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)

Reliable and specific radioimmunoassays have been developed for the gut hormones secretin, gastrin, cholecystokinin, pancreatic glucagon, VIP, GIP, motilin, and enteroglucagon. Using these assays, the relative pattern of distribution of the gut hormones has been determined using the same bowel extracts for all measurements. VIP occurred in high concentration in all regions of the bowel, whereas secretin, GIP, motilin, and CCK were predominantly localised in the proximal small intestine. Pancreatic glucagon was almost exclusively confined to the pancreas. Like VIP, enteroglucagon also exhibited a wide pattern of distribution but was maximal in the ileum. The acid ethanol extraction method that was used was found to be unsuitable for gastrin. On gel chromatography of the extracts, motilin and VIP eluted as single molecular species in identical position to the pure porcine peptides. CCK, pancreatic glucagon, enteroglucagon and GIP were all multiform.
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PMID:Distribution of the gut hormones in the primate intestinal tract. 11 57

In collagenase isolated rat pancreatic islets, CCK-PZ, SHG, secretin and glucagon stimulated the accumulation of cAMP, in physiological ranges. The resulting increment of cAMP showed a good correlation with insulin release stimulated by either glucagon or secretin, but not by SHG or CCK-PZ. In the same system, 14CO2 production from glucose-U-14C was significantly increased by either SHG or CCK-PZ. The results presented in this report are compatible with the hypothesis that insulin release by gastrointestinal hormones may be mediated by cAMP in the B-cell in the case of either glucagon or secretin; whereas, in the case of either SHG or CCK-PZ, it may presumably be mediated by an unknown mechanism in glucose metabolism, other than c-AMP.
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PMID:Stimulation by gastro-intestinal hormones of cyclic adenosine 3': 5'-monophosphate accumulation and insulin release in isolated pancreatic islets of the rat. 20 18

Gastro-entero-pancreatic (GEP) and bronchial endocrine tumours have been studied by immunohistochemistry using specific antisera against a variety of hormonal and neuronal peptides. In gastrinomas numerous tumour cells were found to contain GH-like immunoreactivity. These cells were identical with those storing gastrin. Gastrinomas as a rule were extremely heterogeneous containing a variety of minority cell populations, including CCK immunoreactive cells and neurotensin immunoreactive cells. Glucagonoma cells were found to store GIP-like material in addition to glucagon. In some insulinomas calcitonin-like material was encountered in the insulin producing tumour cells. In both glucagonomas and insulinomas other pancreatic endocrine cell types constituted minority cell populations. One intestinal somatostatinoma contained gastrin cells as a minority cell population. Bronchial endocrine tumours contained scattered cells displaying ACTH-like or enkephalin-like immunoreactivity. Two such tumours in addition contained cells displaying neurophysin immunoreactivity.
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PMID:Majority and minority cell populations in GEP and bronchial endocrine tumours. 22 92

The inhibitory action of both calcitonin (CT) and glucagon (GK) on human pancreatic secretion has been evaluated in detail. The reduction of enzyme secretion expressed as percentage corresponded to 60--80% of the initial values in response to both CT and GK when the hormones were given as single infusions during background stimulation with secretin or with secretin plus cholecystokinin-pancreozymin (CCK-PZ). After withdrawal of GK-infusion the return to normal values of enzyme secretion was distinctly faster than after CT, thus reflecting a more rapid degradation of circulating GK than of CT. In the presence of stimulation with secretin plus CCK-PZ, the combined administration of CT and GK did not enhance the inhibitory actions of CT and GK. Fluid and bicarbonate secretions were not affected by either CT or GK. The results suggest that CT and GK inhibit human pancreatic enzyme secretion by similar modes of action. Therefore, the combined administration of both CT and GK does not offer a reasonable approach to the treatment of acute pancreatitis.
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PMID:Similar modes of action of calcitonin and glucagon in inhibiting pancreatic enzyme secretion in man. 54

Effects of intravenous arginine and cholecystokinin-pancreozymin (CCK-PZ) infusion on hepatic extraction of insulin (EI) and glucagon (EGG) and also on hepatic glucose output (HGO) were studied in anesthetized dogs. Because insulin and glucagon exert antagonistic effects on HGO, insulin:glucagon (I/GG) molar ratios were determined in the portal vein and also in peripheral vessels. During the arginine-CCK-PZ infusion the amount of insulin and glucagon coming to the liver increased 12- and 15-fold, respectively. In contrast EI decreased significantly from a control value of 62 +/- 6% to a nadir of 22 +/- 13%. EGG (control value 19 +/- 9%), however, was unaffected by arginine-CCK-PZ. The absence of any alteration in EGG cannot be attributed to the molecular heterogeneity of the immunoreactive glucagon. HGO increased fourfold in response to the pancreatic stimulation, whereas portal I/GG decreased significantly from 8.2 +/- 0.9 to 5.0 +/- 0.7. The concurrent femoral arterial I/GG (control 3.7 +/- 1.0) and mesenteric venous I/GG (control 2.1 +/- 0.5) increased significantly. These observations indicate that portal, but not peripheral, I/GG measurements reflect hepatic events in anesthetized dogs, probably because of the different extraction patterns for insulin and glucagon.
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PMID:Hepatic insulin and glucagon extraction after their augmented secretion in dogs. 67 14

Pressure responses in guinea-pig antral and fundal pouches were investigated in vitro. Secretin and glucagon in concentrations that did not significantly alter spontaneous activity significantly reduced antral responses to cholecystokinin, but had no depressive effect on the fundal responses. The antral inhibition of CCK-PZ may be specific, since responses to acetylcholine were unaffected by secretin and glucagon. The changes produced by secretin and glucagon in the antral dose-response curve to CCK-PZ suggest that the inhibition might be of a non-competitive type.
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PMID:The inhibitory effect of secretin and glucagon on pressure responses to cholecystokinin-pancreozymin in isolated guinea-pig stomach. 70 48

Synthesis of gastrin, CCK-PZ-octapeptide sulphate ester and secretin, is dealt with in some detail. A gastrin synthesis developed by the author's team is also described. The synthesis of glucagon and caerulein is, though touched upon, but not discussed in any detail.
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PMID:Synthesis of gastrointestinal peptide hormones. 80 96

In addition to established gastrointestinal hormones--secretin, cholecystokinin-pancreozymin (CCK-PZ), gastrin, and glucagon---some 30 polypeptides with gastrointestinal actions can be listed. New aspects of these substances include the following: Gastrin and vasoactive intestinal peptide (VIP) can be also encountered in the central nervous system and may act as transmitters. CCK-PZ-serum concentrations are found markedly elevated in patients with exocrine pancreatic insufficiency; this may provide the opportunity to establish a realtively simple screening test. Moreover, there is evidence that serum-CCK-PZ levels serve as satiety signal. Secretin secretion is said to be enhanced in hunger and then to act as a lipolytic hormone. In addition to enteroglucagon, a gastrintestinal peptide identical to pancreatic glucagon has been detected. Gastric inhibitory polypeptide (GIP) inhibits gastric secretion and motility (enterogastrone activity) and together with glucose it stimulates insulin release (incretin activity). Motilin increases lower esophageal sphincter pressure, enhances gastric pepsin secretion and slows down gastric evacuation. Serum levels of pancreatic polypeptide may be found elevated as a diagnostic index in patients with endocrine peptide tumors of the pancreas. Recently, the potential importance of local (paracrine) actions of gastrointestinal polypeptides has been amphasized. Predominantly paracrine activity is exhibited by some prototype hormones, e.g. somatostatin, substance P, bombesian, and the non-polypeptide compounds, prostaglandins.
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PMID:[New views on gastrointestinal hormones]. 85 99

Gastrin is a peptide hormone originating from G-cells of the antrum, the duodenum and the proximal jejunum. From extracts of gastrinomas and from sera of hypergastrinaemic subjects several gastrin molecules could be isolated which were nominated as "mini gastrin" (G13), "little gastrin" (G17), "big gastrin" (G34) and "big big gastrin". Antisera used for radioimmunological gastrin determinations should be characterized with respect to their specificity, as differeing affinity towards the various gastrins and towards CCK-PZ influences the results of the assay and thus the comparability with values of other laboratories. Gastrin is released by direct vagal stimulation of the antral G-cells and by local chemical and physical stimuli in the antrum and duodenum; probably an oxynto-pyloric reflex also exists. Gastrin stimulates in physiologic doses gastric acid secretion and, as shown in dogs and cats, reveals a trophic action on parietal cell growth. H+-secretion and gastrin release are connected by a feed back mechanism, insofar, as a decrease of intragastric pH below 3 inhibits endogenous gastrin release. Hypergastrinaemia has been demonstrated in patients with gastric anacidity or hypo-secretion, benigne pyloric stenosis, uraemia, short bowel-syndrome, gastric and duodenal ulceration and in patients with gastrinomas (Zollinger-Ellison-syndrome). Hypergastrinaemia in combination with hypersecretion exhibits clinical significance in patients suffering from Zollinger-Ellison-syndrome or excluded antrum syndrome which are due to autonomous gastrin release. The differential diagnosis between these syndromes and other diseases, in which hypergastrinaemia is not associated with gastric hypersecretion, can be achieved by several tests using calcium infusion or intravenous application of secretin and glucagon. The significance of elevated gastrin levels in patients with duodenal ulceration (DU) is pointed out. In DU-patients basal and postprandial hypergastrinaemia has been observed. In these patients gastrin release from gastric and extragastric sites is increased. In these patients hypergastrinaemia due to extragastric gastrin release could cause gastric hypersecretion at a time, when the stomach already has emptied. Furthermore parietal cell hyperplasia could be the result of chronic hypergastrinaemia.
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PMID:[Gastrointestinal hormones. I. Hormones of the gastrin group]. 87 Oct 64

Gastrointestinal hormones are considered to be those that are formed in the gastrointestinal tract and there, in physiological concentrations, develop their effects on motility, secretion, trophism, bloodflow and absorption. Structural analysis, synthesis or a high degree of purity after extraction, and its exact demonstration by means of a useful radioimmunoassay, form the basis for the establishment of a polypeptide as a gastrointestinal hormone. To this category belong, at the present time, gastrin, cholecystokinin-pancreozymin (CCK-PZ) and secretin. GIP, VIP, motilin, glucagon and somatostatin are considered likely candidates. The substances gastrin and CCK-PZ, which are structurally related and have a predominantly stimulating effect, and the structurally dissimilar motilin, contrast with the partially or totally inhibiting hormones of the glucagon family, namely, secretin, VIP, glucagon-enteroglucagon, GIP and somatostatin. By the combined action of these hormones with one another and with the autonomic nervous system, the digestive processes are regulated. Disturbances in the formation of these hormones, in particular an overproduction, give rise to disease syndromes that can now be diagnosed and, in part, treated by surgery. The therapeutic application of gastrointestinal hormones has now also become a possibility.
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PMID:[Gastrointestinal hormones]. 96 Sep 54


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