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Regulation of insulin release by ionic and electrical events in B cells


, : Regulation of insulin release by ionic and electrical events in B cells. Hormone Research 27(3): 168-178

This review article is an attempt to schematize the major alteractions in ionic fluxes and B cell membrane potenial that underlie the changes in insulin release brought about by glucose and by other stimulators or inhibitors. Glucose metabolism in B cells leads to closure of K channels in the plasma membrane. The resulting decrease in K+ permeability causes depolarization with activation of voltage-dependent Ca channels. An increase in Ca2+ influx ensues, which raises the cytoplasmic concentration of free Ca2+ and ultimately triggers insulin release. Tolbutamide induces a similar sequence of events by a direct action on K channels. In contrast, diazoxide antagonizes the effects of glucose by increasing K+ permeability of the B cell membrane. Among amino acids, leucine largely mimics the effects of glucose, whereas arginine depolarizes the B cell membrane because of its transport in a positively charged form.

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Accession: 006288777

PMID: 2447002

DOI: 10.1159/000180806

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