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)

Procedures for the determination of secretin, gastrin, cholecystokinin-pancreozymin, glucagon and villikinin in various species are reported. The sensitivities of the individual methods are dealt with.
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PMID:Biological determination of gastrointestinal peptide hormones. 80 97

Superfusion of twelve human Taenia Coli strips with cholecystokinin (CCK) (boots and GIH Karolinska), CCK-octapeptide and glucagon at doses of 25--1,000 mIDu/ml evoked muscular contractions. Dose-dependent response to acetylcholine (ACH) (0.15--1.0 mug/ml) was not altered by an underlying contraction induced by CCK, CCK-octapeptide or glucagon. Though atropine (0.1 mug/ml) abolished ACH effects, hormonal responses were unaffected. The muscles' sensitivity was highest of CCK (Boots) and lowest to CCK-octapeptide, and the sigmoid colon was more sensitive than other parts of the bowel to both. Addition of glucagon had no effect on CCK-induced (Boots) responses. The results suggest (1) CCK and CCK-octapeptide act directly on the Taenia coli; (2) biologically active impurities in the whole CCK preparations explain their apparent increased activity; (3) glucagon does not block ACH or CCK, nor inhibit, directly, muscle contractions; (4) atropine (0.1) mug/ml)) does not interfere with CCK or CCK-octapeptide on colonic muscle.
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PMID:The effect of cholecystokinin on human taenia coli. 84 75

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

The effects of gastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of pancreozymin-cholecystokinin on immunoreactive somatostatin release were studied in the isolated perfused dog pancreas. Gastrin at a concentration of 65 ng/ml and the octapeptide of pancreozymin-cholecystokinin at a concentration of 25 ng/ml produced a prompt, but transient statistically significant, twofold rise in mean somatostatin concentration. Secretion at a concentration of 0.3 U/ml and gastric inhibitory polypeptide concentration of 58 ng/ml produced a prompt two- to threefold rise in mean somatostatin release, which persisted throughout the perfusion period. With all four polypeptides the pattern of the somatostatin response resembled that of insulin. It appears that pancreatic somatostatin release is stimulated by gastrointestinal hormones that influence the secretion of insulin and glucagon.
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PMID:The effects of gastrin, gastric inhibitory polypeptide, secretin, and the octapeptide of cholecystokinin upon immunoreactive somatostatin release by the perfused canine pancreas. 90 61

We have used 125I-labeled vasoactive intestinal peptide (VIP) to study the kinetics, stoichiometry, and chemical specificity with which the labeled peptide binds to dispersed acinar cells prepared from guinea pig pancreas. Binding of 125I-VIP to pancreatic acinar cells was moderately rapid, reversible, specific, saturable, and depended on incubation temperature. Deterioration of 125I-VIP incubated with pancreatic acinar cells at 37 degrees was reflected in a decrease in acid-precipitable radioactivity and in the amount of tracer which could bind to fresh acinar cells. On the other hand, 125I-VIP bound to pancreatic acinar cells appeared to be protected from deterioration. VIP and secretin but not glucagon or COOH-terminal octapeptide of cholecystokinin inhibited binding of 125I-VIP to pancreatic acinar cells. The dose-response curve for inhibition of 125I-VIP binding by VIP or secretin was biphasic and suggested that pancreatic acinar cells have two classes of binding sites: (a) a relatively small number of sites with a high affinity for VIP and a low affinity for secretin, and (b) a relatively large number of sites with a low affinity for VIP and a high affinity for secretin. The difference between the relative affinities of VIP and secretin for the high affinity VIP binding sites appears to be primarily attributable to the NH2-terminal portions of these molecules since synthetic COOH-terminal fragments VIP 14-28, VIP 15-28, and secretin 14-27 were equipotent in inhibiting 125I-VIP binding. On the other hand, secretin 5-27, [6-tyrosine] secretin and native secretin were equipotent in inhibiting binding of 125I-VIP to its high affinity site, and these three peptides were 5 times more potent than secretin 14-27 but 10,000 times less potent than native VIP.
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PMID:Interaction of porcine vasoactive intestinal peptide with dispersed pancreatic acinar cells from the guinea pig. Binding of radioiodinated peptide. 94

The purpose of the present study was to evaluate the effects of several gastrointestinal hormones on the gastric submucosal arterioles using an in vivo microscopy technique. Alteration in diameter of submucosal arterioles, 40 to 90 mu in diameter, in response to infusion of different agents into the celiac axis, was measured in the anesthetized cat. Pentagastrin, the octapeptide of cholecystokinin, natural secretin, and histamine produced arteriolar dilation. Only with histamine and the octapeptide of cholecystokinin did this occur with doses that might be considered physiological. Synthetic secretin had no vasodilator activity, suggesting the presence of a contaminating agent in natural secretin. Glucagon had no effect on the submucosal arterioles. In addition, the effect of glucagon on the smaller (10 to 30 mu) terminal and subterminal submucosal arterioles was studied in the rat by in vivo microscopy. Again no effect was observed with glucagon, but norepinephrine in small doses produced vasoconstriction.
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PMID:The effect of gastrointestinal hormones on the gastric microcirculation. 95 93

The effects on gallbladder contraction of three structurally related peptides, secretin, glucagon and the vasoactive intestinal peptide (VIP) have been compared in urethane-anesthetized guinea pigs. Secretin and glucagon had no effect alone but augmented cholecystokinin (CCK)-induced contractions. VIP decreased CCK-induced contractions.
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PMID:Effect of secretin, glucagon and VIP on gallbladder contraction. 95 25

During a study of intraluminal motor patterns of the colon and rectum, spontaneous wave activity of a continuous complex type was observed at the rectosigmoid junction in constipated subjects. To assess the frequency and characteristics of this hyperactive segment, 36 subjects with colonic motor disorders and 12 healthy controls were studied. Eighteen of 24 patients with constipation (75%) and 1 of 7 subjects with asymptomatic diverticulosis exhibited a persistent hyperactive segment at the rectosigmoid junction. Neither secretin nor cholecystokinin influenced the wave activity of the hyperactive segment. In contrast, atropine and glucagon inhibited markedly all wave activity and decreased the motility index of this segment significantly, suggesting overactivity of the muscarinic effector cells. It is concluded that a segmental area of overactivity exists at the rectosigmoid junction in most constipated subjects regardless of their underlying disorders.
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PMID:Characterization of a hyperactive segment at the rectosigmoid junction. 95 44

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

Intragastric pressure was measured in dogs with gastric fistulas by using a flaccid balloon containing 500 ml of water. Intravenous infusion of cholecystokinin (20% pure), the carboxyl-terminal octapeptide of cholecystokinin, secretin, and vasoactive intestinal peptide produced dose-related decreases in intragastric pressure with maximal decreases of 40% or more. Glucagon and gastric inhibitory peptide produced smaller decreases in intragastric pressure. Motilin caused a dose-related increase in intragastric pressure that lasted only about 7 min despite continuing infusion of the peptide. The half-dose of cholecystokinin or of octapeptide of cholecystokinin for pancreatic protein secretion and the half-dose of secretin for pancreatic bicarbonate secretion each produced significant inhibition of intragastric pressure, suggesting that these hormones play a physiological reole in regulating gastric pressure.
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PMID:Effect of intestinal hormones and peptides on intragastric pressure in dogs. 96 68


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