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Query: UNIPROT:P01275 (glucagon)
 26,492 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study provides evidence that changes in glucagon secretion are influential in determining the hyperglycemic activity of catecholamines in normal and diabetic rats. In normal fed rats, epinephrine (EPI) stimulated large increments in glucagon release and inhibited insulin secretion. In contrast, the modest hyperglycemic activity of isoproterenol (ISO) in normal fed rats correlated with its weak glucagon-releasing activity and its strong insulin-releasing activity. In alloxan-diabetic rats, the augmented hyperglycemic response to ISO was accompanied by larger increments in plasma glucagon levels than the catecholamine produced in normal fed rats. When glucagon release was inhibited by a concurrent infusion of somatostatin, the hyperglycemic responses of normal fed rats to EPI were reduced by approximately 67%. ISO-induced hyperglycemia in alloxan-diabetic rats was even more sensitive to inhibition by somatostatin since this response was reduced by approximately 90% when glucagon release was inhibited by somatostatin. These findings indicate that more than half of the hyperglycemic response to EPI in normal fed rats and nearly all of the hyperglycemia produced by ISO in diabetic rats result from increased glucagon release. Moreover, the impotence of ISO as a hyperglycemic agent in normal fed rats is probably due to insulin release which tends to suppress glucagon release.
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PMID:The influence of endogenous glucagon release on hyperglycemic responses to catecholamines in normal fed and diabetic rats. 48 Jan 94

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