GIP potentiates CCK stimulated pancreatic enzyme secretion: correlation of anatomical structures with the effects of GIP and CCK on amylase secretion.
Utilizing scanning electron microscopy and isolated, vascularly perfused rat pancreas, we studied the angioarchitecture and the effect of the insulinotropic hormone, gastric inhibitory polypeptide (GIP), on cholecystokinin (CCK)-stimulated exocrine secretion. We tried to correlate the microcirculation with the physiological effect of insulin on the pancreatic secretion in the same species. We found a vascular pattern consisting of direct insuloacinar connections, a venous drainage system of islets, and a direct arterial supply of acini. GIP at a concentration as low as 2 ng/ml or exogenous rat insulin potentiated CCK-stimulated pancreatic enzyme secretion. To have similar effects as insulin which is endogenously released by GIP, about 30 times more exogenous rat insulin has to be infused. We conclude that based on the angioarchitecture, insulinotropic hormones like GIP could link the metabolic and the digestive function of the pancreas.
D000681:Amylases / Q000378:metabolism*; D000818:Animals; D004305:Dose-Response Relationship, Drug; D004357:Drug Synergism; D005749:Gastric Inhibitory Polypeptide / Q000494:pharmacology*; D007328:Insulin / Q000378:metabolism / Q000494:pharmacology; D000078790:Insulin Secretion; D008297:Male; D008833:Microcirculation / Q000648:ultrastructure*; D008855:Microscopy, Electron, Scanning; D010179:Pancreas / Q000098:blood supply* / Q000378:metabolism; D051381:Rats; D011919:Rats, Inbred Strains; D012844:Sincalide / Q000494:pharmacology*
D007328:Insulin; D005749:Gastric Inhibitory Polypeptide; D000681:Amylases; D012844:Sincalide