PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 35356161-4 2022 It has up to 40 times higher affinity for somatostatin receptor subtype 5 in comparison with octreotide, leading to a higher inhibition of insulin release from beta cells. Octreotide 93-103 insulin Homo sapiens 139-146 2686331-4 1989 The 400 micrograms octreotide dose was superior with regard to the duration of plasma GH suppression to below 5 micrograms/l or 25% of the basal GH level, the mean GH as a percentage of the basal level over the first 4 and 8 h, and the integrated reduction of plasma GH during the first 4 and 8 h. The postprandial integrated insulin secretion during the first 3 h after injection of the octapeptide was significantly lower after 50, 100 and 400 micrograms than after the placebo injection. Octreotide 19-29 insulin Homo sapiens 326-333 2687064-0 1989 Sandostatin, a new analogue of somatostatin, reduces the metabolic changes induced by the nocturnal interruption of continuous subcutaneous insulin infusion in type 1 (insulin-dependent) diabetic patients. Octreotide 0-11 insulin Homo sapiens 140-147 2646315-3 1989 We studied in normo- and hypertensive elderly subjects the effects of the synthetic long-acting somatostatin analog octreotide (SMS 201-995) on the BP reduction that follows oral glucose administration in subjects who are recumbent and on their postglucose plasma vasoactive intestinal polypeptide (VIP) and insulin concentrations. Octreotide 116-126 insulin Homo sapiens 308-315 2545062-5 1989 Compared with control levels, octreotide therapy reduced insulin levels. Octreotide 30-40 insulin Homo sapiens 57-64 2466045-4 1989 A sc injection of 50 micrograms octreotide caused a significant (P less than 0.001) decrease in median plasma tachykinins and serum pancreatic polypeptide, GH, and insulin for up to 4 h. Administration of octreotide (50 micrograms, twice daily, sc) caused a 26% decrease in urinary 5-hydroxyindoleacetia acid excretion, but the number of flushing attacks or bowel movements did not change significantly. Octreotide 32-42 insulin Homo sapiens 164-171 2646315-8 1989 After placebo administration the postglucose plasma insulin levels increased from 79 to 519 pmol/L in the hypertensive subjects and from 63 to 464 pmol/L in the normotensive subjects, whereas after octreotide treatment plasma insulin increased little in either group. Octreotide 198-208 insulin Homo sapiens 226-233 2564819-7 1989 In Type 2 diabetes the analogue Octreotide suppresses insulin and glucagon release, leaving glucose levels either unchanged or somewhat elevated. Octreotide 32-42 insulin Homo sapiens 54-61 2899913-3 1988 Treatment with octreotide (SMS 201-995, Sandostatin; Sandoz) resulted in immediate sustained improvement of the hypoglycaemia despite persistent high levels of insulin. Octreotide 15-25 insulin Homo sapiens 160-167 2894388-7 1987 Native somatostatin (SRIF) and the synthetic analog SMS 201-995 inhibited insulin secretion from all cultures. Octreotide 52-63 insulin Homo sapiens 74-81 2898862-3 1988 Subcutaneous somatostatin analogue (SMS 201-995) was shown to increase the blood concentrations of glucose and B-hydroxybutyrate while lowering serum insulin levels. Octreotide 36-47 insulin Homo sapiens 150-157 2898427-2 1988 After octreotide injection, postprandial rises in plasma insulin and glucagon were significantly flattened. Octreotide 6-16 insulin Homo sapiens 57-64 29373734-7 2018 Insulin sensitivity was estimated as the steady-state plasma glucose (SSPG) concentration at equilibrium during octreotide and insulin administration. Octreotide 112-122 insulin Homo sapiens 0-7 2892338-1 1987 SMS 201-995 (Sandostatin) is an octapeptide which differs in its action from native somatostatin in four ways: 1) it inhibits GH hormone secretion in preference to insulin secretion; 2) it can be administered subcutaneously or even orally; 3) it is long-acting (t1/2 after sc administration 113 min), and 4) there is no rebound hypersecretion of hormones when the effect of the analogue lingers off. Octreotide 0-11 insulin Homo sapiens 164-171 2892338-1 1987 SMS 201-995 (Sandostatin) is an octapeptide which differs in its action from native somatostatin in four ways: 1) it inhibits GH hormone secretion in preference to insulin secretion; 2) it can be administered subcutaneously or even orally; 3) it is long-acting (t1/2 after sc administration 113 min), and 4) there is no rebound hypersecretion of hormones when the effect of the analogue lingers off. Octreotide 13-24 insulin Homo sapiens 164-171 31366755-2 2019 Octreotide acetate, a long-acting somatostatin analogue, suppresses the secretion of insulin and is recognized as a possible treatment for sulfonylurea-induced hypoglycemia. Octreotide 0-18 insulin Homo sapiens 85-92 33481251-5 2022 Octreotide was infused throughout both protocols to prevent endogenous insulin release. Octreotide 0-10 insulin Homo sapiens 71-78 33481251-13 2022 Octreotide was infused throughout both protocols to prevent endogenous insulin release. Octreotide 0-10 insulin Homo sapiens 71-78 33150747-2 2020 METHODS: A search of PubMed, Embase, and Cochrane databases was performed to identify randomized controlled trials (up to January 1, 2020) that used drugs that directly suppress insulin secretion (diazoxide or octreotide) in the treatment of obesity. Octreotide 210-220 insulin Homo sapiens 178-185 33150747-4 2020 RESULTS: A total of seven randomized controlled trials were included, with four using diazoxide and three using octreotide to suppress insulin secretion. Octreotide 112-122 insulin Homo sapiens 135-142 28600547-4 2017 ABCC8-deficient insulin-producing cells secreted higher insulin than their wild-type counterparts, and the excess insulin secretion was rescued by nifedipine, octreotide and nicorandil. Octreotide 159-169 insulin Homo sapiens 16-23 28592737-3 2017 The patient refused surgical treatment and octreotide was used to prevent hypoglycemia.It is known that octreotide suppresses the secretion of insulin from the pancreas; however, insulin secretion is not always suppressed in patients with insulinoma. Octreotide 43-53 insulin Homo sapiens 143-150 28592737-3 2017 The patient refused surgical treatment and octreotide was used to prevent hypoglycemia.It is known that octreotide suppresses the secretion of insulin from the pancreas; however, insulin secretion is not always suppressed in patients with insulinoma. Octreotide 104-114 insulin Homo sapiens 143-150 23902932-3 2014 METHODS: We utilized an octreotide, basal glucagon replacement, multistage insulin infusion, and the concomitant infusion of [6,6 (2)H2]glucose to derive insulin-mediated suppression of glucose production and insulin-stimulated glucose disposal in nine older, overweight individuals (body mass index 28.1 +- 1.7 kg m(-2); 39.9% +- 1.9% fat). Octreotide 24-34 insulin Homo sapiens 154-161 27258938-5 2016 During the hyperglycemic clamps, endogenous insulin and C-peptide secretion were inhibited by infusion of the somatostatin analogue octreotide. Octreotide 132-142 insulin Homo sapiens 44-51 25324442-3 2015 Octreotide, a somatostatin analog, suppresses insulin secretion from pancreatic beta cells, and is an effective therapy used for both short and long term in the treatment of CHI. Octreotide 0-10 insulin Homo sapiens 46-53 23902932-3 2014 METHODS: We utilized an octreotide, basal glucagon replacement, multistage insulin infusion, and the concomitant infusion of [6,6 (2)H2]glucose to derive insulin-mediated suppression of glucose production and insulin-stimulated glucose disposal in nine older, overweight individuals (body mass index 28.1 +- 1.7 kg m(-2); 39.9% +- 1.9% fat). Octreotide 24-34 insulin Homo sapiens 154-161 23669130-6 2013 Octreotide, a somatostatin analogue, was given on day 4 of admission in an attempt to inhibit any insulin secretion from the pancreas that might be occurring in response to the dextrose infusion and to minimize the amount of fluid being given. Octreotide 0-10 insulin Homo sapiens 98-105 23046209-9 2012 In humans octreotide markedly inhibited insulin release, increased serum glucose concentration, reduced dextrose requirement, prevented recurrent hypoglycemia and was superior to IV dextrose and diazoxide after administration of sulfonylureas. Octreotide 10-20 insulin Homo sapiens 40-47 21538290-8 2011 21 days after one dose of octreotide-LAR injection, insulin response during OGTT significantly decreased, and the Matsuda index increased significantly. Octreotide 26-40 insulin Homo sapiens 52-59 22399695-4 2012 Insulin sensitivity was assessed directly with insulin suppression test by measuring steady-state plasma glucose (SSPG) concentration during a 240-min infusion of octreotide, glucose, and insulin. Octreotide 163-173 insulin Homo sapiens 0-7 22408121-9 2012 Octreotide given prior to the OGTT attenuated both the GLP1 and insulin responses and abolished hypoglycaemia. Octreotide 0-10 insulin Homo sapiens 64-71 21911723-2 2011 This trial was undertaken to assess whether octreotide would lower insulin and IGF-1 levels and reduce risk of breast cancer recurrence. Octreotide 44-54 insulin Homo sapiens 67-74 21911723-11 2011 CONCLUSION: Octreotide-related changes in circulating IGF-1 and C-peptide levels were statistically significant. Octreotide 12-22 insulin Homo sapiens 64-73 21538290-12 2011 During octreotide-LAR treatment, the early-phase insulin response to OGTT is reduced and plasma glucose levels remained normal in most patients. Octreotide 7-17 insulin Homo sapiens 49-56 20723227-7 2010 Whether this could be ascribed to the effects of octreotide on the insulin requirement or on the GH/IGF-axis remains to be elucidated. Octreotide 49-59 insulin Homo sapiens 67-74 20723227-4 2010 Subsequently, adjuvant infusion of octreotide was applied (3.5 mug/kg/h), suppressing growth hormone (GH) and IGF-1 production and necessitating the insulin dose to be reduced to 0.05 - 0.025 units/kg/h. Octreotide 35-45 insulin Homo sapiens 149-156 17917813-10 2008 Octreotide LAR reduced GH, IGF-1 and insulin resistance index but did not alter levels of CRP and NT-pro BNP. Octreotide 0-10 insulin Homo sapiens 37-44 20484012-6 2010 Compared with the control condition, infusion of octreotide reduced plasma insulin levels in lean (from approximately 3.5 to 0.5 microU/ml) and in obese (from approximately 9 to 2 microU/ml), blunted the exercise-induced rise in plasma GH and epinephrine levels in both groups, and enhanced the exercise-induced natriuretic peptide (NP) levels in lean but not in obese subjects. Octreotide 49-59 insulin Homo sapiens 75-82 18778119-3 2008 Somatostatin and its analogues (octreotide and lanreotide) bind to somatostatin subtype 5 receptors on the beta-cell membrane, which limits insulin release and, consequently, may decrease adipogenesis. Octreotide 32-42 insulin Homo sapiens 140-147 19963157-7 2009 The oral octreotide/insulin suppression test suppressed endogenous insulin secretion for the first 100 minutes of the study. Octreotide 9-19 insulin Homo sapiens 67-74 19417097-5 2009 Infusion of octreotide suppressed plasma insulin and growth hormone levels at rest and during exercise. Octreotide 12-22 insulin Homo sapiens 41-48 19625744-2 2009 Since octreotide inhibits endogenous insulin secretion, the cognitive effects of insulin and octreotide may not be independent. Octreotide 6-16 insulin Homo sapiens 37-44 18353876-8 2008 In conclusion, 1) hyperfiltration responses to ARG require the concurrent, modest, permissive increase in insulin; 2) inhibition of insulin release after ARG reduces proximal reabsorption and prevents the hyperfiltration response; and 3) inhibition of ANG II activity restores the hyperfiltration response, maintains parallel increases in proximal reabsorption, and overrides the arginine/octreotide actions. Octreotide 389-399 insulin Homo sapiens 132-139 18630821-3 2008 Octreotide improves the result of hypertonic glucose infusion in sulfonylurea derivatives intoxications, by blocking insulin release. Octreotide 0-10 insulin Homo sapiens 117-124 18345397-8 2008 CONCLUSIONS: In this series, treatment with octreotide LAR led to a worsening of glucose tolerance in three non-diabetic patients and worsened glycemic control in two diabetics, in spite of reducing insulin resistance. Octreotide 44-54 insulin Homo sapiens 199-206 16423593-1 2006 OBJECTIVE: To assess the use of oral glucose tolerance testing (OGTT) to predict efficacy of insulin sensitization (metformin) or suppression (octreotide) because insulin resistance and insulin hypersecretion may impact pharmacotherapeutic efficacy in obese children. Octreotide 143-153 insulin Homo sapiens 163-170 17185803-12 2006 For treatment of DKA, insulin need was very high in the first days after the onset of ketoacidosis, but decreased after initiation of treatment with octreotide and after successful operation. Octreotide 149-159 insulin Homo sapiens 22-29 16158082-0 2006 A multicenter, randomized, double-blind, placebo-controlled, dose-finding trial of a long-acting formulation of octreotide in promoting weight loss in obese adults with insulin hypersecretion. Octreotide 112-122 insulin Homo sapiens 169-176 17339747-4 2007 There are some reports that insulinogenic index is lower in most Japanese patients with type 2 diabetes mellitus and that early insulin secretions are significantly suppressed after administration of octreotide LAR. Octreotide 200-210 insulin Homo sapiens 28-35 17285009-3 2007 Specific risk factors for hypoglycemia in the intensive care unit with intensive insulin therapy are diabetes, octreotide therapy, nutrition support, continuous venovenous hemofiltration with bicarbonate replacement fluid, sepsis and need for inotropic support. Octreotide 111-121 insulin Homo sapiens 81-88 17229659-8 2006 In 3 of the 6 study subjects, measurements of insulin and C-peptide levels both before and after treatment confirmed the efficacy of the octreotide therapy. Octreotide 137-147 insulin Homo sapiens 46-53 17229659-8 2006 In 3 of the 6 study subjects, measurements of insulin and C-peptide levels both before and after treatment confirmed the efficacy of the octreotide therapy. Octreotide 137-147 insulin Homo sapiens 58-67 16423593-13 2006 Efficacy of octreotide was predicted by insulin hypersecretion and sensitivity. Octreotide 12-22 insulin Homo sapiens 40-47 16356235-6 2005 Octreotide inhibits the secretion of several neuropeptides, including insulin, and has successfully been used to control life-threatening hypoglycaemia caused by insulinoma or persistent hyperinsulinaemic hypoglycaemia of infancy. Octreotide 0-10 insulin Homo sapiens 70-77 16284426-10 2005 Insulin suppression test using 50 microg of octreotide improved plasma glucose and IRI levels, suggesting the usefulness of the treatment, and a monthly administration of 20 mg of long-acting octreotide has successfully controlled her symptoms of hypoglycemia for 10 months. Octreotide 44-54 insulin Homo sapiens 0-7 15827099-10 2005 Conversely, octreotide produced an additional decrease in fasting (P = 0.018) and glucose-stimulated (P = 0.038) insulin levels, an increase in IGFBP-2 (P = 0.042) and IGFBP-3 (P = 0.047), and an improvement in hirsutism (P = 0.004). Octreotide 12-22 insulin Homo sapiens 113-120 15649100-8 2005 In acromegaly, preliminary observations on new octreotide analogs with greater specificity for somatostatin-receptor subtypes indicate that these compounds achieve better control of GH hypersecretion than octreotide, but may also negatively influence insulin release. Octreotide 47-57 insulin Homo sapiens 251-258 15279081-12 2004 CONCLUSION: Our study demonstrates that: 1) octreotide treatment can be effective in controlling endogenous hyperinsulinism during pregnancy; 2) octreotide does not affect physiological changes during pregnancy such as insulin-resistance or placental GH level; 3) exposure of the foetus to octreotide throughout pregnancy does not induce any malformation and does not affect foetal development. Octreotide 44-54 insulin Homo sapiens 113-120 15314628-3 2004 We examined changes in REE and leptin in a cohort of 17 obese subjects during experimental weight loss therapy with the insulin-suppressive agent octreotide-LAR, 40 mg i.m. Octreotide 146-160 insulin Homo sapiens 120-127 14988241-4 2004 Insulin resistance was quantified by determining the steady-state plasma glucose (SSPG) concentration in response to an infusion of octreotide, glucose, and insulin, and degree of adiposity was assessed by BMI. Octreotide 132-142 insulin Homo sapiens 0-7 14984323-1 2004 To assess a possible influence of short-term administration of somatostatin on remission development in adult patients with newly diagnosed diabetes mellitus type 1, the somatostatin analog octreotide was given for two weeks after the establishment of the diagnosis at the daily dose of 150 microg subcutaneously in addition to the regular insulin and metabolic therapy. Octreotide 190-200 insulin Homo sapiens 340-347 14984323-3 2004 Moreover, remission also appeared in patients from the octreotide group with lower endogenous residual secretion of insulin (basal C peptide at the time of diagnosis in patients who later entered remission was 0.23+/-0.16 nmol/l vs. 0.34+/-.18 nmol/l in the control group, p<0.05). Octreotide 55-65 insulin Homo sapiens 116-123 12582462-6 2002 Somatostatin analogues such as octreotide have shown promise as a safe and effective treatment for severe proliferative diabetic retinopathy by blocking the local and systemic production of growth hormone and insulin-like growth factor type 1 associated with angiogenesis and endothelial cell proliferation. Octreotide 31-41 insulin Homo sapiens 209-216 14640992-0 2003 Insulin sensitivity and glucose tolerance improve in patients with acromegaly converted from depot octreotide to pegvisomant. Octreotide 99-109 insulin Homo sapiens 0-7 12898472-7 2003 Endogenous insulin secretion was inhibited by octreotide (0.43 microg kg(-1). Octreotide 46-56 insulin Homo sapiens 11-18 14576502-4 2003 CONCLUSION: We demonstrated that the SSTR 2 agonist and octreotide significantly suppressed insulin secretion. Octreotide 56-66 insulin Homo sapiens 92-99 14510913-3 2003 Twenty-four active acromegalic patients were studied in order to determine the long-term effects of octreotide-LAR and SR-lanreotide on insulin sensitivity and carbohydrate metabolism. Octreotide 100-110 insulin Homo sapiens 136-143 12788859-7 2003 OGTT documented Delta insulin response (peak - basal) of -417 +/- 304 pM after octreotide vs. +216 +/- 215 pM after placebo (P = 0.034). Octreotide 79-89 insulin Homo sapiens 22-29 12788859-9 2003 For the octreotide group, changes in quality of life positively correlated with changes in insulin response (P = 0.041). Octreotide 8-18 insulin Homo sapiens 91-98 12788859-12 2003 Octreotide suppressed insulin, and stabilized weight and BMI. Octreotide 0-10 insulin Homo sapiens 22-29 12727951-9 2003 In patients without diabetes mellitus, serum insulin levels in the surgical group were 19.7 +/- 5.4 microU/ml before surgery and fell to 9.7 +/- 0.93 microU/ml after surgery (P = 0.05); levels in the octreotide group were 13.9 +/- 2.8 microU/ml before and fell to 11.2 +/- 2.8 microU/ml on octreotide (P = 0.03). Octreotide 200-210 insulin Homo sapiens 45-52 12727951-9 2003 In patients without diabetes mellitus, serum insulin levels in the surgical group were 19.7 +/- 5.4 microU/ml before surgery and fell to 9.7 +/- 0.93 microU/ml after surgery (P = 0.05); levels in the octreotide group were 13.9 +/- 2.8 microU/ml before and fell to 11.2 +/- 2.8 microU/ml on octreotide (P = 0.03). Octreotide 290-300 insulin Homo sapiens 45-52 12379575-3 2002 METHODS AND RESULTS: Plasma glucose levels were acutely raised in 20 control and 15 IGT subjects and maintained at 15 mmol/L for 5 hours while endogenous insulin secretion was blocked with octreotide. Octreotide 189-199 insulin Homo sapiens 154-161 12225719-3 2002 METHODS: Insulin resistance was quantified by determining the steady-state plasma glucose (SSPG) concentration during the last 30 min of a 180-min infusion of octreotide, glucose, and insulin. Octreotide 159-169 insulin Homo sapiens 9-16 11833058-2 2002 Insulin-mediated glucose disposal was quantified by the insulin suppression tests, in which the height of the steady-state plasma glucose (SSPG) concentration during the last 30 minutes of a 180-minute infusion of octreotide, insulin, and glucose provides an estimate of insulin resistance. Octreotide 214-224 insulin Homo sapiens 0-7 11931620-1 2002 Somatostatin-14 (somatostatin) and its clinically available analogues octreotide, lanreotide, and vapreotide are potent inhibitors of growth hormone, insulin, and glucagon release. Octreotide 70-80 insulin Homo sapiens 150-157 12081231-2 2002 Ninety minutes after administration, octreotide acetate increased the plasma concentration of uridine by 15% and decreased the plasma concentration of glucagon by 24% and that of insulin to below the detection limits. Octreotide 37-55 insulin Homo sapiens 179-186 12081231-5 2002 From these results, we speculated that octreotide acetate decreases the urinary excretion of uric acid by decreasing the concentration of glucagon and/or urinary excretion of sodium, and increases the plasma concentration of uridine via decreased concentrations of glucagon and insulin. Octreotide 39-57 insulin Homo sapiens 278-285 11932320-8 2002 In contrast, octreotide significantly increased fasting plasma glucose, lowered fasting plasma insulin, and led to deterioration in glucose tolerance; three subjects developed impaired glucose tolerance and one diabetes mellitus by World Health Organization criteria. Octreotide 13-23 insulin Homo sapiens 95-102 11932320-9 2002 Octreotide significantly impaired stimulated release of cholecystokinin, gastrin, insulin, and pancreatic polypeptide. Octreotide 0-10 insulin Homo sapiens 82-89 12071296-5 2002 Insulin resistance was measured by the Insulin Suppression Test using Octreotide. Octreotide 70-80 insulin Homo sapiens 0-7 12071296-5 2002 Insulin resistance was measured by the Insulin Suppression Test using Octreotide. Octreotide 70-80 insulin Homo sapiens 39-46 12002412-0 2002 Effects of octreotide on serum insulin-like growth factor I and insulin-like growth factor binding proteins in patients with cirrhosis. Octreotide 11-21 insulin Homo sapiens 31-38 11137181-1 2001 Aim of this study was to investigate whether octreotide, a synthetic somatostatin analogue that inhibits growth hormone, insulin and glucagon secretion and improves glycaemic control in insulin dependent diabetic patients was able to exert similar effects in insulin treated type 2 diabetic patients with chronic renal failure who have high plasma glucagon levels. Octreotide 45-55 insulin Homo sapiens 121-128 12501980-5 2001 Thereafter, he reduced insulin by 30 to 50% for the first week after each LAR-octreotide injection, and gradually increased it again over the next 3 weeks. Octreotide 78-88 insulin Homo sapiens 23-30 11165689-5 2001 Glucose utilisation increased after octreotide (insulin 0.5 mU kg(-1) min(-1) clamp 3.09+/-0.23 vs. 4.19+/-0.19 mg kg(-1) min(-1); 1 mU kg(-1) min(-1) clamp 5.64+/-0.61 vs. 7.93+/-0.57 mg kg(-1) min(-1); both P<0.05) and endogenous glucose production was similarly suppressed. Octreotide 36-46 insulin Homo sapiens 48-55 10966898-3 2000 DESIGN: Insulin-mediated glucose disposal was determined in 36 healthy, nondiabetic volunteers by measuring their steady-state plasma insulin (SSPI) and glucose (SSPG) concentrations in response to a 180-min constant infusion of octreotide, insulin, and glucose. Octreotide 229-239 insulin Homo sapiens 8-15 10966898-3 2000 DESIGN: Insulin-mediated glucose disposal was determined in 36 healthy, nondiabetic volunteers by measuring their steady-state plasma insulin (SSPI) and glucose (SSPG) concentrations in response to a 180-min constant infusion of octreotide, insulin, and glucose. Octreotide 229-239 insulin Homo sapiens 134-141 11208511-5 2001 Insulin need was very high in the first days after the onset of ketoacidosis, but was considerably reduced after initiation of treatment with octreotide and after successful re-operation. Octreotide 142-152 insulin Homo sapiens 0-7 11137181-1 2001 Aim of this study was to investigate whether octreotide, a synthetic somatostatin analogue that inhibits growth hormone, insulin and glucagon secretion and improves glycaemic control in insulin dependent diabetic patients was able to exert similar effects in insulin treated type 2 diabetic patients with chronic renal failure who have high plasma glucagon levels. Octreotide 45-55 insulin Homo sapiens 186-193 11137181-4 2001 Octreotide treatment lowered endogenous insulin secretion (evaluated by C-Peptide levels assay), GH and glucagon in all patients, but caused a significant reduction of daily insulin requirement (32 +/- 14 I.U. Octreotide 0-10 insulin Homo sapiens 40-47 11137181-4 2001 Octreotide treatment lowered endogenous insulin secretion (evaluated by C-Peptide levels assay), GH and glucagon in all patients, but caused a significant reduction of daily insulin requirement (32 +/- 14 I.U. Octreotide 0-10 insulin Homo sapiens 72-81 11137181-4 2001 Octreotide treatment lowered endogenous insulin secretion (evaluated by C-Peptide levels assay), GH and glucagon in all patients, but caused a significant reduction of daily insulin requirement (32 +/- 14 I.U. Octreotide 0-10 insulin Homo sapiens 174-181 11137181-7 2001 The lowering effect of octreotide on insulin requirement in diabetic patients with renal failure in spite of the contemporaneous inhibition on insulin secretion could be explained on the basis of the greater reduction of glucagon levels which are very elevated in these patients as compared to patients with normal renal function. Octreotide 23-33 insulin Homo sapiens 37-44 10969848-6 2000 Using an octreotide-based quantification of insulin sensitivity, 8 of the remaining 10 study subjects showed pronounced insulin resistance, reflecting a significant difference from the control group (P = 0.001). Octreotide 9-19 insulin Homo sapiens 44-51 10601077-6 1999 Our study is the first report showing that: (i) octreotide does not appear to significantly influence pituitary release of gonadotrophins in this group of PCOS patients; (ii) octreotide is able to reduce insulin release, LH and androgen concentrations in lean PCOS patients with hyperinsulinaemia. Octreotide 175-185 insulin Homo sapiens 204-211 11036882-0 2000 Crucial role of insulin in leptin maintenance: profound decrease in serum leptin by octreotide acetate in insulinoma subjects. Octreotide 84-102 insulin Homo sapiens 16-23 11036882-2 2000 Octreotide acetate induced a prompt decrease in serum insulin level, accompanied with an increase in plasma glucose in both patients. Octreotide 0-18 insulin Homo sapiens 54-61 11036882-3 2000 Following the decrease in serum insulin level, serum leptin concentrations were profoundly decreased by 66% and 44%, 8-12 hrs after octreotide injection; that is, the concentrations decreased from 41.1 to 13.8 ng/ml in patient 1, and from 17.5 to 9.8 ng/ml in patient 2. Octreotide 132-142 insulin Homo sapiens 32-39 10811590-4 2000 In another study, octreotide was infused during the hyperglycemic clamp to block the release of endogenous insulin; this prevented the late fall of plasma sICAM-l levels observed in under control clamp conditions. Octreotide 18-28 insulin Homo sapiens 107-114 10566126-0 1999 The effect of octreotide on glucose and insulin levels in a patient with type 2 diabetes on glibenclamide. Octreotide 14-24 insulin Homo sapiens 40-47 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 insulin Homo sapiens 14-21 10377503-9 1999 During the oGTT, octreotide initially almost abolished the early (0-60 min) and diminished the late (60-180 min) GLP-1 and insulin responses in patients and healthy subjects. Octreotide 17-27 insulin Homo sapiens 123-130 10377503-14 1999 During the St-M the GLP-1 and insulin responses were similarly suppressed by octreotide and recovered during ongoing treatment (GLP-1: 49.6% of pretreatment at D1 versus 79.0% at M6 in NFA and 46.9 versus 52.9% in GHA. Octreotide 77-87 insulin Homo sapiens 30-37 10377503-19 1999 The early insulin response (0-30 min) was abolished by octreotide, followed by a reduced peak at 60 min. Octreotide 55-65 insulin Homo sapiens 10-17 10377503-27 1999 CONCLUSIONS: Octreotide abolishes the early and diminishes the late GLP-1 and insulin responses to oGTT and St-M in NFA and GHA patients and in healthy subjects. Octreotide 13-23 insulin Homo sapiens 78-85 10333081-6 1999 Insulin, GIP and GLP-1 secretion post-carbohydrate was markedly reduced by octreotide in lean and obese subjects. Octreotide 75-85 insulin Homo sapiens 0-7 9768695-8 1998 Therefore, the clinical efficacy of octreotide on glucagon and insulin release can be explained by the presence of sst2A receptors in human A and B pancreatic islet cells. Octreotide 36-46 insulin Homo sapiens 63-70 10065781-9 1999 RESULT(S): Octreotide significantly reduced levels of fasting insulin, insulin-like growth factor 1, and LH in both clomiphene citrate- and urinary FSH-stimulated cycles. Octreotide 11-21 insulin Homo sapiens 62-69 9829612-9 1998 Two patients treated with prednisone or octreotide had insulin levels similar to those of normal TPN children. Octreotide 40-50 insulin Homo sapiens 55-62 9836524-4 1998 Octreotide was infused to suppress endogenous insulin release, and tritiated glucose methodology was used to measure glucose uptake and disposal rates. Octreotide 0-10 insulin Homo sapiens 46-53 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 insulin Homo sapiens 98-105 9657106-5 1998 During the baseline (pre-octreotide) study, patients demonstrated a significant decrease in insulin-mediated glucose uptake compared with controls (5.75 +/- 0.21 vs. 7.98 +/- 0.84 mg/kg/min; P < .03), which was entirely accounted for by an impairment in non-oxidative glucose disposal (P < .04). Octreotide 25-35 insulin Homo sapiens 92-99 9657106-6 1998 Four-day infusion of octreotide to cirrhotic patients: 1) reduced postabsorptive and meal-stimulated plasma insulin levels by approximately 35% to 45% without significantly affecting glucose tolerance; 2) did not significantly alter plasma free fatty acids (FFA), growth hormone, and glucagon levels in the postabsorptive state and during the meal test; 3) normalized insulin-mediated whole-body glucose disposal (7.63 +/- 0.72 mg/kg/min post-octreotide; P = not significant vs. control). Octreotide 21-31 insulin Homo sapiens 108-115 9657106-7 1998 Restoration of insulin-mediated glucose utilization was entirely caused by normalization of non-oxidative glucose disposal; 4) was associated with a considerably more pronounced stimulation by insulin of the fractional glycogen synthase in muscle compared with pre-octreotide results (increment above baseline pre: 0.035 +/- 0.010 vs. post: 0.060 +/- 0.023 nmol/min/mg protein; P < .04). Octreotide 265-275 insulin Homo sapiens 15-22 9854458-12 1998 There were no significant differences in plasma glucose responses between groups: however, after octreotide, the hypertensive subjects had a greater insulin suppression than the controls (P < 0.02). Octreotide 97-107 insulin Homo sapiens 149-156 9766261-0 1998 Different effects of octreotide by continuous night infusion at increasing rate or by evening injections at different times on morning hyperglycemia and growth hormone levels in insulin-dependent diabetic patients. Octreotide 21-31 insulin Homo sapiens 178-185 9540027-11 1998 Diazoxide inhibits hormonal release directly on the beta-cells, whereas octreotide exerts its effect indirectly, presumably by multiple actions on insulin sensitivity and insulin-releasing hormones. Octreotide 72-82 insulin Homo sapiens 147-154 9854458-5 1998 In one of these tests the endogenous insulin response was inhibited with subcutaneous octreotide. Octreotide 86-96 insulin Homo sapiens 37-44 9854458-11 1998 Octreotide completely abolished the immediate insulin response to glucose in all subjects (both P < 0.0001) and caused a delayed and significantly increased glycaemic response in both groups (P < 0.0001). Octreotide 0-10 insulin Homo sapiens 46-53 9688372-5 1998 This increase was associated with a decrease in insulin-like growth factor-I (IGF-I) and IGF binding protein-3 (IGFBP-3) concentrations during treatment with octreotide, but not with a decrease in insulin concentrations. Octreotide 158-168 insulin Homo sapiens 48-55 9540027-11 1998 Diazoxide inhibits hormonal release directly on the beta-cells, whereas octreotide exerts its effect indirectly, presumably by multiple actions on insulin sensitivity and insulin-releasing hormones. Octreotide 72-82 insulin Homo sapiens 171-178 15511959-3 1997 Octreotide significantly reduced LH (31.8%), insulin (52%), IGF-1 (14%), androstenedione (22.6%) and testosterone (20%) and increased IGFBP-3 (25%). Octreotide 0-10 insulin Homo sapiens 45-52 9483371-7 1997 The failure of octreotide to diminish glycaemic values and HGP in type 2 diabetic patients in spite of its ability to lower GH and glucagon may probably depend on temporary blockage of residual endogenous insulin secretion induced by octreotide administration. Octreotide 15-25 insulin Homo sapiens 205-212 9329359-8 1997 In 3 of the 7 patients with diabetes mellitus, treatment with OCT together with low carbohydrate intake normalized blood glucose levels, whereas in 2 patients, insulin could be replaced by oral antidiabetics, and in 2 patients, the insulin dose was reduced. Octreotide 62-65 insulin Homo sapiens 232-239 9187410-6 1997 PAI-1, FVII and fibrinogen levels were significantly correlated with the degree of insulin resistance estimated by the steady state plasma glucose concentration (SSPG) during the continuous infusion of glucose, insulin and octreotide. Octreotide 223-233 insulin Homo sapiens 83-90 9294779-1 1997 Octreotide, a synthetic analogue of somatostatin, may improve metabolic control and reduce GH and glucagon levels in insulin-dependent diabetic patients. Octreotide 0-10 insulin Homo sapiens 117-124 9231061-3 1997 Functional somatostatin receptors were present as octreotide administration decreased basal glucagon and insulin secretion by 52 and 74%, respectively. Octreotide 50-60 insulin Homo sapiens 105-112 9213172-7 1997 In this case, octreotide appears to have improved the insulin sensitivity by reducing the plasma GH level. Octreotide 14-24 insulin Homo sapiens 54-61 9126794-9 1997 Octreotide abolished the insulin postprandial response with no major change in glycemic control. Octreotide 0-10 insulin Homo sapiens 25-32 8770012-5 1996 Octreotide abolished the plasma insulin response to intraduodenal glucose and reversed the changes in ratings and eating behavior. Octreotide 0-10 insulin Homo sapiens 32-39 8905479-0 1996 Effect of chronic treatment with octreotide nasal powder on serum levels of growth hormone, insulin-like growth factor I, insulin-like growth factor binding proteins 1 and 3 in acromegalic patients. Octreotide 33-43 insulin Homo sapiens 92-99 8905479-0 1996 Effect of chronic treatment with octreotide nasal powder on serum levels of growth hormone, insulin-like growth factor I, insulin-like growth factor binding proteins 1 and 3 in acromegalic patients. Octreotide 33-43 insulin Homo sapiens 122-129 8905479-12 1996 During chronic octreotide treatment, positive correlations were found between GH and IGF-I, GH and IGFBP-3, IGF-I and IGFBP-3, insulin and IGFBP-3 and insulin and IGF-I. Octreotide 15-25 insulin Homo sapiens 127-134 8905479-12 1996 During chronic octreotide treatment, positive correlations were found between GH and IGF-I, GH and IGFBP-3, IGF-I and IGFBP-3, insulin and IGFBP-3 and insulin and IGF-I. Octreotide 15-25 insulin Homo sapiens 151-158 8884164-13 1996 In refractory hypoglycaemia due to hyperinsulinaemia such as during sulphonylurea overdosage or quinine treatment, the long-acting somatostatin, octreotide, may suppress insulin release and restore euglycaemia. Octreotide 145-155 insulin Homo sapiens 40-47 8710037-4 1996 Treatments aimed at decreasing endogenous insulin secretion by either dietary intervention alone or in combination with acarbose, octreotide or diazoxide had only limited success, while a 2-week course of immunosuppression with prednisone was without any antihypoglycaemic effect. Octreotide 130-140 insulin Homo sapiens 42-49 8667198-6 1996 Late hypoglycemia was prevented by octreotide, and peak fed insulin levels were reduced from 87 +/- 15 to 26 +/- 9 microU/ml after octreotide (P < .05). Octreotide 131-141 insulin Homo sapiens 60-67 7672138-12 1995 Octreotide significantly reduced insulin and LH exaggerated response to GnRH stimulus, as well as the A and T circulating levels, only in the hyperinsulinemic group. Octreotide 0-10 insulin Homo sapiens 33-40 8720524-4 1996 Insulin sensitivity was determined by the steady-state plasma glucose (SSPG) method using Sandostatin. Octreotide 90-101 insulin Homo sapiens 0-7 8822314-10 1995 These results indicate that octreotide improves insulin resistance at the insulin receptor site by lowering plasma levels of GH and insulin in acromegalic patients with glucose intolerance. Octreotide 28-38 insulin Homo sapiens 48-55 8596492-1 1996 To examine the effect of the somatostatin analog, octreotide, on insulin-mediated glucose uptake, seven insulin-dependent diabetic (IDDM) subjects were studied with and without 4 days of continuous subcutaneous octreotide administration (1 mg/kg/d). Octreotide 50-60 insulin Homo sapiens 65-72 8596492-6 1996 Insulin requirements were reduced during octreotide administration, resulting in significantly lower insulin levels (27.3 +/- 2.7 v 39.9 +/- 9.9 mU/L, P < .5). Octreotide 41-51 insulin Homo sapiens 0-7 8596492-6 1996 Insulin requirements were reduced during octreotide administration, resulting in significantly lower insulin levels (27.3 +/- 2.7 v 39.9 +/- 9.9 mU/L, P < .5). Octreotide 41-51 insulin Homo sapiens 101-108 8596492-11 1996 In conclusion, a low-dose octrotide infusion for 4 days to IDDM subjects leads to significantly increased insulin sensitivity. Octreotide 26-35 insulin Homo sapiens 106-113 8813473-0 1996 Calcium reverses octreotide inhibition of insulin and glucagon levels in patients with insulinoma and glucagonoma. Octreotide 17-27 insulin Homo sapiens 42-49 8813473-5 1996 Patients A and B had elevated fasting plasma levels of glucagon and insulin, respectively, which were reduced by octreotide therapy by 73 and 50%, respectively. Octreotide 113-123 insulin Homo sapiens 68-75 8553400-5 1996 Insulin sensitivity was determined by the steady state plasma glucose method with the use of octreotide acetate. Octreotide 93-111 insulin Homo sapiens 0-7 7792821-8 1995 Octreotide profoundly reduced the elevated plasma insulin concentrations seen with cortisol administration but had no effect on the rise in blood pressure. Octreotide 0-10 insulin Homo sapiens 50-57 8534589-3 1995 Nevertheless, IV injection of somatostatin and octreotide resulted in a significant decrease in peripheral insulin levels. Octreotide 47-57 insulin Homo sapiens 107-114 7762630-3 1995 Constant octreotide infusion 1) decreased postabsorptive and meal-stimulated plasma insulin levels by approximately 30-40% but did not significantly alter overall glucose tolerance, free fatty acid, growth hormone, and glucagon levels and 2) was associated with significant increases in insulin-mediated whole body glucose disposal (pre-drug: 10.29 +/- 0.49 vs. postdrug: 11.42 +/- 0.72 mg.kg-1.min-1, P < 0.04), nonoxidative glucose disposal (6.82 +/- 0.57 vs. 7.68 +/- 0.62, P < 0.03), and fractional glycogen synthase activity (0.14 +/- 0.03 vs. 0.20 +/- 0.04 mU/mg protein, P < 0.02). Octreotide 9-19 insulin Homo sapiens 84-91 7762630-3 1995 Constant octreotide infusion 1) decreased postabsorptive and meal-stimulated plasma insulin levels by approximately 30-40% but did not significantly alter overall glucose tolerance, free fatty acid, growth hormone, and glucagon levels and 2) was associated with significant increases in insulin-mediated whole body glucose disposal (pre-drug: 10.29 +/- 0.49 vs. postdrug: 11.42 +/- 0.72 mg.kg-1.min-1, P < 0.04), nonoxidative glucose disposal (6.82 +/- 0.57 vs. 7.68 +/- 0.62, P < 0.03), and fractional glycogen synthase activity (0.14 +/- 0.03 vs. 0.20 +/- 0.04 mU/mg protein, P < 0.02). Octreotide 9-19 insulin Homo sapiens 287-294 7642173-0 1995 Long-term effect of octreotide in acromegaly on insulin resistance. Octreotide 20-30 insulin Homo sapiens 48-55 7534239-1 1995 OBJECTIVE: To determine if the somatostatin analog, octreotide, affects insulin and related peptides and, hence, androgen levels differently between polycystic ovary syndrome (PCOS) patients and controls. Octreotide 52-62 insulin Homo sapiens 72-79 7534239-10 1995 Octreotide reduced fasting insulin levels significantly but to a similar degree in control and PCOS patients (77% and 90%, respectively). Octreotide 0-10 insulin Homo sapiens 27-34 7534239-15 1995 Although no significant changes could be demonstrated in ovarian androgens after a single dose, octreotide effectively reduced serum LH and insulin and, as such, may prove useful in treating some patients with PCOS. Octreotide 96-106 insulin Homo sapiens 140-147 9420847-8 1995 Daytime fasting and administration of Sandostatin were accompanied by rapid and sustained increases in IGFBP-1 when insulin levels declined to 54 +/- 20 pmol/L. Octreotide 38-49 insulin Homo sapiens 116-123 7525123-0 1994 Inverse correlation between insulin-like growth factor binding protein-1 and insulin in patients with acromegaly during treatment with the somatostatin analogue octreotide. Octreotide 161-171 insulin Homo sapiens 28-35 7525123-6 1994 Serum insulin was determined at 0700, 0800 and 0900 h, and serum IGF-I at 0700 h. RESULTS: Octreotide increased the daily mean IGFBP-1 level by 43% on day 8 and by 35% on day 14. Octreotide 91-101 insulin Homo sapiens 6-13 7525123-8 1994 Octreotide treatment significantly suppressed the insulin levels on all observation days by 40-48% compared to placebo. Octreotide 0-10 insulin Homo sapiens 50-57 7525123-13 1994 CONCLUSIONS: Octreotide treatment, in addition to reducing GH, IGF-I and insulin levels, is associated with an increase in IGFBP-1 concentrations in patients with acromegaly, and it is suggested that the rise in serum IGFBP-1 is a consequence of the decrease in insulin secretion. Octreotide 13-23 insulin Homo sapiens 73-80 8053756-2 1994 In two insulin-dependent diabetic patients with autonomic neuropathy and chronic steatorrheic diarrhea refractory to conventional medications, subcutaneous administration of octreotide markedly improved the volume and frequency of stools in both patients. Octreotide 174-184 insulin Homo sapiens 7-14 8255845-4 1993 Fasting concentrations of proinsulin, and 32-33 split proinsulin, as determined by two-site monoclonal antibody-based immunoradiometric assays, were also suppressed by octreotide. Octreotide 168-178 insulin Homo sapiens 26-36 7988789-0 1994 Evaluation of octreotide to assess insulin-mediated glucose disposal by the insulin suppression test. Octreotide 14-24 insulin Homo sapiens 35-42 7988789-0 1994 Evaluation of octreotide to assess insulin-mediated glucose disposal by the insulin suppression test. Octreotide 14-24 insulin Homo sapiens 76-83 7518781-5 1994 Octreotide therapy improved fluid balance but suppressed gut hormone (insulin, gastrin, glucagon, peptide YY) levels in blood and the uptake of amino acids into pancreatic enzyme and mucosal proteins, increasing oxidative losses. Octreotide 0-10 insulin Homo sapiens 70-77 7917157-11 1994 Insulin concentrations were reduced profoundly after octreotide, both in the control period (12.5 +/- 3.7 mU/L, falling to 1.1 +/- 0.3 mU/L at 30 min) and on cortisol (22.3 +/- 4.5 to 2.3 +/- 0.5 mU/L at 30 min). Octreotide 53-63 insulin Homo sapiens 0-7 7917157-13 1994 Thus, octreotide was effective in lowering plasma insulin concentrations but di not lower blood pressure in normal subjects with cortisol-induced hypertension. Octreotide 6-16 insulin Homo sapiens 50-57 8172227-5 1994 The study revealed that the administration of subcutaneous octreotide resulted in suppression of beta cell function (insulin and c-peptide) but had no effect or a delayed effect on alpha cell secretion (glucagon). Octreotide 59-69 insulin Homo sapiens 117-124 8172227-5 1994 The study revealed that the administration of subcutaneous octreotide resulted in suppression of beta cell function (insulin and c-peptide) but had no effect or a delayed effect on alpha cell secretion (glucagon). Octreotide 59-69 insulin Homo sapiens 129-138 8082872-0 1994 Insulin sensitivity test using a somatostatin analogue, octreotide (Sandostatin). Octreotide 56-66 insulin Homo sapiens 0-7 8082872-0 1994 Insulin sensitivity test using a somatostatin analogue, octreotide (Sandostatin). Octreotide 68-79 insulin Homo sapiens 0-7 8082872-7 1994 In conclusion, measurement of SSPG, using octreotide to suppress endogenous insulin secretion, is a reliable method to assess insulin sensitivity in man. Octreotide 42-52 insulin Homo sapiens 76-83 8049019-0 1994 Octreotide effect on ovarian morphology in insulin-resistant PCOS patients following six-month decapeptyl treatment. Octreotide 0-10 insulin Homo sapiens 43-50 8049019-3 1994 The aim of our study was to analyze the morphologic and hormonal-metabolic response to octreotide therapy for one month in insulin-resistant PCOS patients in whom luteinizing hormone (LH) effect had formerly been separated by a six-month GnRH-agonist (GnRH-a) course. Octreotide 87-97 insulin Homo sapiens 123-130 7911441-10 1994 Octreotide inhibits gastroenteropancreatic secretion, especially of insulin, glucagon, pancreatic polypeptide, gastric inhibitory polypeptide, and gastrin. Octreotide 0-10 insulin Homo sapiens 68-75 8289671-3 1994 Prolonged (270 minutes) hyperglycemic clamps were used to assess octreotide-mediated suppression of glucose-stimulated endogenous insulin secretion. Octreotide 65-75 insulin Homo sapiens 130-137 8289671-4 1994 Compared with a saline-control infusion, octreotide (30 ng/kg/min) suppressed stimulated insulin (P < .0001) and C-peptide (P < .0001) concentrations to basal levels. Octreotide 41-51 insulin Homo sapiens 89-96 8289671-5 1994 During insulin-induced hypoglycemia (plasma glucose < 40 mg/dL), octreotide (30 ng/kg/min) effectively suppressed the secretion of glucagon (P < .05) and growth hormone (P < .0005). Octreotide 68-78 insulin Homo sapiens 7-14 8289671-7 1994 Subsequent infusion of exogenous insulin, glucagon, and growth hormone resulted in predictable and stable concentrations of each hormone during octreotide-mediated suppression of their endogenous secretion. Octreotide 144-154 insulin Homo sapiens 33-40 7963427-7 1994 Octreotide blunted the postprandial increase in serum insulin and glucagon levels observed in the placebo group. Octreotide 0-10 insulin Homo sapiens 54-61 8205258-8 1994 The insulinogenic index (insulin/glucose) response to a glucose challenge decreased uniformly in octreotide-treated patients. Octreotide 97-107 insulin Homo sapiens 4-11 8205258-9 1994 Female patients and those with elevated baseline insulin levels were more likely to develop diabetes mellitus during octreotide therapy. Octreotide 117-127 insulin Homo sapiens 49-56 8215639-8 1993 During one study they, also received an infusion of the somatostatin analogue, octreotide (0.005 micrograms/kg/min), to suppress insulin elaboration for the first 24 hours. Octreotide 79-89 insulin Homo sapiens 129-136 8344648-3 1993 The cirrhotic patients received one week of treatment with 50 micrograms octreotide subcutaneously three times daily which reduced pre-dose fasting insulin levels from 26.2 +/- 7.9 to 18.1 +/- 6.2 mU/l p < 0.005, and post dose levels to 7.0 +/- 3.5 mU/l p < 0.005. Octreotide 73-83 insulin Homo sapiens 148-155 7687525-18 1993 CONCLUSION: The rapid rise of serum IGFBP-1 levels induced by acute hypoglycaemia could be reproduced in euglycaemic conditions with octreotide when insulin secretion was suppressed, whereas IGFBP-1 levels did not rise with hypoglycaemia induced by a prolonged insulin infusion. Octreotide 133-143 insulin Homo sapiens 149-156 8325938-5 1993 A reduced insulin and augmented glucose response to oral glucose during therapy normalized after octreotide withdrawal (insulin, 527 +/- 84, 289 +/- 62, and 733 +/- 110 pmol/L; glucose, 6.2 +/- 0.3, 8.5 +/- 0.4, and 6.8 +/- 0.2 mmol/L; pre-Tx, on and off octreotide, means +/- SE). Octreotide 97-107 insulin Homo sapiens 10-17 1526629-2 1992 The somatostatin analog, octreotide (Sandostatin), widely used in the treatment of acromegaly, is able to produce a decrease in levels of growth hormone (GH), insulin, and Insulin-like Growth Factor 1 (IGF1). Octreotide 25-35 insulin Homo sapiens 159-166 8445035-6 1993 Insulin concentrations were 4-5 times greater with dextrose alone or in combination with diazoxide than with octreotide (P < 0.01). Octreotide 109-119 insulin Homo sapiens 0-7 8422773-3 1993 Subcutaneous octreotide, 50 micrograms 12 hourly, suppressed stimulated endogenous insulin secretion, thereby preventing a further recurrence of hypoglycemia. Octreotide 13-23 insulin Homo sapiens 83-90 7997211-11 1993 In patients with insulin-dependent diabetes mellitus (IDDM) octreotide suppresses GH levels, postprandial blood glucose increases with resultant decrease in daily insulin requirements. Octreotide 60-70 insulin Homo sapiens 17-24 1452087-1 1992 A 22 year old insulin dependent diabetic with high volume, secretory chronic diarrhoea refractory to standard andiarrhoeal drugs was treated with the somatostatin analogue octreotide, 50 micrograms twice daily by subcutaneous injection. Octreotide 172-182 insulin Homo sapiens 14-21 1487608-5 1992 Serum gastrin and insulin levels fell significantly following octreotide infusion, but plasma glucose levels remained unchanged. Octreotide 62-72 insulin Homo sapiens 18-25 1325289-7 1992 When ZR-75-1 tumor cells were exposed in vitro to nanomolar concentrations of octreotide, a dose-dependent inhibition of cell growth was observed in the presence of 5% fetal calf serum or under serum-free conditions using epidermal growth factor, insulin-like growth factor type I, or insulin as growth stimulus. Octreotide 78-88 insulin Homo sapiens 247-254 1325289-7 1992 When ZR-75-1 tumor cells were exposed in vitro to nanomolar concentrations of octreotide, a dose-dependent inhibition of cell growth was observed in the presence of 5% fetal calf serum or under serum-free conditions using epidermal growth factor, insulin-like growth factor type I, or insulin as growth stimulus. Octreotide 78-88 insulin Homo sapiens 285-292 8507446-0 1993 Octreotide, a somatostatin analog, reduces insulin secretion and increases renal Na+ excretion in lean essential hypertensive patients. Octreotide 0-10 insulin Homo sapiens 43-50 8507446-8 1993 Our data showed that octreotide significantly lowered insulin levels in both hypertensives (from 12.2 +/- 2.4 microU/mL at time 0 to undetectable values at time 30 and 60 min) and normotensives (from 11.5 +/- 2.8 microU/mL at time 0, to undetectable values at time 30 and 60 min). Octreotide 21-31 insulin Homo sapiens 54-61 8200182-6 1993 Our data showed that octreotide completely suppressed insulin levels (from time 0 to 60 min). Octreotide 21-31 insulin Homo sapiens 54-61 8200182-9 1993 In conclusion, a short-time insulin suppression, as obtained by the somatostatin analogue octreotide, enhances the natriuretic response to intravenous saline load in lean type II diabetic hypertensives. Octreotide 90-100 insulin Homo sapiens 28-35 8300064-7 1993 During octreotide administration, plasma insulin displayed an early and steep fall (49.7 +/- 4.61% of baseline, p < 0.03, at 60 min) with a tendency to escape from inhibition before termination of the infusion. Octreotide 7-17 insulin Homo sapiens 41-48 7997211-3 1993 Pharmacological effects of octreotide include inhibition of numerous hormones (growth hormone, TSH, insulin, glucagon and all gut hormones), of exocrine secretion (gastric acid, pancreatic enzyme), and of small-bowel absorption. Octreotide 27-37 insulin Homo sapiens 100-107 1526629-2 1992 The somatostatin analog, octreotide (Sandostatin), widely used in the treatment of acromegaly, is able to produce a decrease in levels of growth hormone (GH), insulin, and Insulin-like Growth Factor 1 (IGF1). Octreotide 37-48 insulin Homo sapiens 159-166 1516889-5 1992 Octreotide significantly reduced mean 24 h GH profile (7.2 +/- 0.7 mU/L before; 5.2 +/- 0.5 mU/L on octreotide, p less than 0.01), IGF-I levels (0.62 +/- 0.06 before; 0.47 +/- 0.05 on octreotide, p less than 0.005) mean 24 h blood glucose (14.4 +/- 0.5 mmol/L before; 12.6 +/- 0.4 mmol/L on octreotide, p less than 0.001) and daily insulin requirements (44.8 +/- 3.0 IU before; 37.2 +/- 3.0 IU on octreotide, p less than 0.02). Octreotide 0-10 insulin Homo sapiens 332-339 1516889-8 1992 The results of this study showed that short-term treatment with octreotide given s. c. every eight hours modulates the pattern of GH secretion in C-peptide negative insulin-dependent patients. Octreotide 64-74 insulin Homo sapiens 165-172 2066644-6 1991 Mean serum free insulin levels were significantly (p less than 0.02) greater during octreotide infusion compared with control, despite the similar daily insulin requirements. Octreotide 84-94 insulin Homo sapiens 16-23 1789059-8 1991 Albeit transient, octreotide caused a rapid near total suppression of insulin release in the morning, 15 to 45 min after administration. Octreotide 18-28 insulin Homo sapiens 70-77 1954071-0 1991 Preventive effects of octreotide (SMS 201-995) on diabetic ketogenesis during insulin withdrawal. Octreotide 22-32 insulin Homo sapiens 78-85 1748062-0 1991 Low-dose octreotide is able to cause a maximal inhibition of the glycemic responses to a mixed meal in obese type 2 diabetic patients treated with insulin. Octreotide 9-19 insulin Homo sapiens 147-154 1748062-8 1991 Our findings suggest that with a low dose of octreotide (25 micrograms) it is possible to abolish the postprandial glycemic peak in type 2 diabetic patients treated with insulin. Octreotide 45-55 insulin Homo sapiens 170-177 1653660-12 1991 Octreotide suppressed the release of insulin, glucagon and pancreatic polypeptide in response to feeding and resulted in post-prandial hyperglycaemia. Octreotide 0-10 insulin Homo sapiens 37-44 1563080-0 1992 Impact of octreotide, a long-acting somatostatin analogue, on glucose tolerance and insulin sensitivity in acromegaly. Octreotide 10-20 insulin Homo sapiens 84-91 1563080-10 1992 Insulin infusion during the glucose clamp completely suppressed hepatic glucose production during but not before octreotide treatment (7.9 +/- 2.4 vs 0.7 +/- 2.2 mumol/kg min, P = 0.02). Octreotide 113-123 insulin Homo sapiens 0-7 1563080-13 1992 CONCLUSIONS: Octreotide improves whole body insulin sensitivity by an increased ability of insulin to suppress hepatic glucose production without affecting the substantial impairment of peripheral insulin action. Octreotide 13-23 insulin Homo sapiens 44-51 1563080-13 1992 CONCLUSIONS: Octreotide improves whole body insulin sensitivity by an increased ability of insulin to suppress hepatic glucose production without affecting the substantial impairment of peripheral insulin action. Octreotide 13-23 insulin Homo sapiens 91-98 1495454-0 1992 [Effect of octreotide on blood glucose levels in poorly compensated insulin-dependent diabetics on insulin treatment]. Octreotide 11-21 insulin Homo sapiens 68-75 1495454-0 1992 [Effect of octreotide on blood glucose levels in poorly compensated insulin-dependent diabetics on insulin treatment]. Octreotide 11-21 insulin Homo sapiens 99-106 1970540-7 1990 Pretreatment with SMS 201-995 completely abolished IAPP and insulin secretion to intravenous glucose injection. Octreotide 18-29 insulin Homo sapiens 60-67 2256759-9 1990 Pretreatment with octreotide acetate completely suppressed the rise in plasma insulin response to the meal and this ablated the late hypoglycemia of dumping. Octreotide 18-36 insulin Homo sapiens 78-85 1976930-4 1990 Sandostatin significantly reduced integrated LH concentrations and LH pulse amplitudes, oestradiol, testosterone, and androstenedione concentrations, and LH responses to buserelin; it also suppressed insulin and C-peptide responses to an oral glucose load. Octreotide 0-11 insulin Homo sapiens 200-207 1976930-4 1990 Sandostatin significantly reduced integrated LH concentrations and LH pulse amplitudes, oestradiol, testosterone, and androstenedione concentrations, and LH responses to buserelin; it also suppressed insulin and C-peptide responses to an oral glucose load. Octreotide 0-11 insulin Homo sapiens 212-221 1822761-8 1991 After octreotide, the insulin response in both groups was suppressed. Octreotide 6-16 insulin Homo sapiens 22-29 1975166-2 1990 Sandostatin is an analogue of somatostatin which has characteristics which makes it a better compound for clinical use than native somatostatin: it inhibits GH preferentially over insulin. Octreotide 0-11 insulin Homo sapiens 180-187 34741720-7 2022 In combination, pasireotide sc (150 microg) and octreotide sc (100/300 microg) resulted in numerically greater reductions in insulin levels and a higher incidence of AEs than either single agent; the rapid (within 1 h) increase in plasma glucose after pasireotide was delayed with combination treatment. Octreotide 48-58 insulin Homo sapiens 125-132