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• W2025659430 abstract "The poor glucose-induced insulin release from single purified B cells has been attributed, in part, to the low cellular cAMP levels. The present study demonstrates that isolated B cells exhibit a markedly lower cAMP formation than B cells lodged in intact islets and suggests that this deficiency is caused by their separation from glucagon-containing A cells. cAMP levels in purified B cells are rapidly and potently elevated by glucagon from 10−10m on, reaching the values of islet B cells at 10−9m. In contrast, exogenous glucagon stimulates cAMP formation in isolated islets only from 3.10−9m on, suggesting that endogenously released glucagon is mainly responsible for the higher cAMP levels in islet B cells. Somatostatin counteracts glucagon-induced cAMP production in purified B cells and, therefore, has also the potential to mediate an intraislet regulation of B cell functions. Neither insulin nor pancreatic polypeptide affect cAMP formation in pancreatic B cells. Glucose alone does not influence cAMP levels in purified B cells, but enhances glucagon-induced cAMP formation in these cells. The glucose-dependent increase in islet cAMP is therefore not considered as the nutrient-induced mediator for hormone release but as a minor amplification of the glucagon-dependent signal. Experiments on reaggregated islet cells permit the reconstruction of the events which regulate cAMP levels in isolated islets. Further support is hereby given to the hypothesis that a normal glucose-induced insulin release from intact islets requires the simultaneous synarchic participation of a nutrient-dependent and a hormone-dependent messenger system. (Endocrinology117: 834–840, 1985)" @default.
• W2025659430 created "2016-06-24" @default.
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• W2025659430 date "1985-09-01" @default.
• W2025659430 modified "2023-10-18" @default.
• W2025659430 title "Regulation of Adenosine 3′,5′-Monophosphate Levels in the Pancreatic B Cell*" @default.
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• W2025659430 doi "https://doi.org/10.1210/endo-117-3-834" @default.
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