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Research Article Free access | 10.1172/JCI115714

Evidence that glucose can control insulin release independently from its action on ATP-sensitive K+ channels in mouse B cells.

M Gembal, P Gilon, and J C Henquin

Unité de Diabétologie et Nutrition, Faculty of Medicine, University of Louvain, Brussels, Belgium.

Find articles by Gembal, M. in: PubMed | Google Scholar

Unité de Diabétologie et Nutrition, Faculty of Medicine, University of Louvain, Brussels, Belgium.

Find articles by Gilon, P. in: PubMed | Google Scholar

Unité de Diabétologie et Nutrition, Faculty of Medicine, University of Louvain, Brussels, Belgium.

Find articles by Henquin, J. in: PubMed | Google Scholar

Published April 1, 1992 - More info

Published in Volume 89, Issue 4 on April 1, 1992
J Clin Invest. 1992;89(4):1288–1295. https://doi.org/10.1172/JCI115714.
© 1992 The American Society for Clinical Investigation
Published April 1, 1992 - Version history
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Abstract

Glucose stimulation of insulin release involves closure of ATP-sensitive K+ channels, depolarization, and Ca2+ influx in B cells. Mouse islets were used to investigate whether glucose can still regulate insulin release when it cannot control ATP-sensitive K+ channels. Opening of these channels by diazoxide (100-250 mumol/liter) blocked the effects of glucose on B cell membrane potential (intracellular microelectrodes), free cytosolic Ca2+ (fura-2 method), and insulin release, but it did not prevent those of high K (30 mmol/liter). K-induced insulin release in the presence of diazoxide was, however, dose dependently increased by glucose, which was already effective at concentrations (2-6 mmol/liter) that are subthreshold under normal conditions (low K and no diazoxide). This effect was not accompanied by detectable changes in B cell membrane potential. Measurements of 45Ca fluxes and cytosolic Ca2+ indicated that glucose slightly increased Ca2+ influx during the first minutes of depolarization by K, but not in the steady state when its effect on insulin release was the largest. In conclusion, there exists a mechanism by which glucose can control insulin release independently from changes in K(+)-ATP channel activity, in membrane potential, and in cytosolic Ca2+. This mechanism may serve to amplify the secretory response to the triggering signal (closure of K(+)-ATP channels--depolarization--Ca2+ influx) induced by glucose.

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