Abstract
Glucose regulates Ca2+ influx in beta-cells by controlling a rhythmic electrical activity (slow waves with spikes). However, the glucose-sensitive feedback system that triggers repolarization at the end of the slow waves, and thus stops Ca2+ influx, is unknown. Raising extracellular Ca2+ to 10 mM shortened slow waves in mouse beta-cells perifused with medium containing 15 mM glucose and restored slow waves when persistent depolarization and continuous spike activity were induced by 30 mM glucose. The effects of high Ca2+ were reversed or prevented by tolbutamide, whereas 1 mM tetraethylammonium only increased spike amplitude. This suggests that a feedback action of Ca2+ on ATP-sensitive K+ channels rather than on voltage- and Ca2(+)-activated K+ channels may be involved in slow wave generation. Metabolic modulation of this feedback could be central in the regulation of electrical activity and, hence, insulin release.
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