Effects of ethanol, acetaldehyde and acetate on insulin release from perifused pancreatic islets.
It has been postulated that ethanol-induced changes in carbohydrate hemeostasis are mediated in part by alterations in pancreatic endocrine function. In this study ethanol (40, 120 and 240 mg/dl) produced dose-related suppression of immunoreactive insulin (IRI) release from isolated rat islets perifused with glucose and theophylline. Acetaldehyde inhibited IRI release at a concentration (39 mg/dl) much higher than can be achieved in vivo. A high concentration (29 mg/dl) of acetate did not influence IRI release. These results suggest that the ability of ethanol to inhibit IRI release resides principally in the parent compound and not its metabolites.
D000079:Acetaldehyde / Q000494:pharmacology*; D000085:Acetates / Q000494:pharmacology*; D019342:Acetic Acid; D000818:Animals; D004305:Dose-Response Relationship, Drug; D000431:Ethanol / Q000494:pharmacology*; D007328:Insulin / Q000378:metabolism*; D007515:Islets of Langerhans / Q000378:metabolism*; D007700:Kinetics; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D000085:Acetates; D007328:Insulin; D000431:Ethanol; D000079:Acetaldehyde; D019342:Acetic Acid