Hyperpolarization of muscle by insulin in a glucose-free environment

It is concluded that insulin hyperpolarizes muscle membrane, as a result of which potassium moves into muscle, and that the eventual effect of insulin on potassium movement can be independent of any effect insulin may also have on glucose uptake.

Abstract

In a glucose-free solution, insulin increased resting membrane potential of rat extensor digitorum longus muscle by as much as it had in the presence of glucose. Even in the absence of glucose there was probably net accumulation of potassium by muscle, but the increase in muscle potassium concentration was too small to have been the cause of the observed hyperpolarization. It is concluded that insulin hyperpolarizes muscle membrane, as a result of which potassium moves into muscle, and that the eventual effect of insulin on potassium movement can be independent of any effect insulin may also have on glucose uptake.