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Diabetes 51:S33-S36, 2002
© 2002 by the American Diabetes Association, Inc.

Section 1: Insulin Release: Some Molecular Requisites

Sulfonylurea-Mediated Stimulation of Insulin Exocytosis via an ATP-Sensitive K+ Channel–Independent Action

Erik Renström1, Sebastian Barg1, Frank Thévenod2, and Patrik Rorsman1

1 Department of Molecular and Cellular Physiology, Institute of Physiology, Lund University, Lund, Sweden
2 F.T. School of Biological Sciences, University of Manchester, Manchester, U.K.

Several reports indicate that hypoglycemic sulfonylureas augment Ca2+-dependent insulin secretion via mechanisms other than inhibition of the ATP-sensitive K+ channel. The effect involves a 65-kd protein in the granule membrane and culminates in intragranular acidification. Lowering of granule pH is necessary for the insulin granule to gain release competence. Proton pumping into the granule is driven by a v-type H+-ATPase, but requires simultaneous Cl- uptake into the granule via metabolically regulated ClC-3 Cl- channels to maintain electroneutrality. Here we discuss the possibility that modulation of granule ClC-3 channels represents the mechanism whereby sulfonylureas directly potentiate the ß-cell exocytotic machinery.


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Copyright © 2002 by the American Diabetes Association.