The role of Ca2+ and calmodulin in insulin signalling in mammalian skeletal muscle

Acta Physiol Scand. 2001 Mar;171(3):259-65. doi: 10.1046/j.1365-201x.2001.00828.x.

Abstract

The role of Ca2+ in mediating effects of insulin on skeletal muscle has been widely debated. It is believed that in skeletal muscle Ca2+ has a permissive role, necessary but not of prime importance in mediating the stimulatory actions of insulin. In this review, we present evidence that insulin causes a localized increase in the concentration of Ca2+. Specifically, insulin induces a rise in near-membrane Ca2+ but not the bulk Ca2+ in the myoplasm. The rise in near-membrane Ca2+ is because of an influx through channels that can be blocked by L-type Ca2+ channel inhibitors. Calcium appears to exert some of its subsequent effects via calmodulin-dependent processes as calmodulin inhibitors block the translocation of glucose transporters and other enzymes as well as the insulin-stimulated increase in glucose transport.

Publication types

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

MeSH terms

  • Animals
  • Biological Transport / drug effects
  • Calcium / physiology*
  • Calcium Channel Blockers / pharmacology
  • Calcium Channels / drug effects
  • Calmodulin / physiology*
  • Glucose / metabolism
  • Insulin / metabolism*
  • Mice
  • Muscle Fibers, Skeletal / drug effects
  • Muscle Fibers, Skeletal / metabolism
  • Muscle, Skeletal / drug effects
  • Muscle, Skeletal / metabolism*
  • Rats
  • Signal Transduction*

Substances

  • Calcium Channel Blockers
  • Calcium Channels
  • Calmodulin
  • Insulin
  • Glucose
  • Calcium