Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric inhibitory polypeptide (GIP) is a 42-amino-acid hormone which may have a role in the regulation of insulin secretion. The characterization of cDNA clones encoding this hormone indicates that it is derived by proteolytic processing of a 153-amino-acid precursor. The human gene coding for the human GIP precursor spans approximately 10 kilobase pairs and consists of six exons. Similar to genes encoding other members of the glucagon superfamily, each exon appears to encode a distinct region of the GIP precursor or its mRNA. The promoter region of the human GIP gene contains potential binding sites for a number of transcriptional factors including Sp 1, AP-1, and AP-2. The human GIP gene has been assigned to chromosome 17q21.3----q22.
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PMID:Gastric inhibitory polypeptide: structure and chromosomal localization of the human gene. 273 53

Blood glucose, plasma concentrations of gastric inhibitory polypeptide, insulin, glucagon, cortisol, and thyroid hormones were measured in nonobese and obese human subjects at 30 and 22 degrees C ambient temperature (Ta). Oxygen consumption (VO2), carbon dioxide output (VCO2), and temperatures in the external auditory meatus (Tc) and on the skin surface (Tsk) were also measured. After 1 h, near naked at the chosen Ta, an oral dose of sucrose (approximately 1.5 g/kg) was given and the subjects were then monitored for a further 60 or 90 min. Following sucrose ingestion, both in the nonobese and obese, there were significant (p less than 0.001) increases in the following: glucose, gastric inhibitory polypeptide, insulin, VO2, and respiratory quotient. The effect of Ta on these responses in the nonobese was that gastric inhibitory polypeptide rose more at Ta 30 than at Ta 22 (p less than 0.05) and VO2 rose more at Ta 22 than at Ta 30 (p less than 0.05). In the obese, glucose rose more at Ta 30 than at Ta 22 (p less than 0.02), VO2 rise was less than in the nonobese at Ta 22 (p less than 0.05), and the respiratory quotient was lower than in the nonobese at both Ta 30 and 22 (p less than 0.001). Gastric inhibitory polypeptide changes with respect to Ta in the obese were inconsistent. It is concluded that responses to oral sucrose are modified by environmental temperature.
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PMID:Gastric inhibitory polypeptide, dietary-induced thermogenesis, and obesity. 330 93

The effect of morphine (0.1 mg/kg) on insulin secretion stimulated by oral, intraduodenal, or intravenous administration of glucose was studied in seven healthy volunteers. When glucose was given intravenously, morphine had no effect on plasma glucose, insulin, glucose-dependent insulinotropic polypeptide (GIP), or pancreatic glucagon. Following oral glucose, morphine slowed gastric emptying and reduced plasma concentrations of glucose, insulin, and GIP. 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. We conclude that clinically relevant doses of morphine have no direct effect on insulin secretion and that the changes observed were secondary to slowed gastric emptying and small intestinal transit.
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PMID:Reduction by morphine of human postprandial insulin release is secondary to inhibition of gastrointestinal motility. 351 43

The effect of porcine gastric inhibitory polypeptide on hepatic glycogen metabolism was investigated in the isolated in situ perfused rat liver. Glycogenolysis was stimulated by infusion of glucagon into the portal vein (half maximal effective portal vein concentration approximately 30 pmol/l). When glucagon was infused at a final portal vein concentration of 0.5 nmol/l, simultaneous addition of insulin inhibited the glucagon-dependent glycogenolysis in a dose-dependent way (half maximal effective concentration for insulin about 2 nmol/l). Gastric inhibitory polypeptide alone at a concentration of 1 nmol/l reduced glucagon-dependent glycogenolysis only slightly. However, when infused simultaneously at low insulin concentrations (0.1 nmol/l), gastric inhibitory polypeptide suppressed hepatic glucose production dose-dependently up to 70%. The data suggest that gastric inhibitory polypeptide exerts direct metabolic effects on hepatic glycogen metabolism predominantly in a situation where insulin is simultaneously present, e.g. following ingestion of glucose.
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PMID:Insulin-dependent inhibition of hepatic glycogenolysis by gastric inhibitory polypeptide (GIP) in perfused rat liver. 351 65

The gastroenteropancreatic (GEP) endocrine cells of the Japanese field vole were studied immunohistochemically. Somatostatin-, 5-hydroxytryptamine-, glicentin-, glucagon-, bovine pancreatic polypeptide-, gastrin-, gastric inhibitory polypeptide-, cholecystokinin-, substance P-, secretin-, neurotensin- and insulin-immunoreactive cells were revealed. The characteristic findings of the regional distribution and relative frequency of these immunoreactive cells in the GEP system of the vole were as follows. Somatostatin-immunoreactive cells were more numerous in the oxyntic glands than in the pyloric glands. Some somatostatin-immunoreactive cells were found in small clusters in the oxyntic glands. Gastrin-immunoreactive cells were detected not only in the pyloric glands and small intestine but also in the caecum and spiral colon. Gastric inhibitory polypeptide-immunoreactive cells were also detected in the pyloric glands and no motilin-immunoreactive cell was found in the gastroenteropancreatic system.
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PMID:Immunohistochemical study of gastroenteropancreatic endocrine cells of the herbivorous Japanese field vole, Microtus montebelli. 353 46

Gastric inhibitory polypeptide (GIP) concentrations may be influenced by obesity, diabetes, and glucagon deficiency and be under feedback inhibition by insulin. To assess these factors, insulin-dependent diabetic, totally pancreatectomized diabetic, and lean and obese noninsulin-dependent diabetic patients were studied twice, once during partial insulin withdrawal and again when euglycemia was achieved before and after mixed meal ingestion, using an artificial endocrine pancreas. The results were compared to those from weight-matched lean and obese nondiabetic subjects. No significant differences in postprandial GIP responses were found between lean and obese nondiabetic subjects. Despite basal and postprandial hyperglycemia, the GIP responses to the mixed meal were not significantly different between insulin-deficient (insulin-dependent and totally pancreatectomized) patients and lean nondiabetic subjects. In addition, there were no significant differences in postprandial GIP responses between insulin-dependent and totally pancreatectomized patients. In contrast, lean and obese noninsulin-dependent diabetic patients had reduced GIP responses compared to weight-matched nondiabetic subjects (mean +/- SE, 37.9 +/- 5.4 vs. 67.1 +/- 10.8 ng ml-1 240 min-1, respectively; P less than 0.05). This difference was entirely due to the reduced GIP responses in obese noninsulin-dependent diabetic patients compared to those in obese nondiabetic subjects (32.1 +/- 7.9 vs. 76.9 +/- 18.2 ng ml-1 240 min-1, respectively; P less than 0.05); the postprandial GIP responses were not significantly different between lean noninsulin-dependent diabetic patients and lean nondiabetic subjects. Insulin infusion by an artificial endocrine pancreas resulted in postprandial insulin and glucose profiles that approximated those of nondiabetics, but did not significantly alter GIP responses to the mixed meal (48.2 +/- 5.5 ng ml-1 240 min-1) in the 18 diabetic patients compared to results obtained with sc insulin treatment (42.2 +/- 5.2 ng ml-1 240 min-1). In conclusion, postprandial GIP responses are normal in obese nondiabetic subjects and insulin-deficient diabetic patients and are blunted in obese, but not in lean, noninsulin-dependent diabetic patients. In addition, GIP does not appear to be under feedback inhibition by insulin or influenced by glucagon deficiency in diabetes.
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PMID:Gastric inhibitory polypeptide in obesity and diabetes mellitus. 637 12

Gastrin-releasing peptide (GRP) was infused at two dose levels [GRP I (0-30 min): bolus dose of 1.41 pmol kg-1, followed by 0.12 pmol kg-1 min-1; GRP II (30-60 min): bolus dose of 5.67 pmol kg-1, followed by 1.50 pmol kg-1 min-1] to six normal men to study the pharmacokinetics of GRP using a newly developed RIA and the effect of GRP on gastro-entero-pancreatic hormones and gastric acid secretion. The half-life of disappearance of GRP was 2.8 +/- 0.4 min (+/- SEM). The MCR and the apparent space of distribution were 33.0 +/- 4.0 ml kg-1 min-1 and 133 +/- 31 ml kg-1, respectively. GRP stimulated the secretion of gastrin, pancreatic polypeptide, insulin, glucagon, and glucose-dependent insulinotropic polypeptide in a dose-dependent manner. Gastric acid secretion was stimulated 15 min after the increase in gastrin secretion, suggesting that GRP stimulated gastric acid secretion via release of gastrin. GRP had no significant effect on the secretion of enteroglucagon or neurotensin. In the mammalian gastrointestinal tract, GRP is localized exclusively to nerve tissue. This fact and its potent effects demonstrated here make it a likely candidate for peptidergic nervous control of gastrointestinal function.
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PMID:Gastrin-releasing peptide: pharmacokinetics and effects on gastro-entero-pancreatic hormones and gastric secretion in normal men. 673 5

Gastric inhibitory polypeptide (GIP) is considered to be the principal mediator of the enteroinsular axis. A glucose-insulin clamp technique was used to study the effects of differing blood glucose levels on the insulinotropic and glucagonotropic actions of fat-stimulated GIP in seven healthy subjects, as well as the effect of physiologic hyperinsulinemia on GIP secretion. Blood glucose levels were clamped for 4 h at 43+/-2 mg/dl (hypoglycemic clamp), 88+/-1 mg/dl (euglycemic clamp), and 141+/-2 mg/dl (hyperglycemic clamp) in the presence of a constant insulin infusion (100 m U/kg per h). Under hypoglycemic clamp conditions there was no increase in C-peptide nor glucagon after Lipomul ingestion, despite an increase of GIP of 51.7+/-8.7 ng/ml per 120 min. Under euglycemic clamp conditions, small and inconsistent increases in C-peptide and glucagon were observed after fat ingestion and a concomitant increase of GIP of 35.2+/-9.4 ng/ml per 120 min. Under hyperglycemic clamp conditions after fat ingestion and a GIP increase of 24.0+/-5.7 ng/ml per 120 min, C-peptide increased from 6.4+/-5 ng/ml to 11.0+/-1.1 ng/ml (P < 0.01) but glucagon did not change. These findings confirm that in healthy man GIP exerts its insulinotropic properties only under hyperglycemic conditions and indicate that GIP is not glucagonotropic. Under euglycemic clamp conditions (plasma glucose, 89+/-1 mg/dl) and physiologic hyperinsulinemia (serum immunoreactive insulin, 137+/-3 muU/ml) GIP responses to fat ingestion (39.7+/-9.8 ng/ml per 120 min) were not different from the GIP responses to fat ingestion in the absence of hyperinsulinemia (39.7+/-11.1 ng/ml per 120 min). Therefore, insulin under normoglycemic conditions does not exert an inhibitory effect on fat-stimulated GIP secretion. The higher GIP response to oral fat in the hypoglycemic clamp, and the lower GIP response in the hyperglycemic clamp compared to the response in the euglycemic clamp suggests an effect of glycemia itself on GIP secretion in the presence of hyperinsulinemia.
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PMID:Interaction of fat-stimulated gastric inhibitory polypeptide on pancreatic alpha and beta cell function. 698 57

Gastric inhibitory polypeptide (GIP), pancreatic polypeptide (PP), glucagon, vasoactive intestinal polypeptide (VIP), bombesin, neurotensin, substance P, and cholecystokinin octapeptide (CCK-OP) were examined for their effects upon glucose-stimulated insulin secretion in denervated and isolated islet cells, namely, monolayer cultures of dispersed neonatal rat pancreatic islet cells. Only glucagon (14 nM), GIP (10 and 20 nM), and CCK-OP (20 nM) enhanced glucose-stimulated insulin release during a 60-min incubation period. None of the others altered insulin secretion under the conditions employed, although reported to influence insulin release in other systems.
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PMID:Effect of gut peptides on glucose-stimulated insulin release by monolayer cultures of neonatal rat islet cells. 701 1

Bombesin, a peptide with widespread biological actions, has been demonstrated in human tissues by immunological methods. To investigate its effect in man, synthetic bombesin was infused at low doses in six male volunteers. Bombesin at 2.4 pmol kg-1 min-1 produced significant rises in plasma insulin, glucagon, pancreatic polypeptide, gastrin, cholecystokinin, motilin, glucose-dependent insulinotropic polypeptide, neurotensin, enteroglucagon, vasoactive intestinal polypeptide, and serum calcium. In contrast, bombesin caused a profound fall in parathyroid hormone levels and reduced plasma glucose concentrations. A late rise in plasma calcitonin was also observed. Bombesin had no significant effect on the pituitary hormones, TSH, GH, PRL, or cortisol. No hormonal changes or alterations in calcium were noted during saline infusions. Bombesin has a marked stimulatory effect on gastrointestinal hormones, which is unique and opposite to the effect of somatostatin, a potent inhibitor of gut hormone release. Bombesin also influences calcium-regulating hormones, either directly or through its action on gut hormones. The bombesin concentrations achieved with the dosages used were low enough to indicate a possible physiological role for the endogenous peptide.
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PMID:Bombesin: action on gut hormones and calcium in man. 706 3


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