The Stimulus-Secretion Coupling of Glucose-Induced Insulin Release. XXXIX. Long Term Effects of K+ Deprivation upon Insulin Biosynthesis and Release*

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Abstract
A decrease in the extracellular concentration of K+ provokes a dose-related, progressive, and persistent inhibition of insulin release evoked by high concentrations of glucose or α-ketoisocaproate. The biosynthesis of proinsulin and other peptides is severely decreased in the K+-deprived islets. The functional situation found in the K+-deprived islets can be mimicked, to a limited extent, by exposing the islets to inhibitors of protein biosynthesis and is reminiscent of that found in glucosedeprived islets. It is postulated that the intracellular concentration of K+ in islet cells participates in the long term regulation of insulin release by glucose. (Endocrinology106: 778, 1980)