The stimulus-secretion coupling of glucose-induced insulin release. XXXIX. Long term effects of K+ deprivation upon insulin biosynthesis and release.

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 alpha-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 glucose-deprived islets. It is postulated that the intracellular concentration of K+ in islet cells participates in the long term regulation of insulin release by glucose.