Calcium and pancreatic beta-cell function. 12. Modification of 45Ca fluxes by excess of K+

Glucose stimulation of insulin release is supposed to result from depolarization of the pancreatic beta-cells with subsequent influx of Ca2+. Isolated islets from non-inbred ob/ob-mice were employed for elucidating whether the glucose effects on the beta-cell handling of Ca2+ could be simulated by the depolarization evoked by excess of K+. Addition of 25 mM K+ was as effective as 20 mM glucose in stimulating the intracellular uptake of 45Ca. In both instances the additional amounts of incorporated 45Ca appeared in the mitochondria and the secretory granules. When analysing the washout pattern for 45Ca it was evident that the effects of raising K+ differed from those evoked by glucose. Whereas glucose inhibited 45Ca efflux during perifusion with Ca2+-deficient medium the addition of K+ resulted in a slight stimulation. Furthermore, the 45Ca incorporated in response to K+ was more readily mobilised.