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)

The effect of intrajejunal (i.j.) infusion of fat on meal-stimulated gastric acid secretion and release of pancreatic glucagon (PG), enteroglucagon (EG), gastric inhibitory polypeptide (GIP), and vasoactive intestinal polypeptide (VIP) was studied in seven healthy volunteers. I.j. fat markedly inhibited meal-stimulated acid secretion as compared to a control study with i.j. saline infusion. The acid inhibition was accompanied by augmental plasma concentrations of EG, GIP, and VIP but not of PG, suggesting that EG, GIP, and VIP may be among mediators of fat-induced jejunal inhibition of acid secretion. Concentration-time relationship makes it unlikely that the observed inhibition could be ascribed to any single peptide studied.
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PMID:Fat-induced jejunal inhibition of gastric acid secretion and release of pancreatic glucagon, enteroglucagon, gastric inhibitory polypeptide, and vasoactive intestinal polypeptide in man. 10 75

Possible interactions between gastric inhibitory polypeptide (GIP) and glucagon were investigated in rat adipocytes. GIP was nonlipolytic and inhibited lipolysis stimulated by glucagon but not that stimulated by secretin or vasoactive intestinal polypeptide (VIP). GIP competed with 125I-glucagon for binding to adipocyte receptors, and at physiologic concentrations inhibited the stimulation of AMP produced by glucagon. Thus GIP acts as an inhibitor of actions of glucagon on adipocytes and may be a physiologic modulator of effects of glucagon.
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PMID:Inhibition of actions of glucagon in adipocytes by gastric inhibitory polypeptide. 18 84

Gastric acid secretion by the parietal cell is a single digestive process involving a continuous interplay between nervous and hormonal stimuli. Gastric acid hypersecretion and hypergastrinemia may represent pathologic disturbance of the normal "gastric phase" of acid secretion (excluded antrum syndrome) or abnormal gastrin secretion from a nongastric source as in the Zollinger-Ellison syndrome. Diagnosis of these two syndromes preoperatively is dependent on immunoassay for serum gastrin. A fall in serum gastrin level after the injection of secretin will distinguish the excluded antrum syndrome from the Zollinger-Ellison syndrome. Which hormone or hormones cause the acid hyposecretion of the watery diarrhea hypokalemia achlorhydria syndrome is still uncertain. Potential candidates include secretin, glucagon (alone or combined with gastrin), vasoactive intestinal peptide and gastric inhibitory polypeptide. Secretin has undergone trials as therapy in peptic ulcer whereas glucagon is under investigation for the treatment of acute pancreatitis because of its dual actions as (1) an enterogastrone and (2) an inhibitor of pancreatic secretion.
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PMID:Current concepts on physiological control of gastric acid secretion. Clinical applications. 23 80

The role of gastrointestinal and pancreatic hormones in regulating liver growth was evaluated by measuring their effect on DNA synthesis in the normal and regenerating liver of rats in vivo and in maintenance cultures of adult rat hepatocytes in vitro. After partial liver resection DNA synthesis reached peak levels after 24 hours while serum concentrations of immunoreactive insulin in portal and peripheral blood at this time were still suppressed. Increase of endogenous insulin levels by intravenous glucose infusion or portal infusion of insulin, glucagon or both together with glucose did not change DNA synthesis in normal or regenerating rat liver. After acute carbon tetrachloride poisoning of rats, survival rate and degree of liver necrosis was not changed by intraperitoneal infusion of glucagon and insulin with glucose. In vitro, insulin, glucagon and somatostatin synergistically stimulated the specific thymidine uptake in seven-day-old maintenance cultures of rat hepatocytes. The hormones did not cause cell multiplication but enhanced cell survival, probably by improving the uptake and utilization of nutrients. Gastrin G-17, secretin and cholecystokinin (contaminated with gastric inhibitory polypeptide) had no effect. It is concluded that the results do not support the contention that liver regeneration is regulated by the known pancreatic hormones. However, a trophic effect of pancreatic hormones on liver cells in vitro could be demonstrated. Gastrointestinal hormones had no such effect.
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PMID:Hepatotrophic effects of pancreatic and gastrointestinal hormones in the rat in vivo and in vitro. 24 3

Effect of synthetic gastric inhibitory polypeptide (GIP) on insulin and glucagon secretion was stuied in vivo and in vitro in the rat. Intravenous administration of 1 microng./kg. GIP along with 0.625 gm./kg. glucose caused a more prominent rise of plasma insulin than did 0.625 gm./kg. glucose alone. The suppression of plasma glucagon levels induced by glucose was attenuated partially but not significantly by the concomitant administration of GIP. GIP (1 microng./kg. i.v.) alone raised both plasma insulin and glucago levels. In in-vitro experiments with isolated pancreatic islets, GIP significantly augmented insulin release induced by either 8.3 mM or 16.7 mM glucose, whereas the augmentation of glucagon release was observed at 3.3 mM, 8.3 MM, and 16.7 mM glucose concentrations. Three peptides, consisting of 1-28, 22-43, and 15-43 amino acids of GIP, failed to potentiate insulin and glucagon secretion. These results suggest that synthetic GIP has a stimulating effect on insulin and glucagon secretion.
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PMID:Synthetic gastric inhibitory polypeptide. Stimulatory effect on insulin and glucagon secretion in the rat. 32 91

Gastric inhibitory polypeptide (GIP) is insulinotropic and is released after ingestion of glucose in normal man. Changes in plasma immunoreactive gastric inhibitory polypeptide (IRGIP) were therefore studied during a 50-gm. oral glucose tolerance test in 10 normal subjects and 20 subjects with maturity-onset diabetes mellitus. The diabetics were nonobese and treated by diet alone; they exhibited exaggerated increments of plasma IRGIP in association with delayed and diminished peak increases in plasma immunoreactive insulin, suggesting relative failure of the beta-cell response to GIP. The diabetic subjects also showed a paradoxic rise in mean plasma immunoreactive glucagon, with a peak coinciding with that of plasma IRGIP. It is suggested that the defective beta-cell response may lead to diminished feedback inhibition of GIP secretion by insulin in diabetes mellitus and that the glucagonotropic action of GIP may be expressed under these conditions.
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PMID:Hypersecretion of gastric inhibitory polypeptide following oral glucose in diabetes mellitus. 32 34

To examine gut-islet interrelationships, we entirely separated the gastrointestinal tract from the rat. When we arterially perfused this preparation with an erythrocyte-free solution for 1 h, it remained histologically intact and took up oxygen and glucose. Feedings were given via a duodenal tube. The gut absorbed glucose when glucose in the feeding was high (9.2 g/dl), but not when glucose in the feeding was low (58 mg/dl). With feeding, the portal venous effluent (PVE) from this preparation (stomach to ileum) enhanced late-phase, glucose-induced insulin secretion from pancreas of another rat. This enhancement occurred when the gut was fed either glucose (9.2 g/dl) in electrolyte solution or electrolyte solution alone. PVE from glucose-fed upper gut (stomach, duodenum) was similarly insulinotropic. In contrast, PVE from unfed gut or from glucose-fed gut of old rats was not insulinotropic. PVE from all gut preparations except upper gut produced a glucagon "spike" during basal pancreatic perfusion. Effects of gastrointestinal peptides (gastric inhibitory polypeptide, cholecystokinin octapeptide, secretin, gastrin) and immunoassays of PVE suggested that the insulinotropic substance is not one of these peptides. Thus, an insulinotropic substance that is not dependent on feeding nutrient material is secreted from the intestine.
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PMID:Secretion of an insulinotropic factor from isolated, perfused rat intestine. 37 52

(Pro-)Insulin biosynthesis ([3H]leucine incorporation) and insulin secretion were studied in collagenase-isolated rat islets incubated for 3 hours at 1 and 2 mg/ml glucose in the presence of gastric inhibitory polypeptide (GIP). GIP augmented [3H]leucine incorporation and release of insulin at both glucose concentrations. In a second series of experiments it was found that an amino acid mixture was without influence on the insulotrophic action of GIP. Combined stimulation of insulin release by GIP and glucagon did not result in higher insulin output than observed in the presence of each substance alone. Thus GIP, in constrast to many other gastrointestinal peptides, however similar to glucagon, enhances not only release but also biosynthesis of insulin. This insulinotrophic action can be observed already at a glucose concentration of 1 mg/ml. The results underline the outstanding role which GIP appears to play in the regulation of beta-cell function.
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PMID:Stimulation of (Pro-)insulin biosynthesis and release by gastric inhibitory polypeptide in isolated islets of rat pancreas. 38 25

The direct effect of insulin on the secretion of insulin (as measured by C-peptide), glucagon, gastric inhibitory polypeptide, and gastrin was studied in normal subjects by infusing insulin while the plasma level of glucose was maintained in the normal fasting range (euglycemic clamp). Insulin-induced hypoglycemia resulted in increases in circulating glucagon and gastric inhibitory polypeptide, a decrease in C-peptide, and no change in gastrin levels. In contrast, during the euglycemic clamp, insulin was found to behave a direct suppressive effect on the secretion of glucagon, C-peptide, and gastrin, but no effect on levels of gastric inhibitory polypeptide.
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PMID:Direct effect of insulin on secretion of insulin, glucagon, gastric inhibitory polypeptide, and gastrin during maintenance of normoglycemia. 40 Jul 22

Oral glucose tolerance tests were done in eight insulin-requiring pancreatic diabetic patients to study the effect of withdrawal of insulin treatment on gut hormone release. Basal levels of gastric inhibitory polypeptide (GIP), glucagon-like immunoreactivity, and immunoreactive glucagon levels rose on insulin withdrawal, more so in patients on short-acting insulin, and were lowered by insulin treatment. Insulin treatment did not affect the GIP, glucagon-like immunoreactivity, or IRG responses to oral glucose. 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. Therefore, it is suggested that insulin treatment lowers basal hormones levels, possibly via a metabolic effect, whereas the hormone responses to oral glucose may be controlled by several factors unrelated to insulin administration or changes in glucose homeostasis.
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PMID:Gastric inhibitory polypeptide in acquired pancreatic diabetes: effects of insulin treatment. 40 Jul 25


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