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.
D000818:Animals; D003513:Cycloheximide / Q000494:pharmacology; D005260:Female; D005947:Glucose / Q000494:pharmacology*; D007328:Insulin / Q000096:biosynthesis / Q000378:metabolism*; D007515:Islets of Langerhans / Q000187:drug effects / Q000378:metabolism*; D007700:Kinetics; D011188:Potassium / Q000494:pharmacology*; D011691:Puromycin / Q000494:pharmacology; D051381:Rats; D013806:Theophylline / Q000494:pharmacology
D007328:Insulin; D011691:Puromycin; D003513:Cycloheximide; D013806:Theophylline; D005947:Glucose; D011188:Potassium