Title: Regulation of adenosine 3',5'-monophosphate levels in the pancreatic B cell
Authors: Schuit, Frans
Pipeleers, D G # ×
Issue Date: Sep-1985
Publisher: Association for the Study of Internal Secretions
Series Title: Endocrinology vol:117 issue:3 pages:834-40
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 suggest 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(-10) M on, reaching the values of islet B cells at 10(-9) M. In contrast, exogenous glucagon stimulates cAMP formation in isolated islets only from 3.10(-9) M 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 intra-islet 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.
ISSN: 0013-7227
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Gene Expression Unit
× corresponding author
# (joint) last author

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