correlated positively with the change in insulin/C-peptide ratio (r = 0.69; P less than 0.05). Acarbose 34-42 gastric inhibitory polypeptide Homo sapiens 15-18 3464150-3 1986 The enteral stimulation of insulin secretion (the incretin effect) is diminished in pregnancy--both when determined indirectly and when the gastric inhibitory polypeptide (GIP) response to glucose ingestion is considered. Glucose 189-196 gastric inhibitory polypeptide Homo sapiens 172-175 3512343-3 1986 Following oral glucose, morphine slowed gastric emptying and reduced plasma concentrations of glucose, insulin, and GIP. Morphine 24-32 gastric inhibitory polypeptide Homo sapiens 116-119 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 gastric inhibitory polypeptide Homo sapiens 229-232 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. Morphine 98-106 gastric inhibitory polypeptide Homo sapiens 229-232 3464150-5 1986 In gestational diabetics similar findings as in normal pregnant women were obtained except that the GIP response to glucose ingestion was smaller and the GIP response to lipid ingestion greater than in normal women. Glucose 116-123 gastric inhibitory polypeptide Homo sapiens 100-103 3018690-5 1986 The experimental data: (1) support the enterogastrone activity of GIP, via adenylate cyclase activation and somatostatin release by gastric D cells; (2) demonstrate that HGT-1 cells originating from a human fundic tumor are sensitive to the glucagon-like peptides G-29 and -37, as rat fundic glands; (3) indicate that the pharmacological properties of the VIP receptor in this human gastric cell line are similar to those characterized in normal human gastric glands. enterogastrone 39-53 gastric inhibitory polypeptide Homo sapiens 66-69 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 gastric inhibitory polypeptide Homo sapiens 34-37 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 gastric inhibitory polypeptide Homo sapiens 39-69 3510224-16 1986 We hypothesize that GIP may play a compensatory role to improve both impaired beta-cell insulin release and peripheral glucose utilization which are the recognized pathogenetic mechanisms underlying type II diabetes mellitus. Glucose 119-126 gastric inhibitory polypeptide Homo sapiens 20-23 3513294-0 1986 The priming effect of glucose on the gastric inhibitory polypeptide-induced insulin release. Glucose 22-29 gastric inhibitory polypeptide Homo sapiens 37-67 3886310-0 1985 High-carbohydrate, low-fat diet: effect on lipid and carbohydrate metabolism, GIP and insulin secretion in diabetics. Carbohydrates 5-17 gastric inhibitory polypeptide Homo sapiens 78-81 4050722-5 1985 Xanthan gum also tended to lower fasting and postload levels of gastrin and gastric inhibitory polypeptide (GIP) and fasting levels of total and VLDL triglyceride and cholesterol in VLDL and LDL fractions. xanthan gum 0-7 gastric inhibitory polypeptide Homo sapiens 76-106 4050722-5 1985 Xanthan gum also tended to lower fasting and postload levels of gastrin and gastric inhibitory polypeptide (GIP) and fasting levels of total and VLDL triglyceride and cholesterol in VLDL and LDL fractions. xanthan gum 0-7 gastric inhibitory polypeptide Homo sapiens 108-111 3902421-3 1985 Since elevated glucose and insulin levels are found in hyperthyroidism, we compared the GIP responses to oral glucose ingestion in 12 hyperthyroid patients and 10 age-matched controls. Glucose 110-117 gastric inhibitory polypeptide Homo sapiens 88-91 4088237-7 1985 IRI and GIP responses to oral glucose were impaired following PD without pancreatojejunostomy, while after operating pancreatojejunostomy, those responses restored in part which might suggest the significant role of the pancreatic juice into the jejunum in releasing mechanism of these hormones. Glucose 30-37 gastric inhibitory polypeptide Homo sapiens 8-11 4008608-5 1985 Obese subjects and diabetic patients exceeded lean normal subjects by up to 620% for glucose, up to 640% for insulin, and up to 360% for GIP during the first hour after glucose ingestion or the test meal. Glucose 169-176 gastric inhibitory polypeptide Homo sapiens 137-140 2860876-3 1985 Glucose intolerance, hyperinsulinism, and exaggerated gastric inhibitory polypeptide (GIP) release occurred following glucose ingestion. Glucose 118-125 gastric inhibitory polypeptide Homo sapiens 86-89 2860876-6 1985 Since GIP is insulinotropic in the presence of hyperglycemia, the hyperinsulinism of morbid obesity may be secondary to the abnormally high glucose-stimulated GIP levels in these patients. Glucose 140-147 gastric inhibitory polypeptide Homo sapiens 6-9 2860876-6 1985 Since GIP is insulinotropic in the presence of hyperglycemia, the hyperinsulinism of morbid obesity may be secondary to the abnormally high glucose-stimulated GIP levels in these patients. Glucose 140-147 gastric inhibitory polypeptide Homo sapiens 159-162 3905182-3 1985 Plasma concentrations of GIP tended to be higher during nadolol than placebo treatment. Nadolol 56-63 gastric inhibitory polypeptide Homo sapiens 25-28 3890140-0 1985 Effects of atropine on GIP-induced insulin and pancreatic polypeptide release in man. Atropine 11-19 gastric inhibitory polypeptide Homo sapiens 23-26 3884577-9 1985 These data indicate that fructose ingestion, though causing smaller perturbations in plasma glucose, insulin, and gastrointestinal polypeptide (GIP) levels than glucose ingestion, was no more effective than glucose or placebo in sparing glycogen during a long-term exercise. Fructose 25-33 gastric inhibitory polypeptide Homo sapiens 114-148 6383904-2 1984 The effect of aging, obesity, and non-insulin-dependent diabetes mellitus on glucose-stimulated gastric inhibitory polypeptide (GIP) levels was studied in 55 male subjects, ranging in age from 19 to 84 yr, and in obesity, expressed as body mass index, from 21 to 34. Glucose 77-84 gastric inhibitory polypeptide Homo sapiens 128-131 2988218-5 1985 Changes in blood glucose, serum insulin, GIP, gastrin, and plasma glucagon, caused by Acarbose, reflected delayed glucose absorption and were plausible within the regulatory framework of carbohydrate assimilation. Acarbose 86-94 gastric inhibitory polypeptide Homo sapiens 41-44 2988218-6 1985 When the Acarbose regime was maintained for 5 weeks on a controlled diet, abdominal sensations like e.g. meteorism declined remarkably while carbohydrate fermentation remained high and lowered GIP was sustained. Acarbose 9-17 gastric inhibitory polypeptide Homo sapiens 193-196 3902421-0 1985 Gastric inhibitory polypeptide (GIP) responses after oral glucose ingestion in hyperthyroidism. Glucose 58-65 gastric inhibitory polypeptide Homo sapiens 0-30 3902421-0 1985 Gastric inhibitory polypeptide (GIP) responses after oral glucose ingestion in hyperthyroidism. Glucose 58-65 gastric inhibitory polypeptide Homo sapiens 32-35 6099816-0 1984 Glucose-induced GIP levels in patients with insulinoma. Glucose 0-7 gastric inhibitory polypeptide Homo sapiens 16-19 6099816-2 1984 GIP hypersecretion and an absent correlation between the insulin: glucose ratio and plasma GIP concentration have been observed. Glucose 66-73 gastric inhibitory polypeptide Homo sapiens 91-94 6383904-8 1984 When IR-GIP responses to oral glucose were expressed as a relative change from basal levels, IR-GIP rose 86% in diabetic subjects and 243% in obese subjects, compared with 185% and 165% in their respective controls. Glucose 30-37 gastric inhibitory polypeptide Homo sapiens 8-11 6383904-8 1984 When IR-GIP responses to oral glucose were expressed as a relative change from basal levels, IR-GIP rose 86% in diabetic subjects and 243% in obese subjects, compared with 185% and 165% in their respective controls. Glucose 30-37 gastric inhibitory polypeptide Homo sapiens 96-99 6367676-3 1984 The levels of GIP after glucose ingestion were significantly greater in the preoperative patients than in normal controls throughout 180 minutes. Glucose 24-31 gastric inhibitory polypeptide Homo sapiens 14-17 6148162-7 1984 Plasma GIP rose markedly after carbohydrate, basal 506 +/- 50 pg/ml, peak 1480 +/- 120 pg/ml. Carbohydrates 31-43 gastric inhibitory polypeptide Homo sapiens 7-10 6385345-5 1984 Maximum acid output in response to tetragastrin correlated significantly with integrated GIP response after oral glucose loading. Tetragastrin 35-47 gastric inhibitory polypeptide Homo sapiens 89-92 6385345-5 1984 Maximum acid output in response to tetragastrin correlated significantly with integrated GIP response after oral glucose loading. Glucose 113-120 gastric inhibitory polypeptide Homo sapiens 89-92 6385345-6 1984 In the SV + P group, the response of GIP was slightly greater after surgery. sv + p 7-13 gastric inhibitory polypeptide Homo sapiens 37-40 6385345-8 1984 The integrated GIP response was greater in the SV + P group than in the TV + P group. sv + p 47-53 gastric inhibitory polypeptide Homo sapiens 15-18 6385345-8 1984 The integrated GIP response was greater in the SV + P group than in the TV + P group. tv + p 72-78 gastric inhibitory polypeptide Homo sapiens 15-18 6329177-0 1984 Gastric inhibitory peptide (GIP), pancreatic glucagon and vasoactive intestinal peptide (VIP) are cAMP-inducing hormones in the human gastric cancer cell line HGT-1. Cyclic AMP 98-102 gastric inhibitory polypeptide Homo sapiens 0-26 6329177-0 1984 Gastric inhibitory peptide (GIP), pancreatic glucagon and vasoactive intestinal peptide (VIP) are cAMP-inducing hormones in the human gastric cancer cell line HGT-1. Cyclic AMP 98-102 gastric inhibitory polypeptide Homo sapiens 28-31 6365944-0 1984 Augmented gastric inhibitory polypeptide and insulin responses to a meal after an increase in carbohydrate (sucrose) intake. Carbohydrates 94-106 gastric inhibitory polypeptide Homo sapiens 10-40 6365944-0 1984 Augmented gastric inhibitory polypeptide and insulin responses to a meal after an increase in carbohydrate (sucrose) intake. Sucrose 108-115 gastric inhibitory polypeptide Homo sapiens 10-40 6365944-10 1984 Serum GIP was highest during period B (carbohydrate), when average concentrations were significantly higher (P less than 0.01) 15-60 min after the meal compared to those during the baseline study. Carbohydrates 39-51 gastric inhibitory polypeptide Homo sapiens 6-9 6365944-12 1984 Thus, GIP and insulin secretion were substantially altered by an acute increase in sucrose intake. Sucrose 83-90 gastric inhibitory polypeptide Homo sapiens 6-9 6365944-13 1984 The exaggerated GIP response to a meal in some patients with obesity may possibly be the result of adaptation of intestinal GIP cells to diet, particularly one rich in sucrose. Sucrose 168-175 gastric inhibitory polypeptide Homo sapiens 16-19 6365944-13 1984 The exaggerated GIP response to a meal in some patients with obesity may possibly be the result of adaptation of intestinal GIP cells to diet, particularly one rich in sucrose. Sucrose 168-175 gastric inhibitory polypeptide Homo sapiens 124-127 6505290-1 1984 The Sephadex G-50 gel filtration profile of immunoreactive gastric inhibitory polypeptide (GIP) in porcine and human gastrointestinal mucosa was determined in assays with antisera obtained from five different groups working with GIP. sephadex 4-17 gastric inhibitory polypeptide Homo sapiens 59-89 6505290-1 1984 The Sephadex G-50 gel filtration profile of immunoreactive gastric inhibitory polypeptide (GIP) in porcine and human gastrointestinal mucosa was determined in assays with antisera obtained from five different groups working with GIP. sephadex 4-17 gastric inhibitory polypeptide Homo sapiens 91-94 6745415-1 1984 Human GIP 1-42 and fragments of human GIP corresponding to GIP 10-42, GIP 11-42, and GIP 17-42 were isolated from acid-ethanol extracts of human small intestines with the aid of an anti-GIP serum specific for the extreme C-terminal portion of the GIP molecule. acid-ethanol 114-126 gastric inhibitory polypeptide Homo sapiens 38-41 6745415-1 1984 Human GIP 1-42 and fragments of human GIP corresponding to GIP 10-42, GIP 11-42, and GIP 17-42 were isolated from acid-ethanol extracts of human small intestines with the aid of an anti-GIP serum specific for the extreme C-terminal portion of the GIP molecule. acid-ethanol 114-126 gastric inhibitory polypeptide Homo sapiens 38-41 6745415-1 1984 Human GIP 1-42 and fragments of human GIP corresponding to GIP 10-42, GIP 11-42, and GIP 17-42 were isolated from acid-ethanol extracts of human small intestines with the aid of an anti-GIP serum specific for the extreme C-terminal portion of the GIP molecule. acid-ethanol 114-126 gastric inhibitory polypeptide Homo sapiens 38-41 6745415-1 1984 Human GIP 1-42 and fragments of human GIP corresponding to GIP 10-42, GIP 11-42, and GIP 17-42 were isolated from acid-ethanol extracts of human small intestines with the aid of an anti-GIP serum specific for the extreme C-terminal portion of the GIP molecule. acid-ethanol 114-126 gastric inhibitory polypeptide Homo sapiens 38-41 6745415-1 1984 Human GIP 1-42 and fragments of human GIP corresponding to GIP 10-42, GIP 11-42, and GIP 17-42 were isolated from acid-ethanol extracts of human small intestines with the aid of an anti-GIP serum specific for the extreme C-terminal portion of the GIP molecule. acid-ethanol 114-126 gastric inhibitory polypeptide Homo sapiens 38-41 6745415-4 1984 The sequence of human GIP is thus: (Formula: see text) Amino acid residues 18 and 34 are Arg and Ser, respectively, in porcine GIP. Arginine 89-92 gastric inhibitory polypeptide Homo sapiens 22-25 6745415-4 1984 The sequence of human GIP is thus: (Formula: see text) Amino acid residues 18 and 34 are Arg and Ser, respectively, in porcine GIP. Arginine 89-92 gastric inhibitory polypeptide Homo sapiens 127-130 6745415-4 1984 The sequence of human GIP is thus: (Formula: see text) Amino acid residues 18 and 34 are Arg and Ser, respectively, in porcine GIP. Serine 97-100 gastric inhibitory polypeptide Homo sapiens 22-25 6745415-4 1984 The sequence of human GIP is thus: (Formula: see text) Amino acid residues 18 and 34 are Arg and Ser, respectively, in porcine GIP. Serine 97-100 gastric inhibitory polypeptide Homo sapiens 127-130 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 gastric inhibitory polypeptide Homo sapiens 0-44 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 gastric inhibitory polypeptide Homo sapiens 46-49 6368294-5 1984 glucose, with or without simultaneous GIP infusion, to produce plasma levels of GIP or glucose similar to those seen after oral glucose. Glucose 0-7 gastric inhibitory polypeptide Homo sapiens 80-83 6368294-7 1984 glucose with three times the original dose of GIP was also investigated. Glucose 0-7 gastric inhibitory polypeptide Homo sapiens 46-49 6368294-10 1984 The higher dose of GIP caused a further increase in insulin response (30-min increment, 972 +/- 191 pmol/L; compared with glucose alone, 356 +/- 100 pmol/L, P less than 0.01; and compared with low GIP, 602 +/- 247 pmol/L, P less than 0.02). Glucose 122-129 gastric inhibitory polypeptide Homo sapiens 19-22 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 gastric inhibitory polypeptide Homo sapiens 145-148 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 gastric inhibitory polypeptide Homo sapiens 159-162 6369071-6 1984 In both groups of women the GIP response to triglycerides was impaired in pregnancy. Triglycerides 44-57 gastric inhibitory polypeptide Homo sapiens 28-31 6369071-9 1984 It is concluded that the GIP response to triglycerides is impaired in pregnancy. Triglycerides 41-54 gastric inhibitory polypeptide Homo sapiens 25-28 6372074-3 1984 The fasting levels of serum immunoreactive GIP were moderately elevated and reached significantly higher levels after oral glucose ingestion in both gastrectomized groups as compared with normal subjects. Glucose 123-130 gastric inhibitory polypeptide Homo sapiens 43-46 6372074-6 1984 Thus, glucose-induced GIP release is mainly of duodenal and fat-induced GIP release mainly of jejunal origin. Glucose 6-13 gastric inhibitory polypeptide Homo sapiens 22-25 6372074-6 1984 Thus, glucose-induced GIP release is mainly of duodenal and fat-induced GIP release mainly of jejunal origin. Glucose 6-13 gastric inhibitory polypeptide Homo sapiens 72-75 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 gastric inhibitory polypeptide Homo sapiens 113-157 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 gastric inhibitory polypeptide Homo sapiens 159-162 6357919-0 1983 Failure of fasting to influence the GIP response to oral glucose in non-obese human subjects. Glucose 57-64 gastric inhibitory polypeptide Homo sapiens 36-39 6357919-1 1983 The plasma GIP response to an oral 50 g glucose tolerance test has been compared in eight non-obese human subjects after 12 and 36 h of fasting. Glucose 40-47 gastric inhibitory polypeptide Homo sapiens 11-14 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 gastric inhibitory polypeptide Homo sapiens 247-250 6350544-6 1983 Consumption of 7.5 and 15% Fructose diets increased fasting plasma glucose and GIP responses in both groups. Fructose 27-35 gastric inhibitory polypeptide Homo sapiens 79-82 6359725-0 1983 [The effect of an infusion of glucose-insulin-potassium and of heparin on the plasma free fatty acid levels and on blood glucose]. Fatty Acids, Nonesterified 85-100 gastric inhibitory polypeptide Homo sapiens 30-55 6359725-1 1983 In the treatment of acute myocardial infarction infusion of glucose-insulin-potassium (GIP) and/or heparin are frequently administered. CHEMBL4438930 87-90 gastric inhibitory polypeptide Homo sapiens 60-85 6354520-0 1983 The evidence for the regulatory role of endogenous GIP as a glucose dependent insulinotropic hormone in patients with duodenal ulcer. Glucose 60-67 gastric inhibitory polypeptide Homo sapiens 51-54 6343163-4 1983 During the course the subjects with negative calorie balance showed augmented integrated glucose-induced gastric inhibitory polypeptide (GIP) response (p less than 0.05) and the plasma concentration of GIP after glucose stimulation was higher at 90 and 120 min during the course than in the control experiment. Glucose 89-96 gastric inhibitory polypeptide Homo sapiens 105-135 6354520-3 1983 Plasma GIP and insulin responses to oral glucose loading were significantly higher than normal in both groups. Glucose 41-48 gastric inhibitory polypeptide Homo sapiens 7-10 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 gastric inhibitory polypeptide Homo sapiens 33-36 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 gastric inhibitory polypeptide Homo sapiens 33-36 6354520-6 1983 These findings indicate that the exaggerated GIP response to oral glucose in duodenal ulcer patients may be due not to increased vagal tone, but to more rapid incoming load. Glucose 66-73 gastric inhibitory polypeptide Homo sapiens 45-48 6354520-7 1983 We found also that the hypersecretion of GIP induced by glucose ingestion in patients with duodenal ulcer and total gastrectomy may be responsible for the hyperfunction of the enteroinsular axis in these patients. Glucose 56-63 gastric inhibitory polypeptide Homo sapiens 41-44 6345991-4 1983 The rise in GIP levels during the first hour was similar after the meal and the oral glucose load, but thereafter concentrations following the oral glucose load fell while those after the meal continued to rise. Glucose 85-92 gastric inhibitory polypeptide Homo sapiens 12-15 6345991-4 1983 The rise in GIP levels during the first hour was similar after the meal and the oral glucose load, but thereafter concentrations following the oral glucose load fell while those after the meal continued to rise. Glucose 148-155 gastric inhibitory polypeptide Homo sapiens 12-15 6189515-1 1983 Calmodulin exhibits high-affinity, calcium-dependent binding of 1 mol/mol of the vasoactive intestinal peptide (VIP), secretin, and either the 42- or 43-residue gastric inhibitory peptide (GIP) with dissociation constants of 0.05-0.14 microM. Calcium 35-42 gastric inhibitory polypeptide Homo sapiens 189-192 6344327-0 1983 Gastric inhibitory polypeptide (GIP) response to an oral glucose load in the patients with diabetes mellitus. Glucose 57-64 gastric inhibitory polypeptide Homo sapiens 0-30 6344327-0 1983 Gastric inhibitory polypeptide (GIP) response to an oral glucose load in the patients with diabetes mellitus. Glucose 57-64 gastric inhibitory polypeptide Homo sapiens 32-35 6344327-2 1983 Plasma GIP concentrations increased significantly from the mean basal value following an oral glucose load in both groups. Glucose 94-101 gastric inhibitory polypeptide Homo sapiens 7-10 6344327-4 1983 When diabetics were divided into two groups according to their basal levels of blood glucose, moderate and severe diabetics exhibited more exaggerated increments of plasma GIP than mild diabetics. Blood Glucose 79-92 gastric inhibitory polypeptide Homo sapiens 172-175 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 gastric inhibitory polypeptide Homo sapiens 17-20 6687777-2 1983 Elderly females had higher gastric inhibitory polypeptide (GIP) responses to oral glucose than elderly males. Glucose 82-89 gastric inhibitory polypeptide Homo sapiens 59-62 6337173-13 1983 Thus, during glucose stimulation, the total IR-GIP released 1) is proportional to the absorbable luminal stimulus, 2) is independent of ambient plasma insulin and glucose levels, 3) is composed predominantly of the 5000 mol wt form, and 4) requires an elevation in plasma glucose of 17-20 mg/dl before it augments insulin release, but then stimulates insulin release in a fashion linearly dependent upon the increment in plasma glucose. Glucose 163-170 gastric inhibitory polypeptide Homo sapiens 47-50 6337173-13 1983 Thus, during glucose stimulation, the total IR-GIP released 1) is proportional to the absorbable luminal stimulus, 2) is independent of ambient plasma insulin and glucose levels, 3) is composed predominantly of the 5000 mol wt form, and 4) requires an elevation in plasma glucose of 17-20 mg/dl before it augments insulin release, but then stimulates insulin release in a fashion linearly dependent upon the increment in plasma glucose. Glucose 163-170 gastric inhibitory polypeptide Homo sapiens 47-50 6337173-13 1983 Thus, during glucose stimulation, the total IR-GIP released 1) is proportional to the absorbable luminal stimulus, 2) is independent of ambient plasma insulin and glucose levels, 3) is composed predominantly of the 5000 mol wt form, and 4) requires an elevation in plasma glucose of 17-20 mg/dl before it augments insulin release, but then stimulates insulin release in a fashion linearly dependent upon the increment in plasma glucose. Glucose 163-170 gastric inhibitory polypeptide Homo sapiens 47-50 6343163-4 1983 During the course the subjects with negative calorie balance showed augmented integrated glucose-induced gastric inhibitory polypeptide (GIP) response (p less than 0.05) and the plasma concentration of GIP after glucose stimulation was higher at 90 and 120 min during the course than in the control experiment. Glucose 89-96 gastric inhibitory polypeptide Homo sapiens 137-140 6343163-4 1983 During the course the subjects with negative calorie balance showed augmented integrated glucose-induced gastric inhibitory polypeptide (GIP) response (p less than 0.05) and the plasma concentration of GIP after glucose stimulation was higher at 90 and 120 min during the course than in the control experiment. Glucose 212-219 gastric inhibitory polypeptide Homo sapiens 202-205 6336815-5 1983 On the other hand, serum triglycerides tended to parallel GIP changes for most of the day, being significantly elevated starting from lunch consumption to late night. Triglycerides 25-38 gastric inhibitory polypeptide Homo sapiens 58-61 6337173-7 1983 At each dose of intraduodenally administered glucose, IR-GIP was elevated within 20-40 min (P less than 0.01), remaining at a steady level until the infusion was stopped. Glucose 45-52 gastric inhibitory polypeptide Homo sapiens 57-60 6337173-9 1983 The release of IR-GIP was proportional to the intestinal glucose load but was unchanged from the basal level during iv glucose studies. Glucose 57-64 gastric inhibitory polypeptide Homo sapiens 18-21 6337173-9 1983 The release of IR-GIP was proportional to the intestinal glucose load but was unchanged from the basal level during iv glucose studies. Glucose 119-126 gastric inhibitory polypeptide Homo sapiens 18-21 6337173-11 1983 During intestinal glucose infusion, 58.7 +/- 4.1% of IR-GIP was accounted for by the 5000 mol wt subspecies and 17.3 +/- 3.5% was accounted for by the 7500 mol wt subspecies, with the remaining immunoreactivity found in the void volume of a Sephadex G-50 column. Glucose 18-25 gastric inhibitory polypeptide Homo sapiens 56-59 6337173-13 1983 Thus, during glucose stimulation, the total IR-GIP released 1) is proportional to the absorbable luminal stimulus, 2) is independent of ambient plasma insulin and glucose levels, 3) is composed predominantly of the 5000 mol wt form, and 4) requires an elevation in plasma glucose of 17-20 mg/dl before it augments insulin release, but then stimulates insulin release in a fashion linearly dependent upon the increment in plasma glucose. Glucose 13-20 gastric inhibitory polypeptide Homo sapiens 47-50 6752641-0 1982 Gastric inhibitory polypeptide (GIP) and insulin release in response to oral and intravenous glucose in uremic patients. Glucose 93-100 gastric inhibitory polypeptide Homo sapiens 0-30 6752641-0 1982 Gastric inhibitory polypeptide (GIP) and insulin release in response to oral and intravenous glucose in uremic patients. Glucose 93-100 gastric inhibitory polypeptide Homo sapiens 32-35 6752641-5 1982 It is proposed that a factor of intestinal origin is released during intake of carbohydrates, which blocks the B-cell response to the combined glucose-GIP stimulus. Carbohydrates 79-92 gastric inhibitory polypeptide Homo sapiens 151-154 6752641-5 1982 It is proposed that a factor of intestinal origin is released during intake of carbohydrates, which blocks the B-cell response to the combined glucose-GIP stimulus. Glucose 143-150 gastric inhibitory polypeptide Homo sapiens 151-154 6757523-4 1982 It is suggested that GIP infusion to patients with myocardial infarction has a favourable effect on the metabolism of ischemized myocardium via a series of changes it produces in carbohydrate and lipid metabolism and blood electrolytic composition. Carbohydrates 179-191 gastric inhibitory polypeptide Homo sapiens 21-24 7049625-3 1982 Alpha-adrenergic stimulation (epinephrine + propranolol) significantly reduced the GIP response (P less than 0.02) and completely inhibited the insulin response (P less than 0.005) to oral glucose, compared with control experiments. Epinephrine 30-41 gastric inhibitory polypeptide Homo sapiens 83-86 7049625-3 1982 Alpha-adrenergic stimulation (epinephrine + propranolol) significantly reduced the GIP response (P less than 0.02) and completely inhibited the insulin response (P less than 0.005) to oral glucose, compared with control experiments. Propranolol 44-55 gastric inhibitory polypeptide Homo sapiens 83-86 6749583-8 1982 The abolished GIP response to oral triglycerides could play a causal role in the inactivity of the enteroinsular axis which is seen in both human and animal neonates. Triglycerides 35-48 gastric inhibitory polypeptide Homo sapiens 14-17 6759077-0 1982 The role of gastric inhibitory polypeptide in the augmented insulin response to sucrose. Sucrose 80-87 gastric inhibitory polypeptide Homo sapiens 12-42 6759077-1 1982 To evaluate the role of gastric inhibitory polypeptide (GIP) in the augmented insulin response to sucrose, seven normal volunteers ingested four separate meals of 100 g sucrose (S), 50 g glucose (G), 50 g fructose (F), and 50 g glucose + 50 g fructose (G + F). Sucrose 98-105 gastric inhibitory polypeptide Homo sapiens 24-54 6759077-1 1982 To evaluate the role of gastric inhibitory polypeptide (GIP) in the augmented insulin response to sucrose, seven normal volunteers ingested four separate meals of 100 g sucrose (S), 50 g glucose (G), 50 g fructose (F), and 50 g glucose + 50 g fructose (G + F). Sucrose 98-105 gastric inhibitory polypeptide Homo sapiens 56-59 6753108-0 1982 The correlation between gastric emptying time and the response of GIP and enteroglucagon to oral glucose in duodenal ulcer patients. Glucose 97-104 gastric inhibitory polypeptide Homo sapiens 66-69 6339782-3 1983 The administration of GIP mixture during the acute phase of myocardial infarction was conducive to lowering the levels of cyclic nucleotides and AMP, and raising blood ATP and ADP values. Nucleotides, Cyclic 122-140 gastric inhibitory polypeptide Homo sapiens 22-25 6339782-3 1983 The administration of GIP mixture during the acute phase of myocardial infarction was conducive to lowering the levels of cyclic nucleotides and AMP, and raising blood ATP and ADP values. Adenosine Monophosphate 145-148 gastric inhibitory polypeptide Homo sapiens 22-25 6339782-3 1983 The administration of GIP mixture during the acute phase of myocardial infarction was conducive to lowering the levels of cyclic nucleotides and AMP, and raising blood ATP and ADP values. Adenosine Triphosphate 168-171 gastric inhibitory polypeptide Homo sapiens 22-25 6339782-3 1983 The administration of GIP mixture during the acute phase of myocardial infarction was conducive to lowering the levels of cyclic nucleotides and AMP, and raising blood ATP and ADP values. Adenosine Diphosphate 176-179 gastric inhibitory polypeptide Homo sapiens 22-25 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 gastric inhibitory polypeptide Homo sapiens 35-38 7078422-0 1982 Betazole-induced GIP secretion is not mediated by gastric HCl. Betazole 0-8 gastric inhibitory polypeptide Homo sapiens 17-20 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 gastric inhibitory polypeptide Homo sapiens 129-132 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 gastric inhibitory polypeptide Homo sapiens 129-132 7078422-1 1982 Betazole, a pyrazole analogue of histamine, as well as pentagastrin and HCl stimulate GIP secretion. Betazole 0-8 gastric inhibitory polypeptide Homo sapiens 86-89 7078422-1 1982 Betazole, a pyrazole analogue of histamine, as well as pentagastrin and HCl stimulate GIP secretion. Histamine 33-42 gastric inhibitory polypeptide Homo sapiens 86-89 7078422-1 1982 Betazole, a pyrazole analogue of histamine, as well as pentagastrin and HCl stimulate GIP secretion. Pentagastrin 55-67 gastric inhibitory polypeptide Homo sapiens 86-89 7078422-1 1982 Betazole, a pyrazole analogue of histamine, as well as pentagastrin and HCl stimulate GIP secretion. Hydrochloric Acid 72-75 gastric inhibitory polypeptide Homo sapiens 86-89 7078422-7 1982 Our results have shown that the GIP response to betazole is maintained in achlorhydric subjects as well as during H2 blockade. Betazole 48-56 gastric inhibitory polypeptide Homo sapiens 32-35 7078422-7 1982 Our results have shown that the GIP response to betazole is maintained in achlorhydric subjects as well as during H2 blockade. Hydrogen 114-116 gastric inhibitory polypeptide Homo sapiens 32-35 7078422-8 1982 The results suggest that betazole and therefore histamine may stimulate GIP directly and not necessarily via the mediation of HCl. Betazole 25-33 gastric inhibitory polypeptide Homo sapiens 72-75 7078422-8 1982 The results suggest that betazole and therefore histamine may stimulate GIP directly and not necessarily via the mediation of HCl. Histamine 48-57 gastric inhibitory polypeptide Homo sapiens 72-75 6127792-1 1982 The effect of beta-adrenergic receptor stimulation with isoproterenol and blockade with propranolol on the release of gastric inhibitory polypeptide (GIP) and insulin was investigated in seven healthy volunteers. Propranolol 88-99 gastric inhibitory polypeptide Homo sapiens 118-148 6127792-1 1982 The effect of beta-adrenergic receptor stimulation with isoproterenol and blockade with propranolol on the release of gastric inhibitory polypeptide (GIP) and insulin was investigated in seven healthy volunteers. Propranolol 88-99 gastric inhibitory polypeptide Homo sapiens 150-153 6127792-2 1982 In the control experiment, the concentration of GIP in plasma increased from 30.1 (18.9-58.8) to 77.2 (44.2-121) pM after 30 g oral glucose. Glucose 132-139 gastric inhibitory polypeptide Homo sapiens 48-51 6127792-4 1982 During infusion with isoproterenol, plasma GIP increased from 29.9 (25.7-39.1) to 47.1 (37.2-83.8) pM and insulin from 9 (5-15) to 37 (16-72) mU/l before oral glucose. Isoproterenol 21-34 gastric inhibitory polypeptide Homo sapiens 43-46 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 gastric inhibitory polypeptide Homo sapiens 41-44 6127792-6 1982 When propranolol was given in addition during this beta-receptor stimulation, plasma GIP after glucose increased to 82.2 (49.7-145) pM and serum insulin to 61 (9-133) mU/l. Propranolol 5-16 gastric inhibitory polypeptide Homo sapiens 85-88 6127792-6 1982 When propranolol was given in addition during this beta-receptor stimulation, plasma GIP after glucose increased to 82.2 (49.7-145) pM and serum insulin to 61 (9-133) mU/l. Glucose 95-102 gastric inhibitory polypeptide Homo sapiens 85-88 6127792-7 1982 An isoproterenol-induced increase in the concentration of GIP and insulin was thus counteracted by propranolol. Isoproterenol 3-16 gastric inhibitory polypeptide Homo sapiens 58-61 6127792-7 1982 An isoproterenol-induced increase in the concentration of GIP and insulin was thus counteracted by propranolol. Propranolol 99-110 gastric inhibitory polypeptide Homo sapiens 58-61 7044844-0 1982 [The effect of calcium on the release of gastric inhibitory polypeptide (GIP) - with reference to the release of GIP in patients with hyperparathyroidism (author"s transl)]. Calcium 15-22 gastric inhibitory polypeptide Homo sapiens 41-71 6978077-3 1982 Duodenal HCO3- transport, which could be titrated directly, was stimulated by dibutyryl cAMP (DBcAMP, 10(-6) M), the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-6) M), noradrenaline (10(-6) M), pancreatic glucagon (10(-8) M), and gastric inhibitory peptide (GIP, 10(-10) M). Bicarbonates 9-13 gastric inhibitory polypeptide Homo sapiens 247-273 6978077-3 1982 Duodenal HCO3- transport, which could be titrated directly, was stimulated by dibutyryl cAMP (DBcAMP, 10(-6) M), the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-6) M), noradrenaline (10(-6) M), pancreatic glucagon (10(-8) M), and gastric inhibitory peptide (GIP, 10(-10) M). Bicarbonates 9-13 gastric inhibitory polypeptide Homo sapiens 275-278 6978077-3 1982 Duodenal HCO3- transport, which could be titrated directly, was stimulated by dibutyryl cAMP (DBcAMP, 10(-6) M), the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-6) M), noradrenaline (10(-6) M), pancreatic glucagon (10(-8) M), and gastric inhibitory peptide (GIP, 10(-10) M). dibutyryl 78-87 gastric inhibitory polypeptide Homo sapiens 247-273 6978077-3 1982 Duodenal HCO3- transport, which could be titrated directly, was stimulated by dibutyryl cAMP (DBcAMP, 10(-6) M), the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-6) M), noradrenaline (10(-6) M), pancreatic glucagon (10(-8) M), and gastric inhibitory peptide (GIP, 10(-10) M). dibutyryl 78-87 gastric inhibitory polypeptide Homo sapiens 275-278 6978077-3 1982 Duodenal HCO3- transport, which could be titrated directly, was stimulated by dibutyryl cAMP (DBcAMP, 10(-6) M), the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-6) M), noradrenaline (10(-6) M), pancreatic glucagon (10(-8) M), and gastric inhibitory peptide (GIP, 10(-10) M). Cyclic AMP 88-92 gastric inhibitory polypeptide Homo sapiens 247-273 6978077-3 1982 Duodenal HCO3- transport, which could be titrated directly, was stimulated by dibutyryl cAMP (DBcAMP, 10(-6) M), the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-6) M), noradrenaline (10(-6) M), pancreatic glucagon (10(-8) M), and gastric inhibitory peptide (GIP, 10(-10) M). Cyclic AMP 88-92 gastric inhibitory polypeptide Homo sapiens 275-278 6978077-3 1982 Duodenal HCO3- transport, which could be titrated directly, was stimulated by dibutyryl cAMP (DBcAMP, 10(-6) M), the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-6) M), noradrenaline (10(-6) M), pancreatic glucagon (10(-8) M), and gastric inhibitory peptide (GIP, 10(-10) M). Bucladesine 94-100 gastric inhibitory polypeptide Homo sapiens 247-273 6978077-3 1982 Duodenal HCO3- transport, which could be titrated directly, was stimulated by dibutyryl cAMP (DBcAMP, 10(-6) M), the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-6) M), noradrenaline (10(-6) M), pancreatic glucagon (10(-8) M), and gastric inhibitory peptide (GIP, 10(-10) M). Bucladesine 94-100 gastric inhibitory polypeptide Homo sapiens 275-278 6978077-3 1982 Duodenal HCO3- transport, which could be titrated directly, was stimulated by dibutyryl cAMP (DBcAMP, 10(-6) M), the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-6) M), noradrenaline (10(-6) M), pancreatic glucagon (10(-8) M), and gastric inhibitory peptide (GIP, 10(-10) M). 1-Methyl-3-isobutylxanthine 145-172 gastric inhibitory polypeptide Homo sapiens 247-273 6978077-3 1982 Duodenal HCO3- transport, which could be titrated directly, was stimulated by dibutyryl cAMP (DBcAMP, 10(-6) M), the phosphodiesterase inhibitor 3-isobutyl-1-methylxanthine (10(-6) M), noradrenaline (10(-6) M), pancreatic glucagon (10(-8) M), and gastric inhibitory peptide (GIP, 10(-10) M). 1-Methyl-3-isobutylxanthine 145-172 gastric inhibitory polypeptide Homo sapiens 275-278 6750703-0 1982 Release of gastric inhibitory polypeptide (GIP) during calcium infusion and in hyperparathyroidism. Calcium 55-62 gastric inhibitory polypeptide Homo sapiens 11-41 6750703-0 1982 Release of gastric inhibitory polypeptide (GIP) during calcium infusion and in hyperparathyroidism. Calcium 55-62 gastric inhibitory polypeptide Homo sapiens 43-46 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 gastric inhibitory polypeptide Homo sapiens 63-66 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 gastric inhibitory polypeptide Homo sapiens 63-66 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 gastric inhibitory polypeptide Homo sapiens 203-206 6750703-4 1982 This caused GIP to respond significantly more to glucose ingestion. Glucose 49-56 gastric inhibitory polypeptide Homo sapiens 12-15 6750703-6 1982 However, in the hypercalcaemic state in healthy subjects, glucose-induced GIP and insulin secretion is significantly greater than in the normocalcaemic state. Glucose 58-65 gastric inhibitory polypeptide Homo sapiens 74-77 6750703-7 1982 The potentiated response of insulin to glucose may be caused, in part, by GIP. Glucose 39-46 gastric inhibitory polypeptide Homo sapiens 74-77 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 gastric inhibitory polypeptide Homo sapiens 118-121 6293900-6 1982 Plasma GIP responses after the meal on the days with ranitidine alone or together with the gastrin infusion did not differ significantly from that found on the control day. Ranitidine 53-63 gastric inhibitory polypeptide Homo sapiens 7-10 7037506-3 1982 The peak GIP concentration after oral glucose was 22.3 +/- 1.9 pmol/l (mean +/- SEM), but was higher after GIP infusion at 36.3 +/- 4.6 pmol/l, (p less than 0.005). Glucose 38-45 gastric inhibitory polypeptide Homo sapiens 9-12 6173312-0 1982 Activation of the alternative complement pathway of guinea-gip by liposomes incorporated with trinitrophenylated phosphatidylethanolamine. trinitrophenylated phosphatidylethanolamine 94-137 gastric inhibitory polypeptide Homo sapiens 59-62 7044844-0 1982 [The effect of calcium on the release of gastric inhibitory polypeptide (GIP) - with reference to the release of GIP in patients with hyperparathyroidism (author"s transl)]. Calcium 15-22 gastric inhibitory polypeptide Homo sapiens 73-76 7044844-0 1982 [The effect of calcium on the release of gastric inhibitory polypeptide (GIP) - with reference to the release of GIP in patients with hyperparathyroidism (author"s transl)]. Calcium 15-22 gastric inhibitory polypeptide Homo sapiens 113-116 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 gastric inhibitory polypeptide Homo sapiens 41-44 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 gastric inhibitory polypeptide Homo sapiens 41-44 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 gastric inhibitory polypeptide Homo sapiens 207-210 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 gastric inhibitory polypeptide Homo sapiens 41-44 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. Calcium 103-110 gastric inhibitory polypeptide Homo sapiens 41-44 7044844-10 1982 Consequently, calcium was considered to play a major part in the release of GIP and insulin. Calcium 14-21 gastric inhibitory polypeptide Homo sapiens 76-79 7029674-0 1981 The response of plasma gastric-inhibitory polypeptide (GIP) to slow and fast glucose ingestion in Billroth II resected patients and normal controls. Glucose 77-84 gastric inhibitory polypeptide Homo sapiens 23-53 7029674-0 1981 The response of plasma gastric-inhibitory polypeptide (GIP) to slow and fast glucose ingestion in Billroth II resected patients and normal controls. Glucose 77-84 gastric inhibitory polypeptide Homo sapiens 55-58 7029674-2 1981 In the Billroth II resected group, the integrated plasma GIP release was significantly higher after the fast than after the slow glucose ingestion. Glucose 129-136 gastric inhibitory polypeptide Homo sapiens 57-60 7029674-3 1981 In this group the integrated plasma GIP release was also significantly higher than in the control group, but only after the fast glucose ingestion. Glucose 129-136 gastric inhibitory polypeptide Homo sapiens 36-39 7029674-4 1981 These findings indicate that the rate of glucose delivery into the intestine may be of importance in the plasma GIP response to oral glucose. Glucose 41-48 gastric inhibitory polypeptide Homo sapiens 112-115 7029674-4 1981 These findings indicate that the rate of glucose delivery into the intestine may be of importance in the plasma GIP response to oral glucose. Glucose 133-140 gastric inhibitory polypeptide Homo sapiens 112-115 16435484-0 1981 GIP and insulin responses to oral glucose in coeliac patients before and after treatment. Glucose 34-41 gastric inhibitory polypeptide Homo sapiens 0-3 7134635-3 1982 However, in contrast to previously published data with higher glucose loads the integrated GIP response was slightly decreased after BII resection and significantly decreased not only after jejunoileal bypass but also after PDP. Glucose 62-69 gastric inhibitory polypeptide Homo sapiens 91-94 7134635-5 1982 The results confirm a discrepant behavior of GIP release in dependence on the glucose content of the test meal after PDP compared to the controls. Glucose 78-85 gastric inhibitory polypeptide Homo sapiens 45-48 7134635-6 1982 The hypothesis is discussed that these results reflect a special dose-effect relationship between glucose and GIP release in man. Glucose 98-105 gastric inhibitory polypeptide Homo sapiens 110-113 7014585-5 1981 In contrast, after 1 month of treatment with tolazamide, IR-GIP concentrations were not significantly altered. Tolazamide 45-55 gastric inhibitory polypeptide Homo sapiens 60-63 7230782-0 1981 Parasympathetic neuroendocrine regulation of GIP response to glucose. Glucose 61-68 gastric inhibitory polypeptide Homo sapiens 45-48 16435472-3 1981 On the day without atropine, plasma GIP and serum insulin increased significantly. Atropine 19-27 gastric inhibitory polypeptide Homo sapiens 36-39 16435472-4 1981 The increases in plasma GIP and serum insulin were significantly attenuated by atropine. Atropine 79-87 gastric inhibitory polypeptide Homo sapiens 24-27 7014314-2 1981 The GIP response to glucose was impaired in pregnancy in all three groups. Glucose 20-27 gastric inhibitory polypeptide Homo sapiens 4-7 7014599-6 1981 These results may be interpreted as indicating a role for GIP in the improved tolerance for oral glucose, although other unknown gastrointestinal hormones could theoretically also be involved. Glucose 97-104 gastric inhibitory polypeptide Homo sapiens 58-61 7014599-7 1981 Enhanced release of GIP after oral glucose may compensate for the reduced IRI release in response to hyperglycemia. Glucose 35-42 gastric inhibitory polypeptide Homo sapiens 20-23 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 gastric inhibitory polypeptide Homo sapiens 90-93 7032210-3 1981 The sensitivity of the beta-cells to GIP was glucose independent. Glucose 45-52 gastric inhibitory polypeptide Homo sapiens 37-40 7032210-5 1981 We conclude that GIP is powerful insulin-stimulator even in low physiological concentrations in the presence of glucose concentrations comparable to those seen during an oral glucose load, which makes GIP to one of the strongest incretin candidates known, i.e. the factor(s) contributing to the augmented insulin response after ingestion of glucose. Glucose 112-119 gastric inhibitory polypeptide Homo sapiens 17-20 7250066-1 1981 The response to plasma immunoreactive gastric inhibitory polypeptide (GIP) to oral glucose loading was determined in 10 normal subjects, 10 patients with mild diabetes mellitus, and 10 patients with moderate to severe diabetes mellitus. Glucose 83-90 gastric inhibitory polypeptide Homo sapiens 38-68 7250066-1 1981 The response to plasma immunoreactive gastric inhibitory polypeptide (GIP) to oral glucose loading was determined in 10 normal subjects, 10 patients with mild diabetes mellitus, and 10 patients with moderate to severe diabetes mellitus. Glucose 83-90 gastric inhibitory polypeptide Homo sapiens 70-73 7250066-2 1981 In normal subjects the mean fasting GIP was 167 +/- 17 pg/ml which rose significantly after glucose loading, reaching the peak value of 513 +/- 44 pg/ml at 30 min. Glucose 92-99 gastric inhibitory polypeptide Homo sapiens 36-39 7250066-4 1981 However, the mean peak GIP level following glucose loading was 683 +/- 71 pg/ml, significantly higher than that in normal subjects (p less than 0.05). Glucose 43-50 gastric inhibitory polypeptide Homo sapiens 23-26 7250066-5 1981 In moderate and severe diabetics, oral glucose loading caused an abrupt rise in plasma GIP from the basal level of 304 +/- 31 pg/ml to the peak of 870 +/- 63 pg/ml occurring at 30 min, both of which were significantly higher than the corresponding values in normal subjects (p less than 0.01). Glucose 39-46 gastric inhibitory polypeptide Homo sapiens 87-90 7250066-6 1981 These results suggest that GIP response to oral glucose loading is enhanced in diabetic patients in proportion to the degree of their glucose intolerance. Glucose 48-55 gastric inhibitory polypeptide Homo sapiens 27-30 7250066-6 1981 These results suggest that GIP response to oral glucose loading is enhanced in diabetic patients in proportion to the degree of their glucose intolerance. Glucose 134-141 gastric inhibitory polypeptide Homo sapiens 27-30 7045829-4 1981 GIP was also shown to potentiate insulin release initiated by D-glyceraldehyde, L-leucine/L-glutamine and 2-keto-isocaproic acid. Glyceraldehyde 62-78 gastric inhibitory polypeptide Homo sapiens 0-3 7323697-2 1981 After intraduodenal infusion of glucose (82 ml 1.51 M, pH 6.5) the GIP concentration in plasma increased from 42.3 (23.1-62.2) to 225 (107-460) pM during intravenous NaCl, from 35.6 (17.3-38.9) to 251 (127-387) pM during phentolamine, and from 32.5 (5.5-63.4) to 172 (103-405) pM during propranolol administration. Glucose 32-39 gastric inhibitory polypeptide Homo sapiens 67-70 7323697-2 1981 After intraduodenal infusion of glucose (82 ml 1.51 M, pH 6.5) the GIP concentration in plasma increased from 42.3 (23.1-62.2) to 225 (107-460) pM during intravenous NaCl, from 35.6 (17.3-38.9) to 251 (127-387) pM during phentolamine, and from 32.5 (5.5-63.4) to 172 (103-405) pM during propranolol administration. Sodium Chloride 166-170 gastric inhibitory polypeptide Homo sapiens 67-70 7323697-2 1981 After intraduodenal infusion of glucose (82 ml 1.51 M, pH 6.5) the GIP concentration in plasma increased from 42.3 (23.1-62.2) to 225 (107-460) pM during intravenous NaCl, from 35.6 (17.3-38.9) to 251 (127-387) pM during phentolamine, and from 32.5 (5.5-63.4) to 172 (103-405) pM during propranolol administration. Phentolamine 221-233 gastric inhibitory polypeptide Homo sapiens 67-70 7323697-2 1981 After intraduodenal infusion of glucose (82 ml 1.51 M, pH 6.5) the GIP concentration in plasma increased from 42.3 (23.1-62.2) to 225 (107-460) pM during intravenous NaCl, from 35.6 (17.3-38.9) to 251 (127-387) pM during phentolamine, and from 32.5 (5.5-63.4) to 172 (103-405) pM during propranolol administration. Propranolol 287-298 gastric inhibitory polypeptide Homo sapiens 67-70 7323697-4 1981 It is concluded that the non-selective beta-adrenoceptor antagonist propranolol inhibits the release of GIP after intraduodenal administration of glucose. Propranolol 68-79 gastric inhibitory polypeptide Homo sapiens 104-107 7323697-4 1981 It is concluded that the non-selective beta-adrenoceptor antagonist propranolol inhibits the release of GIP after intraduodenal administration of glucose. Glucose 146-153 gastric inhibitory polypeptide Homo sapiens 104-107 7323698-0 1981 Glucose-induced release of immunoreactive gastric inhibitory polypeptide (IR-GIP) into the duodenal lumen in man. Glucose 0-7 gastric inhibitory polypeptide Homo sapiens 77-80 7323698-2 1981 After extraction with 95% ethanol, IR-GIP in duodenal juice was determined by radioimmunoassay and found to increase from mean basal level of 63 pmol/l to a mean peak of 354 pmol/l after the glucose infusion. Glucose 191-198 gastric inhibitory polypeptide Homo sapiens 38-41 7323698-3 1981 The elution diagrams of IR-GIP in glucose-stimulated duodenal juice and the corresponding plasma from a 16 X 400 mm Sephadex G-50 Fine column were similar, and the radioimmunoassay dilution curves of porcine GIP and duodenal juice IR-GIP were superimposable. juice 62-67 gastric inhibitory polypeptide Homo sapiens 27-30 7002949-1 1980 This study has assessed the effect of oral or intraduodenal HCl, administered alone or in combination with glucose, on gastric inhibitory polypeptide (GIP) and insulin secretion. Hydrochloric Acid 60-63 gastric inhibitory polypeptide Homo sapiens 119-149 7002949-1 1980 This study has assessed the effect of oral or intraduodenal HCl, administered alone or in combination with glucose, on gastric inhibitory polypeptide (GIP) and insulin secretion. Hydrochloric Acid 60-63 gastric inhibitory polypeptide Homo sapiens 151-154 7002949-6 1980 However, HCl did produce an increase in GIP. Hydrochloric Acid 9-12 gastric inhibitory polypeptide Homo sapiens 40-43 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 gastric inhibitory polypeptide Homo sapiens 21-24 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 gastric inhibitory polypeptide Homo sapiens 21-24 7002949-9 1980 There was, however, a potentiation of both the GIP and insulin responses when intraduodenal acid was given with glucose. intraduodenal acid 78-96 gastric inhibitory polypeptide Homo sapiens 47-50 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 gastric inhibitory polypeptide Homo sapiens 47-50 7002949-11 1980 It is concluded that HCl by itself is capable of stimulating GIP secretion. Hydrochloric Acid 21-24 gastric inhibitory polypeptide Homo sapiens 61-64 7002949-12 1980 Since there was only a potentiation of insulin and GIP secretion when large doses of HCl were given together with glucose via the intraduodenal route, the physiological relevance of acid-induced GIP secretion remains to be resolved. Hydrochloric Acid 85-88 gastric inhibitory polypeptide Homo sapiens 51-54 6990366-11 1980 The small GIP rise might be due to a limited secretory capacity of the GIP cells or to a diminished stimulatory capacity of glucose. Glucose 124-131 gastric inhibitory polypeptide Homo sapiens 10-13 6986299-1 1980 The effect of glucose and insulin on fat- and glucose-induced gastric inhibitory polypeptide (GIP) release has been studied in insulin-dependent juvenile-type diabetics. Glucose 14-21 gastric inhibitory polypeptide Homo sapiens 62-92 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 92-99 gastric inhibitory polypeptide Homo sapiens 132-135 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 92-99 gastric inhibitory polypeptide Homo sapiens 132-135 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 gastric inhibitory polypeptide Homo sapiens 112-115 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 gastric inhibitory polypeptide Homo sapiens 80-83 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 gastric inhibitory polypeptide Homo sapiens 120-123 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. Fatty Acids 167-178 gastric inhibitory polypeptide Homo sapiens 80-83 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. Fatty Acids 167-178 gastric inhibitory polypeptide Homo sapiens 120-123 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 gastric inhibitory polypeptide Homo sapiens 80-83 7353457-0 1980 Effect of gastric inhibitory polypeptide on pentagastrin-stimulated acid secretion in man. Pentagastrin 44-56 gastric inhibitory polypeptide Homo sapiens 10-40 7353457-3 1980 At the 222 ng/kg/hr dose of pentagastrin, acid output was significantly lower with GIP; at all other doses of pentagastrin, acid output did not differ significantly in tests with and without GIP. Pentagastrin 28-40 gastric inhibitory polypeptide Homo sapiens 83-86 7390059-3 1980 Apparent immunoreactive fasting plasma GIP was eluted from a Sephadex G-150 Fine column in one peak probably representing plasma GIP bound to plasma proteins and nonspecific plasma effects. sephadex 61-75 gastric inhibitory polypeptide Homo sapiens 39-42 7390059-4 1980 Apparent immunoreactive meal-stimulated plasma GIP was eluted from a Sephadex G-50 Fine column in two large and one diminutive peak. sephadex 69-82 gastric inhibitory polypeptide Homo sapiens 47-50 7010526-3 1980 The magnitude of the increase in plasma GIP after oral glucose load was positively correlated to the length of residual jejunum. Glucose 55-62 gastric inhibitory polypeptide Homo sapiens 40-43 7015475-0 1980 The association between plasma GIP and insulin after oral glucose. Glucose 58-65 gastric inhibitory polypeptide Homo sapiens 31-34 7015475-1 1980 The correlation between the peripheral concentrations of gastric inhibitory polypeptide (GIP), insulin, and glucose has not previously been quantified. Glucose 108-115 gastric inhibitory polypeptide Homo sapiens 89-92 7015475-2 1980 This paper describes the association among the peripheral concentrations of GIP, insulin and glucose during 50-g oral glucose tolerance tests (OGTT) in healthy volunteers and in patients with gastrointestinal disorders, obesity, and uremia. Glucose 93-100 gastric inhibitory polypeptide Homo sapiens 76-79 7015475-2 1980 This paper describes the association among the peripheral concentrations of GIP, insulin and glucose during 50-g oral glucose tolerance tests (OGTT) in healthy volunteers and in patients with gastrointestinal disorders, obesity, and uremia. Glucose 118-125 gastric inhibitory polypeptide Homo sapiens 76-79 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 gastric inhibitory polypeptide Homo sapiens 69-72 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 gastric inhibitory polypeptide Homo sapiens 208-211 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 gastric inhibitory polypeptide Homo sapiens 69-72 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 gastric inhibitory polypeptide Homo sapiens 60-63 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 gastric inhibitory polypeptide Homo sapiens 89-92 510813-2 1979 Since antilipolytic effects of GIP have been demonstrated and the uptake of triglyceride fatty acid by adipose tissue postprandially is a process reciprocally regulated with lipolysis, a stimulatory role of GIP on adipose tissue lipoprotein lipase activity may be present. triglyceride fatty acid 76-99 gastric inhibitory polypeptide Homo sapiens 207-210 510813-5 1979 A dose response relationship was strongest for the effect of GIP on the enzyme activity in extracts of acetone-ether powders of the cells. Acetone 103-110 gastric inhibitory polypeptide Homo sapiens 61-64 510813-5 1979 A dose response relationship was strongest for the effect of GIP on the enzyme activity in extracts of acetone-ether powders of the cells. Ether 111-116 gastric inhibitory polypeptide Homo sapiens 61-64 510813-6 1979 The increased lipoprotein lipase activity produced by GIP could provide a mechanisms for clearance of chylomicron triglyceride after feeding in man. chylomicron triglyceride 102-126 gastric inhibitory polypeptide Homo sapiens 54-57 479351-6 1979 The ingestion of glucose or galactose resulted in a similar increment of GIP (P less than 0.01), followed by a similar increment in the IRI response to iv glucose. Glucose 17-24 gastric inhibitory polypeptide Homo sapiens 73-76 479351-6 1979 The ingestion of glucose or galactose resulted in a similar increment of GIP (P less than 0.01), followed by a similar increment in the IRI response to iv glucose. Galactose 28-37 gastric inhibitory polypeptide Homo sapiens 73-76 479351-10 1979 From these studies we conclude that 1) galactose does not elicit IRI secretion per se, yet, like glucose, potentiates GIP and IRI secretion; 2) mannose, despite weak transport across gut or kidney, evokes significant betacytotropic effects; and 3) mannose- and fructose-induced enhancement of glucose disposal might be mediated by a factor(s) other than GIP. Galactose 39-48 gastric inhibitory polypeptide Homo sapiens 118-121 479351-10 1979 From these studies we conclude that 1) galactose does not elicit IRI secretion per se, yet, like glucose, potentiates GIP and IRI secretion; 2) mannose, despite weak transport across gut or kidney, evokes significant betacytotropic effects; and 3) mannose- and fructose-induced enhancement of glucose disposal might be mediated by a factor(s) other than GIP. Glucose 97-104 gastric inhibitory polypeptide Homo sapiens 118-121 479351-10 1979 From these studies we conclude that 1) galactose does not elicit IRI secretion per se, yet, like glucose, potentiates GIP and IRI secretion; 2) mannose, despite weak transport across gut or kidney, evokes significant betacytotropic effects; and 3) mannose- and fructose-induced enhancement of glucose disposal might be mediated by a factor(s) other than GIP. Mannose 144-151 gastric inhibitory polypeptide Homo sapiens 354-357 516774-2 1979 This glucose-dependent insulinotropic response occurs when a dose of GIP is administered to obtain circulating levels of approximately 1 ng/ml, a physiologic level that can be achieved by the ingestion of glucose or corn oil or a mixed meal. Glucose 5-12 gastric inhibitory polypeptide Homo sapiens 69-72 516774-2 1979 This glucose-dependent insulinotropic response occurs when a dose of GIP is administered to obtain circulating levels of approximately 1 ng/ml, a physiologic level that can be achieved by the ingestion of glucose or corn oil or a mixed meal. Glucose 205-212 gastric inhibitory polypeptide Homo sapiens 69-72 516774-4 1979 In patients with chronic pancreatitis receiving an oral glucose load or mixed liquid test meal, GIP levels have been shown to be exaggerated. Glucose 56-63 gastric inhibitory polypeptide Homo sapiens 96-99 457845-1 1979 The response of gastric inhibitory polypeptide (GIP) levels to oral glucose in 11 insulin-dependent diabetics was compared to that in 8 age- and sex-matched healthy controls to determine whether they would show the pattern of GIP hypersecretion reported by other workers in maturity-onset, insulin-independent diabetes. Glucose 68-75 gastric inhibitory polypeptide Homo sapiens 48-51 457845-2 1979 One gram of glucose per kg bw resulted in a higher level of glycemia and a significantly diminished GIP response in diabetics when compared to controls (6,018 +/- 1,337 vs. 11,343 +/- 2,353 pg/ml.180 min min, respectively). Glucose 12-19 gastric inhibitory polypeptide Homo sapiens 100-103 428694-0 1979 The effect of oral galactose on GIP and insulin secretion in man. Galactose 19-28 gastric inhibitory polypeptide Homo sapiens 32-35 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. Galactose 66-75 gastric inhibitory polypeptide Homo sapiens 17-20 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. Galactose 66-75 gastric inhibitory polypeptide Homo sapiens 260-263 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 gastric inhibitory polypeptide Homo sapiens 17-20 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 gastric inhibitory polypeptide Homo sapiens 260-263 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. Galactose 66-75 gastric inhibitory polypeptide Homo sapiens 17-20 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. Galactose 66-75 gastric inhibitory polypeptide Homo sapiens 260-263 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. Galactose 66-75 gastric inhibitory polypeptide Homo sapiens 17-20 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. Galactose 66-75 gastric inhibitory polypeptide Homo sapiens 260-263 111943-0 1979 Impaired feedback control of fat induced gastric inhibitory polypeptide (GIP) secretion by insulin in obesity and glucose intolerance. Glucose 114-121 gastric inhibitory polypeptide Homo sapiens 73-76 111943-3 1979 When glucose and fat were given together this IR-GIP response was lowered to 46.2 +/- 2.9 ng/ml/120 min while the serum IRI response to i.v. Glucose 5-12 gastric inhibitory polypeptide Homo sapiens 49-52 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 gastric inhibitory polypeptide Homo sapiens 34-37 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 gastric inhibitory polypeptide Homo sapiens 34-37 111943-12 1979 glucose on the IR-GIP response re-established. Glucose 0-7 gastric inhibitory polypeptide Homo sapiens 18-21 34554-6 1979 Also, in humans, intraduodenal infusion of 0.1 N hydrochloric acid releases GIP without changing serum levels of glucose or insulin. Hydrochloric Acid 49-66 gastric inhibitory polypeptide Homo sapiens 76-79 429501-3 1979 Compared to post partum the GIP response to oral glucose was significantly impaired in late pregnancy. Glucose 49-56 gastric inhibitory polypeptide Homo sapiens 28-31 429501-4 1979 It is concluded that the diminished GIP response to oral glucose in late pregnancy might at least partly explain the impaired incretin effect found in this condition. Glucose 57-64 gastric inhibitory polypeptide Homo sapiens 36-39 6112787-5 1981 Mean plasma GIP tended to fall during the initial 1-h saline infusion, fell further during the first part of the 2-h 100 micrograms/h somatostatin infusion, and started to rise first 85 min after termination of the somatostatin infusion. Sodium Chloride 54-60 gastric inhibitory polypeptide Homo sapiens 12-15 7031846-2 1981 This increase was significantly (p = 0.031) attenuated when atropine was given together with insulin, indicating that the vagal nerves play a major role in the release of plasma GIP during hypoglycemia. Atropine 60-68 gastric inhibitory polypeptide Homo sapiens 178-181 7034154-0 1981 Radioimmunoassay of gastric inhibitory polypeptide (GIP) and the effect of intraduodenal acidification on glucose-stimulated and unstimulated GIP release in humans. Glucose 106-113 gastric inhibitory polypeptide Homo sapiens 142-145 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 gastric inhibitory polypeptide Homo sapiens 63-66 7034154-7 1981 The GIP concentration in plasma increased from 36.7 (27.5-62.2) to 134 (78.9-215) pM after infusion of glucose with a pH of 6.5 and from 44.6 (23.4-60.5) to 141 (74.0-246) pM after pH 1.5 glucose. Glucose 103-110 gastric inhibitory polypeptide Homo sapiens 4-7 7034154-7 1981 The GIP concentration in plasma increased from 36.7 (27.5-62.2) to 134 (78.9-215) pM after infusion of glucose with a pH of 6.5 and from 44.6 (23.4-60.5) to 141 (74.0-246) pM after pH 1.5 glucose. Glucose 188-195 gastric inhibitory polypeptide Homo sapiens 4-7 7034154-11 1981 It is concluded that an acid environment in the duodenum neither potentiates the glucose-induced GIP and insulin release nor influences the unstimulated GIP concentration. Glucose 81-88 gastric inhibitory polypeptide Homo sapiens 97-100 7014042-0 1980 The effect of increasing doses of ingested glucose on insulin and gastric inhibitory polypeptide (GIP) concentrations in man. Glucose 43-50 gastric inhibitory polypeptide Homo sapiens 54-96 7014042-0 1980 The effect of increasing doses of ingested glucose on insulin and gastric inhibitory polypeptide (GIP) concentrations in man. Glucose 43-50 gastric inhibitory polypeptide Homo sapiens 98-101 7014042-3 1980 To investigate the GIP response to increasing amounts of oral glucose, and its relationship to glucose levels and insulin secretion, fourteen normal volunteers ingested 25, 50 and 75 g of glucose at random with 5-7 days between each test. Glucose 62-69 gastric inhibitory polypeptide Homo sapiens 19-22 7014042-5 1980 Peak mean responses to glucose, insulin and GIP occurred at 30 min following each glucose ingestion. Glucose 82-89 gastric inhibitory polypeptide Homo sapiens 44-47 7014042-8 1980 Mean GIP concentrations were significantly greater (P less than 0.03) between 15 and 180 min with both the 50 and 75 g glucose stimulus. Glucose 119-126 gastric inhibitory polypeptide Homo sapiens 5-8 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 gastric inhibitory polypeptide Homo sapiens 106-133 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 gastric inhibitory polypeptide Homo sapiens 130-133 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 gastric inhibitory polypeptide Homo sapiens 130-133 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 gastric inhibitory polypeptide Homo sapiens 74-77 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 gastric inhibitory polypeptide Homo sapiens 106-133 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 gastric inhibitory polypeptide Homo sapiens 130-133 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 gastric inhibitory polypeptide Homo sapiens 130-133 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 gastric inhibitory polypeptide Homo sapiens 74-77 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 gastric inhibitory polypeptide Homo sapiens 106-133 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 gastric inhibitory polypeptide Homo sapiens 130-133 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 gastric inhibitory polypeptide Homo sapiens 130-133 6109240-2 1980 The diet protein, fats and carbohydrates stimulate secretion, CCK-P, GIP, and gastrin release and effect insulin and HGH release. Fats 18-22 gastric inhibitory polypeptide Homo sapiens 69-72 6109240-2 1980 The diet protein, fats and carbohydrates stimulate secretion, CCK-P, GIP, and gastrin release and effect insulin and HGH release. Carbohydrates 27-40 gastric inhibitory polypeptide Homo sapiens 69-72 6107191-3 1980 GIP acts on the B-cells of the pancreas by potentiating glucose-induced insulin secretion. Glucose 56-63 gastric inhibitory polypeptide Homo sapiens 0-3 6997121-8 1980 After restoration of the GIP response to fat by pancreatin, the inhibitory effect of IV glucose on fat-induced GIP increase was restored. Glucose 88-95 gastric inhibitory polypeptide Homo sapiens 25-28 6997121-8 1980 After restoration of the GIP response to fat by pancreatin, the inhibitory effect of IV glucose on fat-induced GIP increase was restored. Glucose 88-95 gastric inhibitory polypeptide Homo sapiens 111-114 6997121-9 1980 These data indicate that the GIP response to a mixed meal or triglycerides is dependent on the absorption of nutrients. Triglycerides 61-74 gastric inhibitory polypeptide Homo sapiens 29-32 6995476-1 1980 Glucose-dependent insulin-releasing peptide or gastric inhibitory polypeptide (GIP) is released into the circulation after ingestion of a mixed meal and is thought to enhance glucose-induced insulin release. Glucose 0-7 gastric inhibitory polypeptide Homo sapiens 79-82 6995476-1 1980 Glucose-dependent insulin-releasing peptide or gastric inhibitory polypeptide (GIP) is released into the circulation after ingestion of a mixed meal and is thought to enhance glucose-induced insulin release. Glucose 175-182 gastric inhibitory polypeptide Homo sapiens 79-82 7411011-6 1980 Ingestion of glucose or fat resulted in a similar rise of plasma GIP, whereas no change was observed after the ingestion of protein. Glucose 13-20 gastric inhibitory polypeptide Homo sapiens 65-68 7045829-4 1981 GIP was also shown to potentiate insulin release initiated by D-glyceraldehyde, L-leucine/L-glutamine and 2-keto-isocaproic acid. Leucine 80-89 gastric inhibitory polypeptide Homo sapiens 0-3 7045829-4 1981 GIP was also shown to potentiate insulin release initiated by D-glyceraldehyde, L-leucine/L-glutamine and 2-keto-isocaproic acid. Glutamine 90-101 gastric inhibitory polypeptide Homo sapiens 0-3 7045829-4 1981 GIP was also shown to potentiate insulin release initiated by D-glyceraldehyde, L-leucine/L-glutamine and 2-keto-isocaproic acid. alpha-ketoisocaproic acid 106-128 gastric inhibitory polypeptide Homo sapiens 0-3 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 gastric inhibitory polypeptide Homo sapiens 193-196 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 207-214 gastric inhibitory polypeptide Homo sapiens 193-196 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 gastric inhibitory polypeptide Homo sapiens 27-57 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 gastric inhibitory polypeptide Homo sapiens 59-62 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 gastric inhibitory polypeptide Homo sapiens 124-127 654387-1 1978 Gastric inhibitory polypeptide (GIP) is released from the duodenum and jejunum following the ingestion of glucose, fat and amino acids. Glucose 106-113 gastric inhibitory polypeptide Homo sapiens 0-30 654387-1 1978 Gastric inhibitory polypeptide (GIP) is released from the duodenum and jejunum following the ingestion of glucose, fat and amino acids. Glucose 106-113 gastric inhibitory polypeptide Homo sapiens 32-35 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 gastric inhibitory polypeptide Homo sapiens 16-46 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 gastric inhibitory polypeptide Homo sapiens 48-51 658630-4 1978 The degree of increased GIP response in the patients was positively correlated with the plasma glucose increase during the OGTT. Glucose 95-102 gastric inhibitory polypeptide Homo sapiens 24-27 752033-4 1978 The normal meal-stimulated rise in serum GIP was almost completely inhibited by atropine. Atropine 80-88 gastric inhibitory polypeptide Homo sapiens 41-44 752033-5 1978 We conclude that: 1) the rise in serum gastrin adter a meal preceeds the rise in serum GIP; 2) atropine potentiates the late gastrin response while suppressing the increase in serum GIP after a meal; and 3) the mechanism by which atropine potentiates gastrin release may be related to its suppressive effects on intestinal inhibitors of gastrin secretion, such as GIP. Atropine 95-103 gastric inhibitory polypeptide Homo sapiens 87-90 752033-5 1978 We conclude that: 1) the rise in serum gastrin adter a meal preceeds the rise in serum GIP; 2) atropine potentiates the late gastrin response while suppressing the increase in serum GIP after a meal; and 3) the mechanism by which atropine potentiates gastrin release may be related to its suppressive effects on intestinal inhibitors of gastrin secretion, such as GIP. Atropine 95-103 gastric inhibitory polypeptide Homo sapiens 182-185 752033-5 1978 We conclude that: 1) the rise in serum gastrin adter a meal preceeds the rise in serum GIP; 2) atropine potentiates the late gastrin response while suppressing the increase in serum GIP after a meal; and 3) the mechanism by which atropine potentiates gastrin release may be related to its suppressive effects on intestinal inhibitors of gastrin secretion, such as GIP. Atropine 95-103 gastric inhibitory polypeptide Homo sapiens 182-185 626287-1 1978 Administration of exogenous insulin before and after intraduodenal glucose results in blunting of the GIP response to glucose. Glucose 67-74 gastric inhibitory polypeptide Homo sapiens 102-105 626287-1 1978 Administration of exogenous insulin before and after intraduodenal glucose results in blunting of the GIP response to glucose. Glucose 118-125 gastric inhibitory polypeptide Homo sapiens 102-105 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 gastric inhibitory polypeptide Homo sapiens 128-131 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 gastric inhibitory polypeptide Homo sapiens 218-221 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 gastric inhibitory polypeptide Homo sapiens 264-267 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 gastric inhibitory polypeptide Homo sapiens 264-267 932174-2 1976 This study was designed to investigate the effects of simultaneous fat ingestion, a potent stimulus for GIP release, and intravenous glucose infusion upon endogenous serum GIP and insulin concentrations in normal subjects. Glucose 133-140 gastric inhibitory polypeptide Homo sapiens 172-175 324834-1 1977 Gastric inhibitory polypeptide (GIP) is insulinotropic and is released after ingestion of glucose in normal man. Glucose 90-97 gastric inhibitory polypeptide Homo sapiens 0-30 324834-1 1977 Gastric inhibitory polypeptide (GIP) is insulinotropic and is released after ingestion of glucose in normal man. Glucose 90-97 gastric inhibitory polypeptide Homo sapiens 32-35 830596-0 1977 The effect of gastric inhibitory polypeptide on human jejunal water and electrolyte transport. Water 62-67 gastric inhibitory polypeptide Homo sapiens 14-44 830596-3 1977 During GIP infusion, net water Na, K, and HCO3 absorption was significantly reduced and chloride flux was switched from absorption to secretion when compared to pre- and post-GIP control periods (p less than 0.001). Water 25-30 gastric inhibitory polypeptide Homo sapiens 7-10 830596-3 1977 During GIP infusion, net water Na, K, and HCO3 absorption was significantly reduced and chloride flux was switched from absorption to secretion when compared to pre- and post-GIP control periods (p less than 0.001). Bicarbonates 42-46 gastric inhibitory polypeptide Homo sapiens 7-10 830596-3 1977 During GIP infusion, net water Na, K, and HCO3 absorption was significantly reduced and chloride flux was switched from absorption to secretion when compared to pre- and post-GIP control periods (p less than 0.001). Chlorides 88-96 gastric inhibitory polypeptide Homo sapiens 7-10 856672-0 1977 Lowering of fasting and food stimulated serum immunoreactive gastric inhibitory polypeptide (GIP) by glucagon. Glucagon 101-109 gastric inhibitory polypeptide Homo sapiens 93-96 856672-1 1977 The effect of intravenous glucagon infusion on serum levels of immunoreactive GIP (IR-GIP), insulin (IRI), gastrin (IRG), and on blood glucose has been investigated in six healthy volunteers in the fasting state and during ingestion of a mixed standard meal. Glucagon 26-34 gastric inhibitory polypeptide Homo sapiens 78-81 856672-2 1977 Glucagon (500 ng/kg/min) lowered significantly serum levels of IR-GIP and IRG below the fasting values and increased the levels of IRI and blood glucose. Glucagon 0-8 gastric inhibitory polypeptide Homo sapiens 66-69 856672-3 1977 Glucagon (50 ng/kg/min) infused 30 minutes before and continued 90 minutes after ingestion of a test meal abolished the IR-GIP response, suppressed significantly the IRG response, and left the IRI response unchanged. Glucagon 0-8 gastric inhibitory polypeptide Homo sapiens 123-126 856672-4 1977 The same glucagon dose infused 60 minutes after ingestion of the test meal decreased significantly the raised levels of IR-GIP and IRG to fasting levels without changing IRI values. Glucagon 9-17 gastric inhibitory polypeptide Homo sapiens 123-126 856672-5 1977 It is concluded that exogenous glucagon inhibits Gip release at the level of the GIP-producing cells. Glucagon 31-39 gastric inhibitory polypeptide Homo sapiens 49-52 856672-5 1977 It is concluded that exogenous glucagon inhibits Gip release at the level of the GIP-producing cells. Glucagon 31-39 gastric inhibitory polypeptide Homo sapiens 81-84 830237-0 1977 Localization of gastric inhibitory polypeptide release by intestinal glucose perfusion in man. Glucose 69-76 gastric inhibitory polypeptide Homo sapiens 16-46 976601-11 1976 After the ingestion of glucose, diabetics had significantly higher (p less than 0.001) mean serum GIP levels between five and 120 minutes. Glucose 23-30 gastric inhibitory polypeptide Homo sapiens 98-101 976601-16 1976 The higher serum GIP concentrations observed following glucose ingestion in diabetics could not be attributed to obesity or age. Glucose 55-62 gastric inhibitory polypeptide Homo sapiens 17-20 976601-17 1976 We conclude that both fasting and glucose-stimulated GIP concentrations are higher than normal in obese adult-onset diabetics. Glucose 34-41 gastric inhibitory polypeptide Homo sapiens 53-56 1035142-2 1976 Synthesis of the tritetracontapeptide corresponding to the entire amino acid sequence of porcine gastric inhibitory polypeptide (GIP). tritetracontapeptide 17-37 gastric inhibitory polypeptide Homo sapiens 97-127 1035142-2 1976 Synthesis of the tritetracontapeptide corresponding to the entire amino acid sequence of porcine gastric inhibitory polypeptide (GIP). tritetracontapeptide 17-37 gastric inhibitory polypeptide Homo sapiens 129-132 932174-9 1976 We conclude that the potentiation of glucose-stimulated insulin secretion induced by the ingestion of fat is associated with serum GIP levels that are within the insulinotropic range. Glucose 37-44 gastric inhibitory polypeptide Homo sapiens 131-134 1270574-2 1976 Plasma GIP levels rise rapidly after glucose ingestion before changes in circulating glucose and insulin concentration. Glucose 37-44 gastric inhibitory polypeptide Homo sapiens 7-10 1270574-3 1976 Patients with pancreatitis have a greater than normal GIP response to oral glucose, which may account for the relatively unimparied insulin response to oral glucose in these patients compared with that to iv glucose, as has been previously found. Glucose 75-82 gastric inhibitory polypeptide Homo sapiens 54-57 8883-4 1976 GIP ("gastric inhibitory peptide"), apart form acting upon the intestinal tract, also causes a marked rise in insulin production; this GIP possibly is the factor responsible for the difference in glucose tolerance following i. v. or oral administration of glucose, something that scientists have been trying to discover for a long time. Glucose 196-203 gastric inhibitory polypeptide Homo sapiens 0-3 8883-4 1976 GIP ("gastric inhibitory peptide"), apart form acting upon the intestinal tract, also causes a marked rise in insulin production; this GIP possibly is the factor responsible for the difference in glucose tolerance following i. v. or oral administration of glucose, something that scientists have been trying to discover for a long time. Glucose 196-203 gastric inhibitory polypeptide Homo sapiens 5-33 8883-4 1976 GIP ("gastric inhibitory peptide"), apart form acting upon the intestinal tract, also causes a marked rise in insulin production; this GIP possibly is the factor responsible for the difference in glucose tolerance following i. v. or oral administration of glucose, something that scientists have been trying to discover for a long time. Glucose 196-203 gastric inhibitory polypeptide Homo sapiens 135-138 951347-3 1976 The association of DIP to 4 other fundamental histological varieties of diseases of the pulmonary interstitium (UIP, BIP, LIP, GIP) is at the origin of Liebow"s classification. Creatinine 19-22 gastric inhibitory polypeptide Homo sapiens 127-130 33955602-1 2021 The insulinotropic gut hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are key factors in the regulation of normal postprandial glucose homeostasis, but in most reports, the glucose-lowering effect of GIP has been shown to be blunted or even absent in people with type 2 diabetes (T2D) (1). Glucose 32-39 gastric inhibitory polypeptide Homo sapiens 78-81 4423791-0 1974 Gastric inhibitory polypeptide (GIP) stimulation by oral glucose in man. Glucose 57-64 gastric inhibitory polypeptide Homo sapiens 0-30 4423791-0 1974 Gastric inhibitory polypeptide (GIP) stimulation by oral glucose in man. Glucose 57-64 gastric inhibitory polypeptide Homo sapiens 32-35 33247879-7 2021 Post-glucose GIP (pmol/l) increased in all e.g. FCPD (15.83 to 94.14), T2DM (21.85 to 88.29), control (13.00 to 74.65) (p <0.001 for all). Glucose 5-12 gastric inhibitory polypeptide Homo sapiens 13-16 34022121-12 2021 GIP secretion was suppressed by lixisenatide and liraglutide. lixisenatide 32-44 gastric inhibitory polypeptide Homo sapiens 0-3 33886495-5 2021 We infused a selective GIP receptor antagonist, GIP(3-30)NH2 (1,200 pmol x kg-1 x min-1), or placebo (saline) during two separate, 230-minute, standardized, liquid mixed meal tests followed by an ad libitum meal. Amido radical 57-60 gastric inhibitory polypeptide Homo sapiens 48-51 33886495-7 2021 RESULTS: Compared with placebo, GIP(3-30)NH2 reduced postprandial insulin secretion (Deltabaseline-subtracted area under the curve (bsAUC)C-peptide%+-SEM; -14+-6%, p=0.021) and peak glucagon (Delta%+-SEM; -11+-6%, p=0.046), but had no effect on plasma glucose (p=0.692). Glucose 252-259 gastric inhibitory polypeptide Homo sapiens 32-35 34001166-14 2021 CONCLUSION: Isomaltulose ingestion led to lower baseline postprandial concentrations of glucose, insulin and GIP compared to maltodextrin and glucose. isomaltulose 12-24 gastric inhibitory polypeptide Homo sapiens 109-112 33955602-1 2021 The insulinotropic gut hormones glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide 1 (GLP-1) are key factors in the regulation of normal postprandial glucose homeostasis, but in most reports, the glucose-lowering effect of GIP has been shown to be blunted or even absent in people with type 2 diabetes (T2D) (1). Glucose 32-39 gastric inhibitory polypeptide Homo sapiens 249-252 33712466-0 2021 GIP mediates the incretin effect and glucose tolerance by dual actions on alpha cells and beta cells. Glucose 37-44 gastric inhibitory polypeptide Homo sapiens 0-3 33946158-3 2021 The results showed that the average daily gain (ADG), average daily feed intake (ADFI), and gastric inhibitory polypeptide (GIP) concentration in the jejunum significantly decreased the core temperature, feed conversion ratio (FCR), and ghrelin of the hypothalamus, and cholecystokinin (CCK) in jejunum, and serum significantly increased in the HT group (p < 0.05). Ghrelin 237-244 gastric inhibitory polypeptide Homo sapiens 92-122 33946158-3 2021 The results showed that the average daily gain (ADG), average daily feed intake (ADFI), and gastric inhibitory polypeptide (GIP) concentration in the jejunum significantly decreased the core temperature, feed conversion ratio (FCR), and ghrelin of the hypothalamus, and cholecystokinin (CCK) in jejunum, and serum significantly increased in the HT group (p < 0.05). Ghrelin 237-244 gastric inhibitory polypeptide Homo sapiens 124-127 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 gastric inhibitory polypeptide Homo sapiens 71-87 33459181-3 2021 The objective of this study was to investigate the effect of oral ursodeoxycholic acid (UDCA) and chenodeoxycholic acid (CDCA) on post-prandial secretion of GLP-1, oxyntomodulin (OXM), peptide YY (PYY), glucose-dependent insulinotropic peptide (GIP), glucagon and ghrelin. Ursodeoxycholic Acid 66-86 gastric inhibitory polypeptide Homo sapiens 203-243 33459181-3 2021 The objective of this study was to investigate the effect of oral ursodeoxycholic acid (UDCA) and chenodeoxycholic acid (CDCA) on post-prandial secretion of GLP-1, oxyntomodulin (OXM), peptide YY (PYY), glucose-dependent insulinotropic peptide (GIP), glucagon and ghrelin. Ursodeoxycholic Acid 66-86 gastric inhibitory polypeptide Homo sapiens 245-248 33459181-6 2021 RESULTS UDCA and CDCA provoked differential gut hormone responses: UDCA did not have any significant effects, but CDCA provoked significant increases in GLP-1 and OXM and a profound reduction in GIP. Chenodeoxycholic Acid 17-21 gastric inhibitory polypeptide Homo sapiens 195-198 33459181-6 2021 RESULTS UDCA and CDCA provoked differential gut hormone responses: UDCA did not have any significant effects, but CDCA provoked significant increases in GLP-1 and OXM and a profound reduction in GIP. Ursodeoxycholic Acid 8-12 gastric inhibitory polypeptide Homo sapiens 195-198 33459181-6 2021 RESULTS UDCA and CDCA provoked differential gut hormone responses: UDCA did not have any significant effects, but CDCA provoked significant increases in GLP-1 and OXM and a profound reduction in GIP. Chenodeoxycholic Acid 114-118 gastric inhibitory polypeptide Homo sapiens 195-198 33459181-8 2021 On the other hand, CDCA reduced post-prandial secretion of GIP, with an associated reduction in post-prandial insulin secretion. Chenodeoxycholic Acid 19-23 gastric inhibitory polypeptide Homo sapiens 59-62 33317160-7 2020 Consistent improvements from anthocyanin intake were found in glycemic, gastric inhibitory peptide (GIP), interleukin-6 (IL-6), and oxygen radical absorbance capacity (ORAC) responses. Anthocyanins 29-40 gastric inhibitory polypeptide Homo sapiens 72-98 33515092-0 2021 Co-ingestion of NUTRALYS pea protein and a high-carbohydrate beverage influences the glycaemic, insulinaemic, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) responses: preliminary results of a randomised controlled trial. Carbohydrates 49-61 gastric inhibitory polypeptide Homo sapiens 157-160 33547046-2 2021 The aim of this study was to develop a Positron Emission Tomography (PET) radioligand for the GIPR, to enable the assessment of target distribution and drug target engagement in vivo.The GIPR selective peptide S02-GIP was radiolabeled with Gallium-68. Gallium-68 240-250 gastric inhibitory polypeptide Homo sapiens 94-97 33461430-0 2022 Effect of 6 weeks of very low-volume high-intensity interval training on oral glucose-stimulated incretin hormone response. Glucose 78-85 gastric inhibitory polypeptide Homo sapiens 97-113 33461430-1 2022 INTRODUCTION: Decreased fasting and oral glucose-stimulated incretin hormone concentrations following moderate-intensity continuous endurance training interventions have been reported in glucose-tolerant people, however results are conflicting. Glucose 41-48 gastric inhibitory polypeptide Homo sapiens 60-76 33461430-1 2022 INTRODUCTION: Decreased fasting and oral glucose-stimulated incretin hormone concentrations following moderate-intensity continuous endurance training interventions have been reported in glucose-tolerant people, however results are conflicting. Glucose 187-194 gastric inhibitory polypeptide Homo sapiens 60-76 33938181-5 2021 While GIP was devoid of direct antimicrobial activity, it has a potent membrane depolarizing effect, and at low concentrations, it significantly potentiated the activity of eight antibiotics and bile salt by reducing MICs by 4-8-fold in E. coli TG1 and 4-20-fold in E. amylovora 1189. Bile Acids and Salts 195-204 gastric inhibitory polypeptide Homo sapiens 6-9 32991046-10 2021 L-phenylalanine also increased GIP concentrations relative to D-phenylalanine (P=0.0420) and placebo (P=0.0249) 70 minutes following ingestion. Phenylalanine 0-15 gastric inhibitory polypeptide Homo sapiens 31-34 32991046-13 2021 CONCLUSIONS: Ingestion of L-phenylalanine, but not D-phenylalanine, increases insulin, glucagon and GIP concentrations without appearing to have a large effect on appetite. Phenylalanine 26-41 gastric inhibitory polypeptide Homo sapiens 100-103 33317160-7 2020 Consistent improvements from anthocyanin intake were found in glycemic, gastric inhibitory peptide (GIP), interleukin-6 (IL-6), and oxygen radical absorbance capacity (ORAC) responses. Anthocyanins 29-40 gastric inhibitory polypeptide Homo sapiens 100-103 33053504-1 2020 Glucose-dependent insulinotropic polypeptide (GIP) is a gut hormone impacting glucose, lipid and bone metabolism through the GIP receptor (GIPR). Glucose 78-85 gastric inhibitory polypeptide Homo sapiens 0-44 32936440-6 2020 The intestinal mucosa has carbohydrate sensors that stimulate the release of two "incretin" hormones (GIP and GLP-1) whose actions range from the secretion of insulin to appetite regulation. Carbohydrates 26-38 gastric inhibitory polypeptide Homo sapiens 102-105 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 gastric inhibitory polypeptide Homo sapiens 50-53 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 gastric inhibitory polypeptide Homo sapiens 64-67 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 gastric inhibitory polypeptide Homo sapiens 64-67 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 gastric inhibitory polypeptide Homo sapiens 64-67 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 gastric inhibitory polypeptide Homo sapiens 0-3 32769216-7 2020 (D-Ala2)GIP and xenin-25-Gln increased glycerol release from 3T3-L1 adipocytes, but this lipolytic effect was significantly less apparent with combined treatment. Glycerol 39-47 gastric inhibitory polypeptide Homo sapiens 8-11 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 gastric inhibitory polypeptide Homo sapiens 24-27 33053504-1 2020 Glucose-dependent insulinotropic polypeptide (GIP) is a gut hormone impacting glucose, lipid and bone metabolism through the GIP receptor (GIPR). Glucose 78-85 gastric inhibitory polypeptide Homo sapiens 46-49 33043692-1 2020 BACKGROUND: Glucagon-like peptide-1 (GLP-1), a gut-derived incretin hormone, plays a pivotal role in glucose-induced insulin secretion. Glucose 101-108 gastric inhibitory polypeptide Homo sapiens 59-75 32518064-2 2020 Treatment based on the incretin hormones glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP-1) is characterized by their glucose-dependent insulinotropic actions without risk of hypoglycemia. Glucose 41-48 gastric inhibitory polypeptide Homo sapiens 83-86 32983244-12 2020 In conclusion, glutamine supplementation could improve glycemic control and levels of incretins (such as GLP-1 and GIP) in diabetes mellitus. Glutamine 15-24 gastric inhibitory polypeptide Homo sapiens 115-118 32825124-5 2020 Importantly, consumption of a diet rich in saturated fatty acids such as meat dishes before carbohydrate increases secretions of not only GLP-1 but also glucose-dependent insulinotropic polypeptide (GIP), which promotes energy storage in adipose tissue and may lead to weight gain in the long term. Fatty Acids 43-64 gastric inhibitory polypeptide Homo sapiens 153-197 32825124-5 2020 Importantly, consumption of a diet rich in saturated fatty acids such as meat dishes before carbohydrate increases secretions of not only GLP-1 but also glucose-dependent insulinotropic polypeptide (GIP), which promotes energy storage in adipose tissue and may lead to weight gain in the long term. Fatty Acids 43-64 gastric inhibitory polypeptide Homo sapiens 199-202 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 gastric inhibitory polypeptide Homo sapiens 48-51 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 gastric inhibitory polypeptide Homo sapiens 79-82 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 gastric inhibitory polypeptide Homo sapiens 260-263 31974732-3 2020 METHODS: GIP concentrations were successfully measured during OGTTs in two independent populations (Malmo Diet Cancer-Cardiovascular Cohort [MDC-CC] and Prevalence, Prediction and Prevention of Diabetes in Botnia [PPP-Botnia]) in a total of 8044 subjects. 2-methoxy-5-(2',4'-dimethoxyphenyl)-2,4,6-cycloheptatrien-1-one 141-147 gastric inhibitory polypeptide Homo sapiens 9-12 31299132-8 2020 Moreover, in Galphas signalling (cAMP production) GIP(1-42) was ~2-fold more potent and more efficacious on GIPR-[E354Q] compared to wt with 17.5% higher basal activity. galphas 13-20 gastric inhibitory polypeptide Homo sapiens 50-53 31299132-8 2020 Moreover, in Galphas signalling (cAMP production) GIP(1-42) was ~2-fold more potent and more efficacious on GIPR-[E354Q] compared to wt with 17.5% higher basal activity. Cyclic AMP 33-37 gastric inhibitory polypeptide Homo sapiens 50-53 31299132-11 2020 This could explain the long-term functional impairment of the GIP system in bone metabolism and blood sugar maintenance for [E354Q] carriers and may shed light on the desensitization of the insulinotropic action of GIP in patients with T2DM. Sugars 102-107 gastric inhibitory polypeptide Homo sapiens 62-65 32543789-1 2020 Incretin hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) play a major role in regulation of postprandial glucose and the development of type 2 diabetes mellitus. Glucose 54-61 gastric inhibitory polypeptide Homo sapiens 100-103 32543789-3 2020 We developed a physiologically-based (PB) quantitative systems pharmacology model of GLP-1 and GIP and their metabolites that describes the secretion of the incretins in response to intraduodenal glucose infusions and their degradation by DPP4 and NEP. Glucose 196-203 gastric inhibitory polypeptide Homo sapiens 95-98 31848710-9 2020 CONCLUSIONS: There is a weak relationship between oral glucose-induced GIP and GLP-1 secretions in non-diabetic subjects. Glucose 55-62 gastric inhibitory polypeptide Homo sapiens 71-74 32182123-2 2020 Dietary glucose drives GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) secretion postoperatively. Glucose 8-15 gastric inhibitory polypeptide Homo sapiens 33-77 32182123-2 2020 Dietary glucose drives GLP-1 and glucose-dependent insulinotropic polypeptide (GIP) secretion postoperatively. Glucose 8-15 gastric inhibitory polypeptide Homo sapiens 79-82 32182123-11 2020 Canagliflozin reduced GIP (iAUC -28%, P = 0.01; peak concentrations -57%, P < 0.01), insulin, and glucose excursions, whereas plasma glucagon (AUC 3,216 vs. 4,160 min pmol L-1, P = 0.02) and amino acids were increased. Canagliflozin 0-13 gastric inhibitory polypeptide Homo sapiens 22-25 32182123-13 2020 The results suggest that SGLT1-mediated glucose absorption contributes to incretin hormone secretion after RYGB. Glucose 40-47 gastric inhibitory polypeptide Homo sapiens 74-90 32305124-11 2020 GIP levels at 120th was lower in cyclosporine-treated renal transplant patients when compared to control group (p = 0,003). Cyclosporine 33-45 gastric inhibitory polypeptide Homo sapiens 0-3 31848710-4 2020 We aimed to evaluate the relationship between plasma GIP and GLP-1 responses to a 75-g oral glucose load in individuals with normal (NGT) and impaired glucose tolerance (IGT). Glucose 92-99 gastric inhibitory polypeptide Homo sapiens 53-56 31928498-4 2020 Results: Using false discovery rate <0.05, three loci were related to all five MetS components (rs7575523; nearest gene LINC0112, rs3936511; intron of C5orf67, and rs111970447; intron of GIP). CYTL1 protein, human 154-161 gastric inhibitory polypeptide Homo sapiens 190-193 32390941-1 2020 Objective: We recently observed a greater increase in plasma levels of bioactive glucose-dependent insulinotropic polypeptide (GIP) than glucagon-like peptide 1 (GLP-1) using the receptor-mediated bioassays in the subjects with normal glycemic tolerance (NGT) treated with dipeptidyl peptidase 4 (DPP-4) inhibitors, which may be unappreciated using conventional enzyme-linked immunosorbent assays (ELISAs) during oral glucose tolerance test. Glucose 81-88 gastric inhibitory polypeptide Homo sapiens 127-130 32390941-8 2020 Results: During the single MTT study, postprandial active GIP bioassay levels of T2DM with DPP-4 inhibitor treatment were drastically higher than those of NGT and T2DM without DPP-4 inhibitor, although the DPP-4 inhibitor-treated group showed moderate increase of active GIPELISA and active GLP-1 bioassay , while active GLP-1 bioassay levels of T2DM subjects without DPP-4 inhibitor were comparable to those of NGT subjects. monooxyethylene trimethylolpropane tristearate 27-30 gastric inhibitory polypeptide Homo sapiens 58-61 32305935-5 2021 And moreover, a new activation function is designed based on the hyperbolic tangent function, and its initial connection weights are optimized by adopting GIP similarity for microbes, which can improve the training speed of BPNNHMDA efficiently. bpnnhmda 224-232 gastric inhibitory polypeptide Homo sapiens 155-158 31693916-1 2020 Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) potentiate glucose-induced insulin secretion and are therefore thought to be responsible for the incretin effect. Glucose 98-105 gastric inhibitory polypeptide Homo sapiens 0-44 32068442-5 2020 In the RYGB group the responses of GLP-1, GIP, glicentin, FGF-21, and C-peptide were increased after glucose compared with the other meals. Glucose 101-108 gastric inhibitory polypeptide Homo sapiens 42-45 32077470-8 2020 RESULTS: Infusion of GIP(3-30)NH2+exendin(9-39)NH2 significantly increased plasma glucose excursions (bsAUC: 261 +- 142 mmol/L x min) during the liquid mixed meals compared with GIP(3-30)NH2 (180 +- 141 mmol/L x min; P = 0.048), exendin(9-39)NH2 (171 +- 114 mmol/L x min; P = 0.046), and placebo (116 +- 154 mmol/L x min; P = 0.015). Glucose 82-89 gastric inhibitory polypeptide Homo sapiens 21-24 32077470-9 2020 Correspondingly, C-peptide:glucose ratios during GIP(3-30)NH2+exendin(9-39)NH2 infusion were significantly lower than during GIP(3-30)NH2 (P = 0.0057), exendin(9-39)NH2 (P = 0.0038), and placebo infusion (P = 0.014). Glucose 27-34 gastric inhibitory polypeptide Homo sapiens 49-52 32077470-13 2020 CONCLUSIONS: Endogenous GIP and GLP-1 lower postprandial plasma glucose excursions and stimulate insulin secretion but only endogenous GIP affects gallbladder motility. Glucose 64-71 gastric inhibitory polypeptide Homo sapiens 24-27 31689454-4 2020 Furthermore, GIP has been suggested to control vasodilation via secretion of nitric oxide, and vascular leukocyte adhesion and inflammation via expression and secretion of endothelin 1. Nitric Oxide 77-89 gastric inhibitory polypeptide Homo sapiens 13-16 31751656-2 2020 GIP is released in response to glucose or fat absorption and acts on the GIP receptor (GIPR) to potentiate insulin release from pancreatic beta cells. Glucose 31-38 gastric inhibitory polypeptide Homo sapiens 0-3 31751656-7 2020 Recently, longer-acting GIP agonists that exhibit enzymatic stability, as well as dual GLP-1/GIP agonists which provide simultaneous improvement in glucose and weight control have been generated and successfully tested in animal T2D models. Glucose 148-155 gastric inhibitory polypeptide Homo sapiens 93-96 31756367-1 2020 Glucose-dependent insulinotropic polypeptide (GIP) is a gut hormone secreted from the upper small intestine, which plays an important physiological role in the control of glucose metabolism through its incretin action to enhance glucose-dependent insulin secretion. Glucose 171-178 gastric inhibitory polypeptide Homo sapiens 0-44 31756367-1 2020 Glucose-dependent insulinotropic polypeptide (GIP) is a gut hormone secreted from the upper small intestine, which plays an important physiological role in the control of glucose metabolism through its incretin action to enhance glucose-dependent insulin secretion. Glucose 171-178 gastric inhibitory polypeptide Homo sapiens 46-49 31756367-1 2020 Glucose-dependent insulinotropic polypeptide (GIP) is a gut hormone secreted from the upper small intestine, which plays an important physiological role in the control of glucose metabolism through its incretin action to enhance glucose-dependent insulin secretion. Glucose 229-236 gastric inhibitory polypeptide Homo sapiens 0-44 31756367-1 2020 Glucose-dependent insulinotropic polypeptide (GIP) is a gut hormone secreted from the upper small intestine, which plays an important physiological role in the control of glucose metabolism through its incretin action to enhance glucose-dependent insulin secretion. Glucose 229-236 gastric inhibitory polypeptide Homo sapiens 46-49 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 gastric inhibitory polypeptide Homo sapiens 16-19 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 gastric inhibitory polypeptide Homo sapiens 0-30 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 gastric inhibitory polypeptide Homo sapiens 32-35 31949084-6 2020 Plasma glucagon and glucose were higher during GIP infusion compared with placebo infusion (P = 0.026 and P = 0.017) as assessed by area under the curve. Glucagon 7-15 gastric inhibitory polypeptide Homo sapiens 47-50 31949084-6 2020 Plasma glucagon and glucose were higher during GIP infusion compared with placebo infusion (P = 0.026 and P = 0.017) as assessed by area under the curve. Glucose 20-27 gastric inhibitory polypeptide Homo sapiens 47-50 31949084-7 2020 CONCLUSIONS: In patients with type 2 diabetes, GIP infusion on top of treatment with metformin and a long-acting GLP-1R agonist did not affect energy intake, appetite, or energy expenditure but increased plasma glucose compared with placebo. Metformin 85-94 gastric inhibitory polypeptide Homo sapiens 47-50 31949084-7 2020 CONCLUSIONS: In patients with type 2 diabetes, GIP infusion on top of treatment with metformin and a long-acting GLP-1R agonist did not affect energy intake, appetite, or energy expenditure but increased plasma glucose compared with placebo. Glucose 211-218 gastric inhibitory polypeptide Homo sapiens 47-50 31785304-7 2020 GIP stimulates glucagon secretion in a glucose-dependent manner in healthy people, with enhanced activity at lower glycemia. Glucose 39-46 gastric inhibitory polypeptide Homo sapiens 0-3 31809770-2 2020 The incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) and the related hormone glucagon-like peptide-2 (GLP-2) are all rapidly N-terminally truncated with severe loss of intrinsic activity. Nitrogen 182-183 gastric inhibitory polypeptide Homo sapiens 23-67 31809770-5 2020 Like GIP(1-42), GIP(1-30)NH2 is a substrate for DPP-4 generating GIP(3-30)NH2 which, compared to GIP(3-42), binds with higher affinity and very efficiently inhibits GIP receptor (GIPR) activity with no intrinsic activity. Ammonia 25-28 gastric inhibitory polypeptide Homo sapiens 5-8 31809770-5 2020 Like GIP(1-42), GIP(1-30)NH2 is a substrate for DPP-4 generating GIP(3-30)NH2 which, compared to GIP(3-42), binds with higher affinity and very efficiently inhibits GIP receptor (GIPR) activity with no intrinsic activity. Ammonia 25-28 gastric inhibitory polypeptide Homo sapiens 16-19 31809770-5 2020 Like GIP(1-42), GIP(1-30)NH2 is a substrate for DPP-4 generating GIP(3-30)NH2 which, compared to GIP(3-42), binds with higher affinity and very efficiently inhibits GIP receptor (GIPR) activity with no intrinsic activity. Ammonia 25-28 gastric inhibitory polypeptide Homo sapiens 16-19 31809770-5 2020 Like GIP(1-42), GIP(1-30)NH2 is a substrate for DPP-4 generating GIP(3-30)NH2 which, compared to GIP(3-42), binds with higher affinity and very efficiently inhibits GIP receptor (GIPR) activity with no intrinsic activity. Ammonia 25-28 gastric inhibitory polypeptide Homo sapiens 16-19 31809770-6 2020 Here, we review the action of these four and multiple other N- and C-terminally truncated forms of GIP with an emphasis on molecular pharmacology, i.e. ligand binding, subsequent receptor activation and desensitization. Nitrogen 60-61 gastric inhibitory polypeptide Homo sapiens 99-102 31809770-6 2020 Here, we review the action of these four and multiple other N- and C-terminally truncated forms of GIP with an emphasis on molecular pharmacology, i.e. ligand binding, subsequent receptor activation and desensitization. Carbon 67-68 gastric inhibitory polypeptide Homo sapiens 99-102 31809770-7 2020 Our overall conclusion is that the N-terminus is essential for receptor activation as GIP N-terminal truncation leads to decreased/lost intrinsic activity and antagonism (similar to GLP-1 and GLP-2), whereas the C-terminal extension of GIP(1-42), as compared to GLP-1, GLP-2 and glucagon (29-33 amino acids), has no apparent impact on the GIPR in vitro, but may play a role for other properties such as stability and tissue distribution. Nitrogen 35-36 gastric inhibitory polypeptide Homo sapiens 86-89 31809770-7 2020 Our overall conclusion is that the N-terminus is essential for receptor activation as GIP N-terminal truncation leads to decreased/lost intrinsic activity and antagonism (similar to GLP-1 and GLP-2), whereas the C-terminal extension of GIP(1-42), as compared to GLP-1, GLP-2 and glucagon (29-33 amino acids), has no apparent impact on the GIPR in vitro, but may play a role for other properties such as stability and tissue distribution. Nitrogen 35-36 gastric inhibitory polypeptide Homo sapiens 236-239 31809770-7 2020 Our overall conclusion is that the N-terminus is essential for receptor activation as GIP N-terminal truncation leads to decreased/lost intrinsic activity and antagonism (similar to GLP-1 and GLP-2), whereas the C-terminal extension of GIP(1-42), as compared to GLP-1, GLP-2 and glucagon (29-33 amino acids), has no apparent impact on the GIPR in vitro, but may play a role for other properties such as stability and tissue distribution. Nitrogen 90-91 gastric inhibitory polypeptide Homo sapiens 86-89 31809770-7 2020 Our overall conclusion is that the N-terminus is essential for receptor activation as GIP N-terminal truncation leads to decreased/lost intrinsic activity and antagonism (similar to GLP-1 and GLP-2), whereas the C-terminal extension of GIP(1-42), as compared to GLP-1, GLP-2 and glucagon (29-33 amino acids), has no apparent impact on the GIPR in vitro, but may play a role for other properties such as stability and tissue distribution. Carbon 212-213 gastric inhibitory polypeptide Homo sapiens 236-239 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 gastric inhibitory polypeptide Homo sapiens 0-44 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 gastric inhibitory polypeptide Homo sapiens 46-49 32081451-0 2020 The early history of GIP 1969-2000: From enterogastrone to major metabolic hormone. enterogastrone 41-55 gastric inhibitory polypeptide Homo sapiens 21-24 32081451-1 2020 This paper describes the early history of Gastric Inhibitory Polypeptide, better referred to simply as GIP, from its isolation by purification from a crude preparation of CCK-PZ (cholecystokinin/pancreozymin) to its recognition as a key play in the pathogenesis of obesity and other metabolic disorders far removed from the enterogastrone properties by which it was originally identified. Cholecystokinin 171-177 gastric inhibitory polypeptide Homo sapiens 103-106 32081451-1 2020 This paper describes the early history of Gastric Inhibitory Polypeptide, better referred to simply as GIP, from its isolation by purification from a crude preparation of CCK-PZ (cholecystokinin/pancreozymin) to its recognition as a key play in the pathogenesis of obesity and other metabolic disorders far removed from the enterogastrone properties by which it was originally identified. Cholecystokinin 179-194 gastric inhibitory polypeptide Homo sapiens 103-106 32081451-1 2020 This paper describes the early history of Gastric Inhibitory Polypeptide, better referred to simply as GIP, from its isolation by purification from a crude preparation of CCK-PZ (cholecystokinin/pancreozymin) to its recognition as a key play in the pathogenesis of obesity and other metabolic disorders far removed from the enterogastrone properties by which it was originally identified. Cholecystokinin 195-207 gastric inhibitory polypeptide Homo sapiens 103-106 32081451-1 2020 This paper describes the early history of Gastric Inhibitory Polypeptide, better referred to simply as GIP, from its isolation by purification from a crude preparation of CCK-PZ (cholecystokinin/pancreozymin) to its recognition as a key play in the pathogenesis of obesity and other metabolic disorders far removed from the enterogastrone properties by which it was originally identified. enterogastrone 324-338 gastric inhibitory polypeptide Homo sapiens 103-106 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 gastric inhibitory polypeptide Homo sapiens 97-100 32069846-6 2020 Fasting GIP was associated with ALT [beta = 0.16 (confidence interval (CI): 0.01-0.32)], triglycerides [beta = 0.21 (95% CI: 0.06-0.36], and FGF-21 [beta = 0.20 (95%CI: 0.03-0.37)]; and postprandial GIP with GGT [beta = 0.17 (95%CI: 0.03-0.32)]. Triglycerides 89-102 gastric inhibitory polypeptide Homo sapiens 8-11 31813891-9 2020 Compared with the model group, in the treatment group, blood glucose decreased, body weight increased, incretin-cAMP signaling pathway related factors glucose-dependent insulin-promoting polypeptide (GIP), glucagon-like peptide-1 (GLP-1), GLP-1R, cAMP, P-protein kinase A (PKA), AKT were up-regulated, insulin secretion was increased, liporing protein interaction protein (TXNIP) expression was down-regulated. Cyclic AMP 112-116 gastric inhibitory polypeptide Homo sapiens 151-198 31813891-9 2020 Compared with the model group, in the treatment group, blood glucose decreased, body weight increased, incretin-cAMP signaling pathway related factors glucose-dependent insulin-promoting polypeptide (GIP), glucagon-like peptide-1 (GLP-1), GLP-1R, cAMP, P-protein kinase A (PKA), AKT were up-regulated, insulin secretion was increased, liporing protein interaction protein (TXNIP) expression was down-regulated. Cyclic AMP 112-116 gastric inhibitory polypeptide Homo sapiens 200-203 31757794-0 2020 Effects of Pioglitazone on Glucose Dependent Insulinotropic Polypeptide Mediated Insulin Secretion and Adipocyte Receptor Expression in Patients with Type 2 Diabetes. pioglitazone 11-23 gastric inhibitory polypeptide Homo sapiens 27-71 31757794-5 2020 To test this, we conducted a randomized, double-blind, placebo-controlled trial of pioglitazone therapy on GIP-mediated insulin secretion and adipocyte GIP-R expression in subjects with well controlled T2DM. pioglitazone 83-95 gastric inhibitory polypeptide Homo sapiens 107-110 31693916-1 2020 Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) potentiate glucose-induced insulin secretion and are therefore thought to be responsible for the incretin effect. Glucose 98-105 gastric inhibitory polypeptide Homo sapiens 46-49 31693916-6 2020 However, using incretin hormone receptor antagonists: the novel GIP receptor antagonist GIP(3-30)NH2 and the widely used GLP-1 receptor antagonist exendin(9-39)NH2, we can now distinguish between the effects of the two hormones. Ammonia 97-100 gastric inhibitory polypeptide Homo sapiens 64-67 31693916-6 2020 However, using incretin hormone receptor antagonists: the novel GIP receptor antagonist GIP(3-30)NH2 and the widely used GLP-1 receptor antagonist exendin(9-39)NH2, we can now distinguish between the effects of the two hormones. Ammonia 97-100 gastric inhibitory polypeptide Homo sapiens 88-91 31706956-2 2020 Together with the other incretin hormone, glucagon-like peptide-1 (GLP-1), it plays an important role in regulating glucose homeostasis. Glucose 116-123 gastric inhibitory polypeptide Homo sapiens 24-40 31706956-6 2020 Therefore, given that studies with incretin receptor antagonists indicate that not all of the glucose-lowering effects of DPP-4 inhibition can be accounted for by GLP-1 alone, evidence supports the notion that GIP may play a role in mediating the anti-hyperglycaemic effects of DPP-4 inhibition, while its glucagonotropic actions at lower glucose levels may contribute to the low risk of hypoglycaemia associated with DPP-4 inhibitors. Glucose 339-346 gastric inhibitory polypeptide Homo sapiens 210-213 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 gastric inhibitory polypeptide Homo sapiens 0-44 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 gastric inhibitory polypeptide Homo sapiens 46-49 31733230-2 2020 Despite a recognised physiological role for GIP as an insulin secretagogue to control postprandial blood glucose levels, growing evidence reveals important actions of GIP on adipocytes and promotion of fat deposition in tissues. Glucose 105-112 gastric inhibitory polypeptide Homo sapiens 44-47 31622777-1 2020 Infusion of the incretin hormone glucose-dependent insulinotropic polypeptide (GIP) suppresses the bone resorption marker carboxy-terminal type 1 collagen crosslinks (CTX). Glucose 33-40 gastric inhibitory polypeptide Homo sapiens 79-82 31622777-1 2020 Infusion of the incretin hormone glucose-dependent insulinotropic polypeptide (GIP) suppresses the bone resorption marker carboxy-terminal type 1 collagen crosslinks (CTX). carboxy phosphate 122-129 gastric inhibitory polypeptide Homo sapiens 79-82 31622777-8 2020 The peak value of the bone formation marker N-terminal propeptide of type 1 procollagen (P1NP) peaked at higher levels during GIP (109 +- 6.7% of baseline) than during GIP(3-30)NH2 infusion (101 +- 8.9%) (P = 0.049) and GIP suppressed PTH levels compared to GIP(3-30)NH2 alone (P = 0.0158). Nitrogen 44-45 gastric inhibitory polypeptide Homo sapiens 126-129 31377992-9 2020 A linear increase was seen in post-glucose GIP response at 1 month and 6 months and 4 years. Glucose 35-42 gastric inhibitory polypeptide Homo sapiens 43-46 31958096-0 2020 The Novel Dual GLP-1/GIP Receptor Agonist DA-CH5 Is Superior to Single GLP-1 Receptor Agonists in the MPTP Model of Parkinson"s Disease. JMV 641 45-48 gastric inhibitory polypeptide Homo sapiens 21-24 31958096-4 2020 OBJECTIVE: We tested DA-CH5, a novel dual GLP-1/GIP receptor agonist. JMV 641 24-27 gastric inhibitory polypeptide Homo sapiens 48-51 31958096-5 2020 METHODS: DA-CH5 activity was tested on cells expressing GLP-1, GLP-2, GIP or glucagon receptors. JMV 641 12-15 gastric inhibitory polypeptide Homo sapiens 70-73 31816909-7 2019 MUFA induced higher GIP response than PUFA. mufa 0-4 gastric inhibitory polypeptide Homo sapiens 20-23 31816909-11 2019 Ghrelin and GIP, but not GLP1, were associated with acute appetite control, especially after MUFA meal. mufa 93-97 gastric inhibitory polypeptide Homo sapiens 12-15 31506889-1 2019 INTRODUCTION: To investigate canagliflozin-induced changes in postprandial total glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) levels in patients with type 2 diabetes mellitus (T2DM). Canagliflozin 29-42 gastric inhibitory polypeptide Homo sapiens 117-161 31506889-1 2019 INTRODUCTION: To investigate canagliflozin-induced changes in postprandial total glucagon-like peptide 1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP) levels in patients with type 2 diabetes mellitus (T2DM). Canagliflozin 29-42 gastric inhibitory polypeptide Homo sapiens 163-166 31506889-5 2019 A transient reduction in the postprandial GIP level at only 30 min (mean difference - 80.3 pg/mL) during an MTT was observed. monooxyethylene trimethylolpropane tristearate 108-111 gastric inhibitory polypeptide Homo sapiens 42-45 31669625-13 2019 CONCLUSIONS: In patients with type 2 diabetes maintained endogenous insulin secretion, anagliptin increased the plasma level of active GLP-1 and GIP in association with a slight stimulation of insulin secretion and slight inhibition of glucagon secretion, but did not delay gastric emptying. anagliptin 87-97 gastric inhibitory polypeptide Homo sapiens 145-148 31393567-0 2019 Longitudinal changes in fasting and glucose-stimulated GLP-1 and GIP in healthy older subjects. Glucose 36-43 gastric inhibitory polypeptide Homo sapiens 65-68 31393567-12 2019 CONCLUSIONS: Fasting GIP, and glucose-stimulated GLP-1 and GIP concentrations correlate within individuals over a follow-up period of ~ 5.9 years. Glucose 30-37 gastric inhibitory polypeptide Homo sapiens 59-62 31539554-0 2019 The early history of GIP 1969-2000: from enterogastrone to major metabolic hormone. enterogastrone 41-55 gastric inhibitory polypeptide Homo sapiens 21-24 31539554-1 2019 This paper describes the early history of Gastric Inhibitory Polypeptide, better referred to simply as GIP, from its isolation by purification from a crude preparation of CCK-PZ (cholecystokinin/pancreozymin) to its recognition as a key play in the pathogenesis of obesity and other metabolic disorders far removed from the enterogastrone properties by which it was originally identified. enterogastrone 324-338 gastric inhibitory polypeptide Homo sapiens 103-106 31539554-2 2019 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 gastric inhibitory polypeptide Homo sapiens 97-100 31781045-0 2019 Insights Into GLP-1 and GIP Actions Emerging From Vildagliptin Mechanism Studies in Man. vildagliptin 50-62 gastric inhibitory polypeptide Homo sapiens 24-27 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. vildagliptin 0-12 gastric inhibitory polypeptide Homo sapiens 56-100 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. vildagliptin 0-12 gastric inhibitory polypeptide Homo sapiens 102-105 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. vildagliptin 0-12 gastric inhibitory polypeptide Homo sapiens 163-166 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. vildagliptin 0-12 gastric inhibitory polypeptide Homo sapiens 163-166 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. vildagliptin 271-283 gastric inhibitory polypeptide Homo sapiens 102-105 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 gastric inhibitory polypeptide Homo sapiens 102-105 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 344-351 gastric inhibitory polypeptide Homo sapiens 102-105 31689951-1 2019 BACKGROUND: The ingestion of whey protein and amino acids with carbohydrate (CHO) enhances the release of glucagon-like peptide-1 (GLP-1) and glucose-dependent-insulinotropic peptide (GIP) that promote insulin secretion. Carbohydrates 63-75 gastric inhibitory polypeptide Homo sapiens 142-182 31689951-1 2019 BACKGROUND: The ingestion of whey protein and amino acids with carbohydrate (CHO) enhances the release of glucagon-like peptide-1 (GLP-1) and glucose-dependent-insulinotropic peptide (GIP) that promote insulin secretion. Carbohydrates 63-75 gastric inhibitory polypeptide Homo sapiens 184-187 31689951-3 2019 The purpose of this study was to examine how Ile and Leu influence both GLP-1 and GIP, subsequent pancreatic hormones, and glycemia in healthy, inactive adults. Isoleucine 45-48 gastric inhibitory polypeptide Homo sapiens 82-85 31689951-3 2019 The purpose of this study was to examine how Ile and Leu influence both GLP-1 and GIP, subsequent pancreatic hormones, and glycemia in healthy, inactive adults. Leucine 53-56 gastric inhibitory polypeptide Homo sapiens 82-85 31689951-10 2019 The ingestion of Ile prior to CHO augmented GIP concentration greater than Leu or Pla. Isoleucine 17-20 gastric inhibitory polypeptide Homo sapiens 44-47 31689951-12 2019 CONCLUSIONS: Ile impacts GIP concentration, which did not relate to either insulin or glucose concentrations. Isoleucine 13-16 gastric inhibitory polypeptide Homo sapiens 25-28 31816909-8 2019 GIP was associated with all the VAS measurements except preoccupation for MUFA meal. mufa 74-78 gastric inhibitory polypeptide Homo sapiens 0-3 31816909-10 2019 In conclusion, the results demonstrate that ghrelin, GIP and VAS respond differently to MUFA and PUFA meals. mufa 88-92 gastric inhibitory polypeptide Homo sapiens 53-56 31816909-10 2019 In conclusion, the results demonstrate that ghrelin, GIP and VAS respond differently to MUFA and PUFA meals. Fatty Acids, Omega-3 97-101 gastric inhibitory polypeptide Homo sapiens 53-56 31466840-0 2019 Low-carbohydrate diet by staple change attenuates postprandial GIP and CPR levels in type 2 diabetes patients. Carbohydrates 4-16 gastric inhibitory polypeptide Homo sapiens 63-66 31466840-6 2019 CONCLUSIONS: These results indicate that changing only the carbohydrate content of the staple food has benefits on glucose and lipid metabolism in T2DM patients concomitant with the decrease of insulin and GIP secretion, which ameliorate body weight gain and insulin resistance. Carbohydrates 59-71 gastric inhibitory polypeptide Homo sapiens 206-209 31443356-2 2019 Furthermore, GLP-1 inhibits glucagon secretion when plasma glucose concentrations are above normal fasting concentrations while GIP acts glucagonotropically at low glucose levels. Glucose 164-171 gastric inhibitory polypeptide Homo sapiens 128-131 31572300-3 2019 Materials and Methods: Cortisol response was measured during in vivo tests that transiently modulated the levels of ligands for potential aberrant receptors, including GIP. Hydrocortisone 23-31 gastric inhibitory polypeptide Homo sapiens 168-171 31572300-6 2019 Results: In vivo, cortisol increased in response to mixed meals (+353%), oral 75 g glucose (+71%), GIP infusion (+416%), and hLH IV (+243%). Hydrocortisone 18-26 gastric inhibitory polypeptide Homo sapiens 99-102 31572300-7 2019 Suppression of GIP by pasireotide improved cortisol secretion but produced hyperglycemia. pasireotide 22-33 gastric inhibitory polypeptide Homo sapiens 15-18 31572300-7 2019 Suppression of GIP by pasireotide improved cortisol secretion but produced hyperglycemia. Hydrocortisone 43-51 gastric inhibitory polypeptide Homo sapiens 15-18 31346639-8 2019 In preclinical studies, polyagonists targeting the receptors for glucagon-like peptide-1 (GLP-1), glucagon, or glucose-dependent insulinotropic peptide (GIP) were promising to reduce body weight and blood glucose. Blood Glucose 199-212 gastric inhibitory polypeptide Homo sapiens 111-151 31346639-8 2019 In preclinical studies, polyagonists targeting the receptors for glucagon-like peptide-1 (GLP-1), glucagon, or glucose-dependent insulinotropic peptide (GIP) were promising to reduce body weight and blood glucose. Blood Glucose 199-212 gastric inhibitory polypeptide Homo sapiens 153-156 30787473-4 2019 Finally, the review will clarify the molecular characteristics of sucrose regarding the release of the gastrointestinal glucose-dependent insulinotropic peptide (GIP) compared to other energy-providing nutrients and its relevance in metabolic diseases. Sucrose 66-73 gastric inhibitory polypeptide Homo sapiens 120-160 30787473-4 2019 Finally, the review will clarify the molecular characteristics of sucrose regarding the release of the gastrointestinal glucose-dependent insulinotropic peptide (GIP) compared to other energy-providing nutrients and its relevance in metabolic diseases. Sucrose 66-73 gastric inhibitory polypeptide Homo sapiens 162-165 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 gastric inhibitory polypeptide Homo sapiens 93-109 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 241-248 gastric inhibitory polypeptide Homo sapiens 93-109 30844053-2 2019 OBJECTIVE: To investigate distal [GLP-1; peptide YY (PYY)] and proximal [glucose-dependent insulinotropic polypeptide (GIP)] gut hormone secretion in response to carbohydrates hydrolyzed at different rates. Carbohydrates 162-175 gastric inhibitory polypeptide Homo sapiens 73-117 29872922-7 2019 RESULTS: Our novel observation shows that the incremental area under curve (iAUC) 0-6 h of plasma GIP concentration was on average 16% lower following IPO meal compared with PO and HOS (P < 0.05) meals. PARA-IODO-D-PHENYLALANINE HYDROXAMIC ACID 151-154 gastric inhibitory polypeptide Homo sapiens 98-101 30844053-2 2019 OBJECTIVE: To investigate distal [GLP-1; peptide YY (PYY)] and proximal [glucose-dependent insulinotropic polypeptide (GIP)] gut hormone secretion in response to carbohydrates hydrolyzed at different rates. Carbohydrates 162-175 gastric inhibitory polypeptide Homo sapiens 119-122 30844053-12 2019 In both groups, GIP secretion was reduced by isomaltulose and even more so by sucrose plus acarbose when compared with sucrose intake. isomaltulose 45-57 gastric inhibitory polypeptide Homo sapiens 16-19 30844053-12 2019 In both groups, GIP secretion was reduced by isomaltulose and even more so by sucrose plus acarbose when compared with sucrose intake. Sucrose 78-85 gastric inhibitory polypeptide Homo sapiens 16-19 30844053-12 2019 In both groups, GIP secretion was reduced by isomaltulose and even more so by sucrose plus acarbose when compared with sucrose intake. Acarbose 91-99 gastric inhibitory polypeptide Homo sapiens 16-19 31061246-5 2019 Fluorescent-labelled GIP was added to fresh human plasma and subjected to clear native polyacrylamide gel electrophoresis (CN-PAGE). polyacrylamide 87-101 gastric inhibitory polypeptide Homo sapiens 21-24