Abstract
Pancreatic islets prelabelled with either 86Rb or 45Ca were exposed to a rise in D-glucose concentration from 2.8 to 16.7 mM whilst perifused in the presence of 2 μM glibenclamide, 30 mM extracellular K + and both 30 mM K + and 250 μM diazoxide. In all three situations, the rise in glucose concentration provoked a dramatic increase in insulin output, despite unchanged or even increased efflux of 86Rb from the prelabelled islets. Also in all three situations, glucose sharply decreased effluent radioactivity from islets prelabelled with 45Ca but perifused in the absence of extracellular Ca 2+, whilst augmenting 45Ca efflux, to a variable extent, from islets perifused at normal extracellular Ca 2+ concentration (1.0 mM). It is proposed, therefore, that the insulinotropic action of D-glucose in depolarized islets, and presumably also under normal conditions, may involve the gating of voltage-insensitive Ca 2+ channels.
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