The role of metabolism in the control of cyclic AMP efflux, cyclic AMP content, and insulin secretion from rat islets of Langerhans.
Glucose, alpha-ketoisocaproate, and N-acetylglucosamine all initiate insulin release and stimulate cyclic AMP efflux and cyclic AMP accumulation. Mannoheptulose inhibited these islet responses to glucose but not to N-acetylglucosamine or alpha-ketoisocaproate. On the other hand, menadione inhibited these responses to all three secretagogues. Nicotinamide enhanced the insulin release due to glucose and alpha-ketoisocaproate and also enhanced cyclic AMP efflux and intracellular cyclic AMP accumulation. N-acetylglucosamine-mediated insulin release, cyclic AMP efflux, and cyclic AMP accumulation were unaffected by nicotinamide. These results suggest that the metabolic state of the islet is a primary determinant of the ability of a secretagogue to raise cyclic AMP efflux and intracellular cyclic AMP, and these actions may be mediated in part by alterations in the redox state of the pyridine nucleotide system.
D000117:Acetylglucosamine / Q000494:pharmacology; D000818:Animals; D000242:Cyclic AMP / Q000502:physiology*; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000502:physiology*; D007651:Keto Acids / Q000494:pharmacology; D008356:Mannoheptulose / Q000494:pharmacology; D009243:NAD / Q000378:metabolism; D010084:Oxidation-Reduction; D051381:Rats; D014812:Vitamin K / Q000494:pharmacology
D007328:Insulin; D007651:Keto Acids; D009243:NAD; D014812:Vitamin K; D008356:Mannoheptulose; C013082:alpha-ketoisocaproic acid; D000242:Cyclic AMP; D005947:Glucose; D000117:Acetylglucosamine