Abstract
Summary
In studies pertinent to pathophysiologic changes in diabetes and reactive hypoglycemia, we have investigated, in dogs, the effect of gastroenteropancreatic hormones upon gastric inhibitory polypeptide (GIP), since it is a potent insulin-releasing hormone. Intravenous infusion of pharmacologic doses of vasoactive inhibitory polypeptide (VIP), acetylcholine, isoproterenol, epinephrine (with or without phentolamine or propranolol), serotonin, or pancreatic polypeptide (PP) did not change fasting plasma GIP levels, despite the fact that several of them increased plasma insulin. However, glucose-induced increase in GIP was inhibited by acetylcholine, iosproterenol, and epinephrine (aloninhibitory polypeptide (GIP), since it is a potent insulin-releasing hormone. Intravenous infusion of pharmacologic doses of vasoactive inhibitory polypeptide (VIP), acetylcholine, isoproterenol, epinephrine (with or without phentolamine or propranolol), serotonin, or pancreatic polypeptide (PP) did not change fasting plasma GIP levels, despite the fact that several of them increased plasma insulin. However, glucose-induced increase in GIP was inhibited by acetylcholine, iosproterenol, and epinephrine (alone or plus phentolamine or plus propranolol), but was not affected by gastrin, VIP, or PP. Corn oil-stimulated GIP rise was inhibited by acetylcholine but not by isoproterenol. By infusing the hormones systemically we were testing an endocrine effect, but their endogenous release in the gut would conceivably promote neurocrinic and /or paracrinic actions. Their release in close proximity to the K cells (GIP-producing) would presumably provide higher concentrations and stronger actions on these cells.
We are deeply indebted to: Drs. Joel Brodsky, Gerald Van Belle, and C. B. Bell for statistical analyses; Drs. John Brown, Werner Creutzfeldt, Roger Unger, Ronald Chance, Morton Grossman, and Sami Said for special hormones and/or antibodies; James Champagne (research technician); Patricia Hulin (secretary).
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