Microdissected β-cell-rich pancreatic islets from ob/ob-mice were used in studies of transmembrane36Cl efflux. The mean rate coefficient for36Cl efflux was stable at 0.158 min−1 during the initial 10 min. Depolarization of the β-cell plasma membrane by acute increases in extracellular K+ (5–130mM) stimulated the36Cl efflux in a concentration-dependent manner. Glucose-induced (20mM) and K+-induced increases in36Cl efflux were largely overlapping, but even at 135.9 mM K+, glucose slightly further enhanced the36Cl efflux rate. The data suggest (1) that pancreatic β-cells are equipped with a voltage-dependent Cl permeability, (2) that glucose-induced increase in Cl permeability may, at least partly, be mediated by primary membrane depolarization, and (3) that glucose in addition may activate other mechanisms for β-cell Cl transport.

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