Regulation of Insulin Release by Ionic and Electrical Events in B Cells

Horm Res. 1987;27(3):168-78. doi: 10.1159/000180806.

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.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Amino Acids / pharmacology
  • Animals
  • Calcium / metabolism*
  • Diazoxide / pharmacology
  • Glucose / pharmacology
  • Insulin / metabolism*
  • Ion Channels / metabolism*
  • Islets of Langerhans / drug effects
  • Islets of Langerhans / metabolism*
  • Membrane Potentials
  • Permeability
  • Potassium / metabolism
  • Sulfonylurea Compounds / pharmacology
  • Tolbutamide / pharmacology

Substances

  • Amino Acids
  • Insulin
  • Ion Channels
  • Sulfonylurea Compounds
  • Tolbutamide
  • Glucose
  • Diazoxide
  • Potassium
  • Calcium