Insulin action on membrane potential and glucose uptake: Effects of high potassium

K. Zierler, E. M. Rogus, R. W. Scherer, F. S. Wu

Research output: Contribution to journalArticlepeer-review

15 Scopus citations

Abstract

These experiments were designed to test the hypothesis that insulin-induced hyperpolarization is a link in the chain of events leading to stimulation of glucose transport. External potassium concentration, [K+]0, was increased by equimolar substitution of KCl for NaCl, a method known to cause cell swelling, and by substitution of [K+]0 for [Na+]0 with maintenance of constant [K+]0. [Cl-]0 product, a method that does not cause cell swelling. When there was constant KCl product, even at 76.8 meq [K+]0 insulin continued to hyperpolarize, although by only ~44% as much as in normal [K+]0, and insulin-stimulated 2-deoxyglucose uptake was only ~60% of that at normal [K+]0. With equimolar substitution of KCl for NaCl: 1) electrical potential difference across cell membranes of surface fibers of rat caudofemoralis muscle decreased with logarithm [K+]0, in the presence or absence of insulin. 2) Insulin-induced hyperpolarization decreased as [K+]0 increased and disappeared at 36 mM [K+]0. 3) The amount of insulin bound to its receptors in 1 h was not affected by [K+]0 over the range studied. 4) Insulin effects on membrane potential and on 2-deoxyglucose uptake, as both were altered by [K+]0, correlated well. As the probe moved in depth through the first six fibers there was stepwise decrease in depolarization in high [K+]0 in the absence of insulin. Insulin hyperpolarized the deepest of these fibers, even when it did not hyperpolarize the outermost. The decrease in insulin-induced hyperpolarization as [K+]0 increases is consistent with the hypothesis that insulin hyperpolarizes by decreasing the ratio P(Na)/P(K).

Original languageEnglish (US)
Pages (from-to)E17-E25
JournalAmerican Journal of Physiology - Endocrinology and Metabolism
Volume12
Issue number1
DOIs
StatePublished - Jan 1 1985

ASJC Scopus subject areas

  • Endocrinology, Diabetes and Metabolism
  • Physiology
  • Physiology (medical)

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