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 distribution of endocrine cells in the gastrointestinal tract of the house musk shrew, Suncus murinus (Family Soricidae, Order Insectivora) was studied immunohistochemically. The hormones investigated were gastrin, cholecystokinin (CCK), somatostatin, secretin, glucagon, gastric inhibitory polypeptide (GIP), motilin and neurotensin. In the gastric mucosa, gastrin and somatostatin cells were only found in the pyloric regions, and no other hormonal cell-types were observed. In the intestinal mucosa, the largest number of endocrine cells belonged to the gastrin and glucagon/glicentin cell-types, whereas CCK-33/39 and secretin cells were the least numerous. Numbers of other cell-types were intermediate between these two groups. The gastrin and GIP cells were mostly localized in the proximal portion of the intestine, decreasing in number towards the distal portion. The motilin and CCK-33/39 cells were restricted to the proximal half. The glucagon/glicentin and neurotensin cells were most abundant in the middle portion. The somatostatin and secretin cells, although only present in small numbers, were randomly distributed throughout the intestine. This characteristic distribution of gastrointestinal endocrine cells is discussed in comparison with the distribution patterns of other mammals.
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PMID:The distribution of endocrine cells in the mucosa of the gastrointestinal tract of the house musk shrew, Suncus murinus (Insectivora). 258 80

After colectomy, continent ileal reservoirs are an accepted alternative to conventional ileostomy for patients with ulcerative colitis. To assess the effect of these reservoirs on digestive function, circulating and morphologic gut endocrine responses were measured in patients with a continent ileostomy or with a pelvic pouch and compared to patients with conventional ileostomy, with active ulcerative colitis and healthy controls. Eight subjects were studied in each group. Basal and postprandial plasma gastrin, enteroglucagon, neurotensin, vasoactive intestinal polypeptide, insulin, pancreatic glucagon, and pancreatic polypeptide in both groups with ileal reservoirs were equivalent to controls. Basal plasma motilin and postprandial plasma gastric inhibitory polypeptide were raised in ileal reservoir patients, but similar changes also occurred in ulcerative colitis patients and those with conventional ileostomy. In one half of patients, cell populations of enteroglucagon, peptide YY, and neurotensin were decreased in pouch mucosa that corresponded with the presence of mucosal inflammation. On the other hand, with pouch inflammation vasoactive intestinal polypeptide immunoreactive nerves were increased and a proportion of the fibres were moderately coarsened. Mucosal concentrations of vasoactive intestinal polypeptide did not, however, exceed that of controls. After an ileal reservoir sufficient reserve remains for gut hormone release into the circulation, suggesting compensation for the presence of a reservoir and the absence of a colon; circulating hormone changes do occur but are consequent upon previous ulcerative colitis. Reservoirs may show neuromorphologic alterations that appear to be related to mucosal inflammation.
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PMID:Gut hormone responses after reconstructive surgery for ulcerative colitis. 261 86

The gastrointestinal hormone, gastric inhibitory polypeptide (GIP), has been isolated and characterized because of its enterogastrone-type effects. It is also named glucose-dependent insulinotropic polypeptide and is actually considered to be the main incretin factor of the entero-insular axis. Besides these well-described effects on gastric secretion and pancreatic beta cells, it also has direct metabolic effects on other tissues and organs, such as adipose tissue, liver, muscle, gastrointestinal tract and brain. In adipose tissue it is involved in the activation and regulation of lipoprotein lipase (LPL); it also inhibits glucagon-induced lipolysis and potentiates the effect of insulin on incorporation of fatty acids into triglycerides. It may play a role in the development of obesity because of the hypersensitivity of adipose tissue of obese animals to some of these actions. In the liver it does not modify insulin extraction, and its incretin effects are due only to the stimulation of insulin secretion and synthesis. It reduces hepatic glucose output and inhibits glucagon-stimulated glycogenolysis. It might increase glucose utilization in peripheral tissues such as muscle. GIP also has an effect on the volume and/or electrolyte composition of intestinal secretion and saliva. The functional importance of its effect on the hormones of the anterior pituitary lobe remains to be established, as it has never been detected in the brain. Its links with insulin are very close and the presence of insulin is sometimes necessary for the greater efficiency of both hormones. GIP can be considered as a true metabolic hormone, with most of its functions tending to increase anabolism.
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PMID:Gastric inhibitory polypeptide: a gut hormone with anabolic functions. 266 79

Gastrointestinal hormones and regulatory peptides of the gastrointestinal tract (GIT) influence many digestive functions and therefore it is essential in diseases of the GIT to search also for changes of GIT hormones in plasma or for an altered response of the target organ to hormonal abnormalities. An unequivocal physiological function is known so far only in gastrin, cholecystokinin, secretin, gastric inhibitory polypeptide, vasoactive intestinal polypeptide, motilin, somatostatin, glucagon and pancreatic polypeptide. The authors analyzes therefore different nosological unites, or clinical syndromes associated with excessive production of gastrin, vasoactive intestinal polypeptide, glucagon and somatostatin. He discusses also the syndrome of malignant carcinoid caused by excessive formation of serotonin in the enterochromaffin cells of the GIT which by its symptoms can imitate some apudomas of the GIT.
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PMID:[Hormonal changes in diseases of the gastrointestinal tract]. 280 Mar 78

The presence of vasoactive intestinal peptide (VIP) binding sites and the adenylate cyclase activity in response to VIP were examined in the human term placenta. Slices were used in order to preserve the physicochemical environment and the structural integrity of this heterogeneous organ. 125I-VIP binding to placental slices was saturable. The steady state was reached after 90 min at 37 degrees C and was maintained up to 3 h. Unlabeled VIP was able to compete in a dose-dependent manner with an IC50 value of 5.2 +/- 1.3 x 10(-10) M. Autoradiography and histological analysis showed that VIP binding sites were essentially located on fetal vascularization, especially arteries of stem villi. VIP produced a stimulatory effect on cAMP synthesis at a concentration as low as 10(-10) M. The dose-response curve was monophasic with an ED50 value of 2.9 +/- 1.6 x 10(-9) M. The specificity of the VIP effect was tested with peptides structurally related to VIP such as glucagon, secretin, gastric inhibitory polypeptide and human growth-hormone releasing factor. Only secretin at high concentrations (greater than 10(-6) M) increased cAMP production. Leu-enkephalin or insulin were ineffective. The presence of both VIP binding sites on fetal vascularization and VIP-induced adenylate cyclase activation would seem to suggest a regulatory role of the peptide on fetoplacental blood flow.
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PMID:Autoradiographic localization of vasoactive intestinal peptide (VIP) binding sites in the human term placenta. Relationship with activation of adenylate cyclase. 282 91

1. Dietary fibre has a moderating impact on glucose metabolism. To test the hypothesis that this effect of fibre may be mediated by its breakdown product acetate, oral glucose tolerance tests were carried out in healthy volunteers with and without acetate. 2. Five subjects received 50 g of glucose orally while taking either acetate (15 mmol every 15 min) by mouth or chloride as control. Oral acetate made no detectable difference to glucose tolerance or to levels of free fatty acids, 3-hydroxybutyrate, lactate, insulin, glucagon and gastric inhibitory polypeptide. 3. The 50 g dose of glucose temporarily depressed acetate levels in blood. This was probably due to an interaction between glucose and acetate in the gastrointestinal lumen as the same effect was seen with 50 g of xylose in three subjects. 4. Plasma acetate concentrations were unaffected by 50 g of oral glucose in one subject when acetate was instilled into the sigmoid colon. 5. It is unlikely that the improvement of glucose tolerance by dietary fibre is mediated by acetate.
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PMID:Effect of gut-derived acetate on oral glucose tolerance in man. 284 52

1. The effect of acetate absorbed from the gut on glucose turnover has been determined in four healthy subjects during both fasting and an intravenous glucose infusion by using [U-13C]glucose. 2. In the first part of the study, after an overnight fast, a tracer dose of [U-13C]glucose was infused at a constant rate along with an infusion of saline for 7 h. In the second part the saline infusion was replaced by glucose at 4.25 mg min-1 kg-1. In both studies 15 mmol of sodium acetate was given by mouth at 15 min intervals from the fourth to the sixth hour. Glucose turnover, respiratory quotient, metabolic rate and blood levels of acetate, 3-hydroxybutyrate, lactate, insulin, glucagon and gastric inhibitory polypeptide were measured. 3. Glucose turnover rates (means +/- SEM) were 1.88 +/- 0.1 mg min-1 kg-1 during fasting and 4.0 +/- 0.08 mg min-1 kg-1 during glucose infusion. Acetate had no effect on glucose turnover, insulin, glucagon and gastric inhibitory polypeptide levels, but temporarily halted the rise in free fatty acids seen during the fasting study. No changes in oxygen consumption or carbon dioxide output occurred, in keeping with previous observations that acetate substitutes for lipid oxidation during metabolism and has no direct effect on glucose turnover.
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PMID:Effect of gut-derived acetate on glucose turnover in man. 284 53

The hypothalamic peptide vasoactive intestinal peptide (VIP) stimulates ACTH and endorphin secretion by the AtT20/D16 clonal strain of mouse pituitary tumor cells. The dose dependence for VIP stimulation of hormone release is biphasic, indicating that VIP is able to activate at least two classes of receptors in D16 cells (ED50 = 1.6 and 160 nM). We show that at high concentrations (ED50 greater than or equal to 150 nM), other natural peptides with primary structures homologous to that of VIP also increased ACTH secretion by D16 cells, whereas structurally unrelated peptides did not. The stimulatory actions of GH-releasing factor (GRF) and porcine heptacosapeptide with amino-terminal histidine and carboxy-terminal isoleucine amide (PHI) were mediated by high affinity VIP receptors because their effects were not additive with that of 10 nM VIP. In addition, GRF and PHI behaved as antagonists at low affinity VIP receptors; both peptides inhibited stimulation by 1 microM VIP. In contrast, glucagon and gastric inhibitory polypeptide appeared to stimulate ACTH release via low affinity VIP receptors because their effects were additive with that of 10 nM, but not 1 microM, VIP. Since all of the VIP-like peptides increased ACTH secretion only at high concentrations, they were unlikely to represent a physiological ligand for the receptor activated by high concentrations of VIP. Therefore, we determined whether cross-reactivity occurred between VIP-like peptides and corticotropin-releasing factor (CRF), a potent stimulator of ACTH secretion both in vitro and in vivo. The dose-response curve for CRF stimulation of ACTH secretion by D16 cells extended over more than a 1000-fold range of concentrations and was biphasic (ED50 = 2.6 and greater than 300 nM), indicating that CRF interacted with multiple receptor types in D16 cells. However, since the effect of 10 nM CRF was additive with that of 1 microM VIP, the CRF receptor was not the site at which high concentrations of VIP stimulated ACTH release. In contrast, the effect of 1 microM CRF was not additive with that of 1 microM VIP or other VIP-like peptides. Therefore, high concentrations of CRF and the previously recognized VIP-like peptides stimulated ACTH secretion by overlapping pathways. Comparison of the amino acid sequence of CRF with those of the VIP-like peptides showed that 18 of the 41 amino acids in CRF match a corresponding amino acid in at least 1 member of the VIP peptide family.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Peptide specificity for stimulation of corticotropin secretion: activation of overlapping pathways by the vasoactive intestinal peptide family and corticotropin-releasing factor. 285 86

Pancreatic islet peptides, as well as other gastrointestinal hormones, have been implicated in both the pathogenesis of obesity and the etiology of associated metabolic derangements. This study evaluated the pancreatic islet and gastrointestinal (GI) hormone response to oral glucose in 20 morbidly obese (151% above ideal body weight) patients. Glucose intolerance, hyperinsulinism, and exaggerated gastric inhibitory polypeptide (GIP) release occurred following glucose ingestion. Significant release of PP occurred in 14 patients, while only six patients had release of somatostatin. No significant changes in plasma concentrations of glucagon occurred. 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. Failure of glucagon suppression in response to oral glucose many contribute to the hyperglycemia noted. Somatostatin and pancreatic polypeptide may be responsible for some of the metabolic derangements of morbid obesity.
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PMID:Pancreatic islet hormone response to oral glucose in morbidly obese patients. 286 Aug 76

Barrett's epithelium refers to the presence of ectopic mucosal types in the squamous-lined oesophagus. Previous studies have documented argentaffin and argyrophil-positive cells as well as gastrin-like immunoreactivity in oesophageal tissue extracts from patients with Barrett's mucosa. In the present study, 125 oesophageal biopsies obtained under direct vision at endoscopy from 22 patients with Barrett's oesophagus were systematically studied using fluorescence and peroxidase antiperoxidase single and double-staining immunocytochemical methods employing highly specific antibodies to localize the following peptide-containing cell types in Barrett's mucosa: gastrin, somatostatin, gastric inhibitory polypeptide, motilin, neurotensin and pancreatic glucagon. In addition, EC cells were localized using a cytochemical silver staining method. The results of this study indicate that EC cells and gastrin- and somatostatin-containing endocrine cells are detectable in Barrett's epithelium.
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PMID:Regulatory peptides in Barrett's oesophagus. 286 40


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