Regulation of insulin release by ionic and electrical events in B cells.
(1987) Hormone Research — Vol. 27, n° 3, p. 168-178 (1987)
Files
No attached file found for this publication.
Details
- Authors
- Abstract
- 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.
- Affiliations
Citations
Henquin, J.-C. (1987). Regulation of insulin release by ionic and electrical events in B cells. Hormone Research, 27(3), 168-178. https://doi.org/10.1159/000180806 (Original work published 1987)