Regulation of insulin release by ionic and electrical events in B cells.
This review article is an attempt to schematize the major alterations in ionic fluxes and B cell membrane potential 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.
D000596:Amino Acids / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D003981:Diazoxide / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology; D007328:Insulin / Q000378:metabolism*; D007473:Ion Channels / Q000378:metabolism*; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D008564:Membrane Potentials; D010539:Permeability; D011188:Potassium / Q000378:metabolism; D013453:Sulfonylurea Compounds / Q000494:pharmacology; D014044:Tolbutamide / Q000494:pharmacology
D000596:Amino Acids; D007328:Insulin; D007473:Ion Channels; D013453:Sulfonylurea Compounds; D014044:Tolbutamide; D005947:Glucose; D003981:Diazoxide; D011188:Potassium; D002118:Calcium