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 mechanism by which intestinal secretagogues evoke fluid secretion in the small bowel and colon has been suggested to involve mucosal adenylate cyclase. Adenylate cyclase activity was assayed by conversion of [32P]ATP to [32P]cyclic AMP in a system of pure epithelial cells isolated from the small intestine of the hamster by vibration in buffer. Several gastrointestinal hormones were tested for their capacity to stimulate adenylate cyclase; vasoactive intestinal peptide and impure cholecystokinin-pancreozymin (but not the 99% pure preparation or pure cholecystokinin octapeptide) were potent stimuli, but pentagastrin, glucagon, secretin, and gastric inhibitory peptide were impotent. Two prostaglandins, PGE1 and PGE2, were potent stimuli of adenylate cyclase. Two other compounds that provoke intestinal secretion of fluid, deoxycholic acid and ricinoleic acid (castor oil), were ineffective stimuli of adenylate cyclase. These experiments do not support a clear-cut relationship between a compound's ability to stimulate adenylate cylase and its activity as an intestinal secretagogue.
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PMID:Stimulation of adenylate cyclase in homogenates of isolated intestinal epithelial cells from hamsters. Effects of gastrointestinal hormones, prostaglandins, and deoxycholic and ricinoleic acids. 56 12

The duodenums of opossums and cats were cut into strips 2 mm wide and 2-2.5 cm long. Strips cut in the oral-caudal axis were called longitudinal strips; those cut at 90 degrees to that axis were called circular strips. Cholecystokinin (CCK) and cerulein stimulated phasic contractions of circular muscle of opossum duodenum, but had no effect on the longitudinal muscle. The effect of CCK was not blocked by tetrodotoxin (10(-7)M), indicating a direct muscle stimulation. CCK had no effect of both muscle layers of the cat duodenum. Vasoactive intestinal peptide raised tension in longitudinal muscle, but reduced tension in circular muscle of opossum duodenum. Glucagon slightly reduced tension in both longitudinal and circular muscle of opossum duodenum. It also inhibited contractions of circular muscle caused by acetylcholine. Pentagastrin and secretin had no effect on either muscle layer in either species. These findings suggest that the circular and longitudinal muscle layers of the duodenum respond differently to at least some gastrointestinal hormones. Also, there is species variation in response to gastrointestinal hormones.
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PMID:Effects of some gastrointestinal hormones on two muscle layers of duodenum. 62 51

The effect of glucagon infusion on secretin and combined secretin and cholecystokinin stimulated exocrine pancreatic secretion was studied in normal subjects and in patients after acute and with chronic pancreatic disease. Glucagon inhibited pancreatic protein secretion and had no inhibitory effect on volume or bicarbonate secretion.
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PMID:Glucagon inhibition of secretin and combined secretin and cholecystokinin stimulated pancreatic exocrine secretion in health and disease. 62 17

Dispersed mucosal cells (approx. 70% parietal cells) prepared from guinea pig stomach maintained their cellular concentration of potassium (65--80 nmol potassium/10(6) cells) for at least 5 h in vitro. Uptake of 42K by dispersed gastric mucosal cells depended on temperature, H+ concentration and oxidative metabolism. Carbachol and, in some instances, gastrin caused a 40--50% increase in cellular uptake of 42K as a consequence of the ability of these agents to increase 42K influx. Ouabain reduced uptake of 42K by 70% but did not alter the effect of carbachol. Cellular uptake of 42K was not altered by histamine, prostaglandin, E1, glucagon, secretin, vasoactive intestinal peptide or C-terminal octapeptide of cholecystokinin. Uptake of 42K was also increased by dibutyryl cyclic AMP or dibutyryl cyclic GMP but not by cyclic AMP, cyclic GMP or their 8-bromo derivatives. Theophylline caused a small (10--15%) increase in 42K uptake and potentiated the increase caused by submaximal concentrations of carbachol. The increase in 42K uptake caused by either dibutyryl cyclic nucleotide and carbachol was additive.
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PMID:Potassium transport in dispersed mucosal cells from guinea pig stomach. 63 44

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

A radioimmunoassay for the measurement of gastric inhibitory polypeptide (GIP) in unextracted plasma in man has been developed using a rabbit antiserum raised against porcine GIP. Porcine GIP was employed also as standard and to produce a 125I-labelled tracer. The assay was able to distinguish 110 pg/ml GIP from zero in plasma samples. Negligible cross-reactivity was demonstrated with cholecystokinin, insulin, pancreatic polypeptide, glucagon, secretin, and vasoactive intestinal polypeptide. The mean overnight fasting plasma GIP level in 28 normal subjects was 203 pg/ml (range: undetectable--420 pg/ml). Plasma GIP levels rose, within 45 minutes of eating a mixed meal, to a mean level of 1573 pg/ml.
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PMID:Radioimmunoassay of gastric inhibitory polypeptide. 67 95

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

It has previously been shown that dopamine stimulates pancreatic exocine secretion and inhibits acid secretion in the dog. In this study, the authors have investigated the effect of dopamine on human gastric and pancreatic secretions. In 6 subjects, dopamine produced a dose-dependent inhibition of pentagastrin-stimulated acid secretion, an effect that was suppressed when the subjects received haloperidol. In 6 other subjects, dopamine infusion did not modify basal pancreatic secretion, and dopamine inhibited pancreatic enzyme secretion during secretin-cholecystokinin infusion. Dopamine also caused a rise in plasma glucagon and insulin. The effects on pancreatic enzyme secretion and plasma glucagon were not antagonized by haloperidol. The results suggest that dopamine is inhibitory for human gastric secretion. The authors did not observe a stimulatory effect of dopamine on human pancreatic exocrine secretion as has been observed in dogs.
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PMID:Effect of dopamine on human gastric and pancreatic secretion. 75 61

Gastrin- and cholecystokinin (C.C.K.)-containing cells were detected by using anti-gastrin and anti-C.C.K. sera in the gastrointestinal tract of human fetuses and premature infants and in the stomach and duodenum of adult man obtained by biopsy from eight patients with normal gastro-duodenal endoscopy. The specificity of immunocytological reactions was ascertained by studying the inhibition of the reaction by gastrin, C.C.K., secretin, somatostatin, glucagon, insulin, serotonin, histamin, caerulein and octapeptide of C.C.K. In adult man, the gastrin cells are located only in the antrum and juxtapyloric region; C.C.K. was detected in the duodenum. In the human fetus, the first gastrin cells are seen in the antrum at 14 weeks of age and in the duodenum as early as 10 weeks; the C.C.K. cells are seen in the small intestine at 10 weeks of age.
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PMID:Identification of gastrin-secreting cells and cholecystokinin-secreting cells in the gastrointestinal tract of the human fetus and adult man. 79 24

The history of the discovery of gastrointestinal hormones and the modern methods of their isolation are discussed in the first chapter. The origin of structural relationships of gastrointestinal hormones and the possible ways of evolution are analyzed in the second chapter. The methods used for isolation and identification of secretin and cholecystokinin are dealt with in detail; the isolation of vasoactive intestinal peptide, gastrin, "gastric inhibitory peptide" and enteroglucagon is discussed but briefly in the first chapter. The second chapter is of speculative character. It deals with the structural resemblances between gastrin-type (gastrin, cholecystokinin-pancreozyzimin, caerulein) and secretin-type (secretin, vasoactive intestinal peptide, glucagon, "gastric inhibitory peptide") hormones. The resemblances are explained by different evolutionary mechanisms.
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PMID:Isolation and evolution of the gastrointestinal hormones. 80 95


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