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

Laboratory of Experimental Medicine, Brussels Free University Brussels, Belgium

Address requests for reprints to: Dr. W. J. Malaisse, Laboratory of Experimental Medicine, Boulevard de Waterloo 115, B-1000 Brussels,Belgium.

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 -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. (Endocrinology 106: 778, 1980)

Footnotes

^* This work was supported by grants from the Belgian Foundation for Scientific Medical Research. A preliminary account of this work was published in abstract form (36).

Received May 7, 1979.