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)

1. The effect of octapeptide of cholecystokinin-pancreozymin (CCK(8)), bethanechol, cholera toxin, glucagon and vasoactive intestinal polypeptide (VIP) on amylase secretion and lactic dehydrogenase (LDH) release from isolated rat pancreatic acini was studied.2. In isolated rat pancreatic acini, in the absence of theophylline in the medium, amylase secretion was increased by 65-78% with 10(-7) and 10(-6) M-cholera toxin. In the presence of theophylline, amylase secretion was increased by 43-56% with 10(-7) and 10(-6) M-cholera toxin following a 90 min incubation. No effect was observed in the presence of theophylline at 30 and 60 min. The effect of cholera toxin was potentiated by CCK(8) at 60 and 90 min.3. In the absence of theophylline in the medium, amylase secretion was increased by 81-118% with 10(-5) and 10(-4) M-glucagon and 86% with 10(-6) M-VIP at 60 min. In the presence of theophylline in the medium, amylase secretion was increased by 53-246% with 10(-9) to 10(-6) M-glucagon and 111-158% with 10(-7) and 10(-6) M-VIP respectively. The effect of glucagon and VIP was potentiated by CCK(8).4. Potentiation of the rate of amylase release due to glucagon (10(-5) M) and VIP (10(-6) M) occurred during the first 15 min of incubation.5. Release of LDH was not increased by any of these agents.6. It is concluded that cyclic AMP rise (due to cholera toxin, glucagon and VIP effect) increased amylase secretion from rat pancreatic acinar cells. This effect is less marked than in the guinea-pig pancreas and is potentiated by agents mobilizing cellular Ca(2+) (CCK(8) and bethanechol).7. These data indicate species-specific variation in the action of cyclic AMP in the pancreas.
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PMID:Role of cyclic adenosine monophosphate in amylase release from dissociated rat pancreatic acini. 618 68

The effects of dietary soybean trypsin inhibitor (SBTI, Kunitz type) or repeated i.p. injections of 95% pure cholecystokinin (CCK-39) on rat pancreas were investigated in a 10-day experiment. SBTI and CKK -39 induced similar increases in pancreatic weight, which led to both cellular hypertrophy and hyperplasia. Trypsin and chymotrypsin activity increased with an increase in pancreatic weight. Amylase activity increased only after CCK-39 injection, whereas lipase activity was not affected by either SBTI or CCK-39 treatment. After both treatments, insulin content showed only a slight tendency to increase, whereas glucagon content was not different from controls. The results indicate that SBTI and CCK-39 mainly exert their effects on the exocrine pancreas in a similar but not identical manner. It is therefore suggested that SBTI is not only a potent stimulator of the secretion of CCK activity but also of other unidentified gastrointestinal factor(s).
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PMID:The effect of feeding soybean trypsin inhibitor and repeated injections of cholecystokinin on rat pancreas. 620 62

Influence of amino acids upon pancreatic exocrine secretion has been investigated in the isolated perfused pancreas of rats. Arg produced significant and dose-related inhibition of pancreatic juice flow, protein output and amylase output evoked by CCK-PZ (1.25 pM). The secretory response evoked by CCK-PZ was inhibited by other amino acids (Ala, Asp, Asn, Gly, Ile, Leu, Lys, Met, Phe, Pro, Thr, Trp, Val, in each 20 mM). A similar inhibitory pattern was observed using 10 mixed amino acids of 2 mM each (Pro, Phe, Thr, Met, Lys, Asp, Leu, Trp, Val, Gly). Gly at a concentration of 20 mM produced significant inhibition of exocrine secretion evoked by ACh (50 nM) or GRP (36 pM). The inhibitory response induced by amino acids could not be repeated by using exogenous insulin (1 microM) and glucagon (280 nM). The inhibitory response was also not changed by increased extracellular Ca (5 or 10 mM). However, Gly (20 mM) produced inhibition of exocrine secretion evoked by Ca reintroduction into a pancreas which was pretreated with A 23187. It was suggested that the inhibitory effects of some amino acids on exocrine secretion are mainly caused by suppression of Ca influx in a stimulus-secretion coupling process.
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PMID:Inhibitory influence of amino acids on secretagogues induced exocrine secretion in isolated perfused rat pancreas. 620 12

Nutrients in the lumen of the small intestine may cause the release of enteric hormones which directly or indirectly stimulate intestinal mucosal growth. Male Sprague-Dawley rats with either an intact small bowel or following jejunal resection were maintained on total parenteral nutrition (TPN). C-terminal octapeptide-cholecystokinin alone or combined with secretin, or glucagon alone were added to the intravenous nutrient solution and continuously infused. Control rats received only TPN or gastric infusion of isocaloric amounts of TPN solution. After 7 days, intestinal hypoplasia was noted in rats with an intact bowel maintained on TPN alone compared with the gastrically infused group. TPN did not maintain the proximal-distal gradient of mucosal mass. Continuous intravenous infusion of octapeptide-cholecystokinin alone and together with secretin in rats maintained on TPN significantly stimulated small bowel mucosal growth, partially restoring the proximal-distal gradient. Glucagon infusion did not stimulate mucosal growth. Rats with a jejunal resection and maintained on TPN for 7 or 14 days failed to develop mucosal hyperplasia of the ileum in contrast to rats given the TPN solution intragastrically. Continuous intravenous infusion of octapeptide-cholecystokinin in rats maintained on TPN after jejunal resection caused significant mucosal growth in the ileum compared with the rats maintained on TPN alone, but not to the extent seen in gastrically fed animals. Intravenous infusion of octapeptide-cholecystokinin stimulates small-bowel mucosal growth. Secretin appears to have an additional effect when given together with octapeptide-CCK. Although a direct trophic action by these hormones on the intestinal mucosa is possible, this effect is more likely mediated via stimulation of pancreaticobiliary secretions.
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PMID:Effects of octapeptide-cholecystokinin, secretin, and glucagon on intestinal mucosal growth in parenterally nourished rats. 626 70

The aim of this work was to compare the action of gastrointestinal (GI) hormones on the myoelectrical activity of the sphincter of Oddi. Using an experimental design previously described, we studied the electrical activity of the sphincter of Oddi and compared the percentage variation in the number of spikes before and after injection of hormones. Increasing doses of the following hormones were injected i.v. at random: CCK, OP-CCK, caerulein, bombesin, gastrin, secretin and glucagon. CCK and caerulein (as previously found), and also bombesin, OP-CCK and gastrin increased the spikes activity of the sphincter of Oddi. Secretin had no effect and glucagon decreased this activity. There was no tachyphylaxis, but a good dose-effect relationship for each hormone. Compared on a molar basis caerulein is 8 times more effective than CCK and OP-CCK which in turn are more potent than bombesin. Gastrin acts only at pharmacological doses.
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PMID:Action of gastrointestinal hormones on the myoelectric activity of the sphincter of Oddi in living rabbit. 626 80

The secretory effect of sulfated and nonsulfated cholecystokinin octapeptide (CCK-8) was studied on the isolated perfused porcine pancreas. Both CCKs in concentrations from 10(-11) to 10(-8) mol/l in the presence of glucose (7.5, 5.0 or 3.5 mmol/l) were without effect on insulin and glucagon release. The exocrine secretion was stimulated by both CCKs in a dose-dependent manner, but sulfated CCK-8 was considerably more potent. The study shows that CCK-8, a major constituent of endogenous CCK, does not contribute to the incretin mechanism, irrespective of degree of sulfation. In contrast, CCK-8 is a potent stimulator of exocrine pancreatic secretion. For this effect sulfation is crucial.
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PMID:Effect of sulfation of CCK-8 on its stimulation of the endocrine and exocrine secretion from the isolated perfused porcine pancreas. 627 14

A biologically active gastrin analogue, [125I](Nle11)-HG-13, appears to bind specifically to saturable binding sites on isolated rabbit gastric mucosal cells: Kd = 70 pM at pH 7.4 and at 37 degrees C. Increasing incubation temperature from +4 degrees C to +37 degrees C increased specific binding. Gastrin binding was shown to be reversible and the dissociation rate was enhanced with cold gastrin. The binding sites were saturated with 0.2 fmol of labelled gastrin per 10(6) mucosal cells. Gastrin binding was not inhibited by secretin, glucagon, Met-enkephalin, physalaemin, eledoisin, BPP, VIP, carbachol, histamine, atropine or cimetidine. Gastrin analogues (HG-4, HG-8, (Leu15)-HG-17), CCK-7 and gastrin antagonists (proglumide or benzotript) inhibited [125I](Nle11)-HG-13 specific binding. We concluded that isolated cells from rabbit gastric fundic mucosa contain high-affinity binding sites for a gastrin analogue (Nle11)-HG-13.
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PMID:High-affinity binding sites for gastrin on isolated rabbit gastric mucosal cells. 629 Feb 32

Rats equipped with biliary, duodenal, and vena cava cannulae and supplemented with Na taurocholate received 4 hour infusions of gastrointestinal hormones. Boots secretin increased bile flow by 63% and bile acid, cholesterol, and phospholipid output by 75, 96, and 73% respectively. This stimulatory effect on bile flow and bile acid secretion was observed also in the four hour postinfusion period. Kabi secretin had practically no effect on bile secretion. Boots pancreozymin stimulated bile flow by 45% and to some extent also stimulated bile acid output. OP-CCK and glucagon stimulated mainly bile flow rate.
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PMID:Effect of secretin, pancreozymin OP-CCK, and glucagon on bile flow and bile lipid secretion in rats. 630 17

Both radiotrace labeled and high specific activity 125I-labeled derivatives of secretin were prepared by direction iodination of the histidyl residue with chloramine T [( 125I]secretin) and by conjugation of a preiodinated Bolton-Hunter group (iodo-3-(4-hydroxyphenyl)propionate) to the free alpha-amino group at the N-terminus [( 125I]BH-secretin). Following purification, the biological, immunological and receptor binding properties of both secretin derivatives were compared. [125I]secretin and [125I]BH-secretin were equally effective in a sensitive radioimmunoassay that detected secretin and secretin (5-27) but not CCK-8, VIP and glucagon. Although both derivatives retained 60% of the biological potency of secretin as measured by cAMP accumulation in pancreatic acinar cells, only the directly iodinated peptide [( 125I]secretin) could be used to characterize specific binding sites on rat pancreatic membranes. The N-terminal blocked derivative [( 125I]BH-secretin) in contrast dissociated rapidly from pancreatic membranes reflecting an unstable hormone-receptor complex. These results suggest that a free alpha-amino group at the N-terminus may be essential for an optimal interaction of secretin with its pancreatic receptor.
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PMID:Effect of N-terminal iodination on the biological, immunological and receptor binding properties of secretion. A role for the alpha-amino group of histidine in stabilizing hormone-receptor interactions. 632 57

Previous studies in anesthetized dogs demonstrated that basal hepatic extraction of insulin and glucagon are approximately 50 and 10-20%, respectively. Because of the stress of anesthesia and surgery, these values may not be relevant to normal physiology. In this study, hepatic extraction of insulin and glucagon were compared in conscious and anesthetized dogs. The conscious dogs had chronically implanted catheters in the portal and hepatic vein and the carotid artery and Doppler flow probes on the portal vein and hepatic artery. The mean basal portal vein insulin (42 +/- 10 and 44 +/- 7 microU/ml, respectively) and glucagon (247 +/- 37 and 219 +/- 20 pg/ml, respectively) concentrations were similar in conscious and anesthetized animals. The mean basal portal vein, but not hepatic artery, plasma flow was significantly increased in conscious dogs (462 +/- 62 vs. 294 +/- 35 ml/min, respectively). Despite the increased portal vein plasma flow in conscious animals, the basal hepatic extractions of insulin (42 +/- 6 vs. 39 +/- 6%, respectively) and glucagon (12 +/- 7 vs. 7 +/- 7%, respectively) were similar in both types of animals. Arginine and cholecystokinin-pancreozymin (CCK-PZ) infusion, which increased the amount of insulin and glucagon presented to the liver in conscious and anesthetized dogs, significantly decreased the hepatic extraction of insulin. Hepatic extraction of glucagon did not change in either group of animals. In contrast, infusion of insulin (1.0 mU/kg X min) and glucagon (4 ng/kg X min) into the portal system did not alter hepatic extraction of insulin even though the amounts of insulin and glucagon presented to that organ were similar to those obtained with arginine and CCK-PZ. The basal arterial glucose level was significantly lower in the conscious dogs but the basal hepatic glucose output was similar in the two groups. The glucose response to the infusion of arginine and CCK-PZ and exogenous hormones was significantly greater in the anesthetized animals.
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PMID:Comparison of hepatic extraction of insulin and glucagon in conscious and anesthetized dogs. 633 43


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