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)

In dogs with denervated fundic pouches, antrectomy, and gastrojejunostomy, feeding a meal of cooked liver and 5 percent bone dust stimualted acid secretion from the fundic pouches without increasing serum gastrin concentrations. Simultaneous administration of pentagastrin, histamine, octapeptide of cholecystokinin, or bethanecol produced potentiation of acid secretion, suggesting that the mediator of the intestinal phase is different from these secretagogues. Secretin and glucagon failed to inhibit the intestinal stimulus but both atropine and metiamide were potent inhibitors. We conclude that entero-oxyntin, the hormone responsible for the intestinal phase of gastric secretin, has a unique pattern of effects for acid secretion.
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PMID:The intestinal phase of gastric secretion: a pharmacological profile of entero-oxyntin. 23 96

Smooth muscle adenylate cyclase of a membrane preparation of canine gastric antrum has been characterized, and the effect of hormonal and neuronal agents examined. The enzyme is active in the presence of Mg2+ or Mn2+, but is inhibited by Ca2+. The Km is 0.5 mM ATP, similar to the Km of skeletal muscle adenylate cyclase. The enzyme is activated by isoproterenol but not norepinephrine, consistent with a beta 2-catecholamine receptor-adenylate cyclase interaction. Secretin activates the enzyme in concentrations as low as 1 . 10(-11) M, while glucagon was effective only at 1 . 10(-6) M. Prostaglandin E1 and E2 have a biphasic effect with activation of adenylate cyclase at 1 . 10(-5) M and a small but significant inhibition of enzyme activity at 1 . 10(-11) M.
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PMID:Effect of hormonal and neuronal agents on adenylate cyclase from smooth muscle of the gastric antrum. 45 75

The inhibitory effects of intravenous infusions of secretin, glucagon and caerulein on the gastric acid response to bombesin were studied in 8 duodenal ulcer patients. Bombesin was found to be a very potent stimulator of gastric acid secretion in patients with duodenal ulcer. There were no significant differences in acid outputs per 15-min period between bombesin infused in a dose of 0.9 microgram/kg/h and pentagastrin infusion administered in a maximal dose, at a rate of 6.0 microgram/kg/h. Secretin (1 U/kg/h), glucagon (30 microgram/kg/h) and caerulein (0.1 microgram/kg/h) produced significant decreases in gastric acid secretion evoked by bombesin given in a dose of 0.9 microgram/kg/h. Percentages of inhibition were 48.6, 45.2 and 35.5, respectively. It is supposed that secretin and glucagon given in pharmacological doses are capable of interfering with the action of gastrin released from antrum by means of bombesin on the parietal cell by noncompetitive kinetics. Caerulein administered in a pharmacological dosis, however, can inhibit the effect of gastrin released by bombesin on the parietal cells by a competitive kinetic.
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PMID:Inhibition of bombesin-stimulated gastric acid secretion by secretin, glucagon and caerulein in patients with duodenal ulcer. 48 52

Enteropeptidase, trypsin, and chymotrypsin activity in basal and secretin-stimulated duodenal juice of 20 normal adult volunteers and 15 patients with gastrotestinal disease were determined. All enzyme concentrations showed skew distributions, but fluctuations in the secretin-stimulated juices were less pronouced than in the basal secretions. Secretin administration had no influence on the release of enteropeptidase from human duodenal mucosa, but resulted in a very small increase in secretion of pancreatic enzymes. Six out of seven patients with chronic alcoholic pancreatitis or cancer of the pancreas exhibited highly significant elevations of enteropeptidase in their basal as well as secretin-stimulated duodenal juice. It is suggested that raised luminal enteropeptidase activity may be the result of pancreatic insufficiency or elevated blood glucagon concentrations.
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PMID:Enteropeptidase levels in duodenal juice of normal subjects and patients with gastrointestinal disease. 66 28

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

The effects of glucagon, gastric inhibitory peptide (GIP), and secretin on the concentrating mechanism and the motility in the feline gallbladder have been studied in vivo. A technique by which the gallbladder in situ was perfused by an electrolyte solution made possible a simultaneous study of the motility and of the net transport of water and electrolytes across the gallbladder wall. Secretin (0.6 microgram per kg/h) was found to abolish the net absorption of water, Na+, and HCO3- and strongly reduce the net absorption of K+ and Cl-, whereas neither glucagon (1--20 microgram per kg/h) nor GIP (1--30 microgram per kg/h) was found to significantly influence the concentrating function of the gallbladder. The motility of the gallbladder was not influenced by the peptides. The formation of bile and pancreatic secretion was not changed by glucagon or GIP, whereas secretin had a potent effect.
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PMID:A comparison of glucagon, gastric inhibitory peptide, and secretin on gallbladder function, formation of bile, and pancreatic secretion in the cat. 72 15

Carbonized microspheres, 15 mu in diameter and labelled with 85Sr or 51Cr were injected into the left ventricle of unanesthetized male rats to investigate the changes induced by secretin and glucagon in the distribution of cardiac output to various organs including splanchnic organs. Secretin (0.5 U/100 g i.v.) significantly increased the cardiac output distribution to the stomach, small intestine and pancreas, while the percentage distribution of the cardiac output to the heart, lungs and kidneys was unchanged. On the other hand, glucagon (10 microgram/100 g i.v.) significantly increased the cardiac output distribution to the heart, lungs and kidneys, while the distribution to the major splanchnic organs remained unchanged with the exception of hepatic arterial perfusion which was significantly increased by glucagon.
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PMID:Differences in the effects of secretin and glucagon on the blood circulation of unanesthetized rats. 72 16

Fasting levels of 5 gut hormones were studied in 30 patients with advanced uraemia (CRF), 40 undergoing regular dialysis (RD) and 555 renal transplant patients (RT). Mean values of gastrin and total glucagon were markedly elevated in CRF and RD patients compared with 20 normal subjects; there were lesser elevations in pancreatic glucagon, insulin and vasoactive intestinal peptide (VIP). Secretin levels were unchanged. In RT patients, fasting levels of VIP and pancreatic glucagon had returned to normal, while levels of gastrin, total glucagon and insulin remained slightly elevated compared with controls. Food stimulated hormone levels were measured in 18 RD patients and compared with 18 controls. After eating, RD patients failed to show the late increase in total glucagon, or the suppression of VIP and secretin seen in normal subjects; the pattern of gastrin and insulin response was similar to controls, but after the initial increase plasma levels in RD patients tended to show a slower decline. Thus involvement of the gastrointestinal tract in uraemia is associated with functional disturbance of the endocrine system of the gut.
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PMID:Elevations of gastrointestinal hormones in chronic renal failure. 74 Jun 78

1 The sympathetically-innervated arterial vascular bed of the dog's liver was perfused from a femoral artery. Arterial blood flow and perfusion pressure were monitored continuously and the hepatic arterial vascular resistance (HAVR) calculated from these measurements. 2 Commercial preparations of secretin, pancroezymin, glucagon and pentagastrin were administered by intra-arterial (i.a.) injection and infusion. 3 Secretin and pancreozymin by injection caused dose-dependent hepatic arterial vasodilatation, and on a molar basis were both more potent than glucagon or pentagastrin. 4 Intra-arterial infusions of secretin and pancreozymin caused hepatic arterial vasodilatation at calculated blood concentrations close to those measured under physiological conditions by other investigators. The vasodilatation was of the same duration as that of the hormone infusions. 5 Pentagastrin by i.a. injection caused dose-dependent hepatic arterial vasodilatation; by i.a. infusion, vasodilatation occurred but there was marked 'escape' from the effects during the continued infusion. 6 As reported previously, glucagon by injection caused dose-dependent hepatic arterial vasodilatation of long duration; by infusion, glucagon caused vasodilatation that persisted after the cessation of the infusion. 7 Glucagon infused i.a. inhibited the vasoconstricter effects of i.a. noradrenaline, over the same range of infusions that caused hepatic arterial vasodilatation. 8 Secretin or pancreozymin did not antagonize the effects of noradrenaline on the hepatic arterial vascular bed at any doses used. 9 Pentagastrin did not antagonize the vasoconstrictor effect of noradrenaline whether hepatic arterial vasodilatation resulted from the pentagastrin infusion, or not. 10 These results are discussed with respect to the possible control of the hepatic arterial vascular bed by gastrointestinal hormones.
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PMID:The effects of glucagon, secretin, pancreozymin and pentagastrin on the hepatic arterial vascular bed of the dog. 83 95

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


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