Evidence for glucose stimulation of intracellular buffering of calcium in the pancreatic beta-cell.

Glucose-induced movements of Ca2+ in pancreatic beta-cells were analysed using islets isolated from ob/ob mice and insulin-releasing cells from a clonal cell line (RINm5F). Addition of glucose to a perifusion medium resulted in an inhibited efflux of 45Ca from the islets both when the extracellular Ca2+ concentration was lower or higher than that in the cytosol. Glucose inhibition of 45Ca efflux was seen also after altering the Na+ gradient across the plasma membrane provided that the cytosolic K+ activity was maintained. The glucose suppression of 45Ca efflux corresponded to a stimulated net uptake of Ca2+ in the RINm5F cells. Also in this case the glucose effect was maintained when Na+ was replaced with K+ and suppressed after substitution with choline. During perifusion of islets with a Ca2+-deficient medium the removal of glucose resulted in a temporary stimulation of insulin release. The results suggest that glucose, in addition to stimulating the entry of Ca2+, also promotes active sequestration of the ion in intracellular stores. The balance between these processes will determine the activity of cytosolic Ca2+ and consequently the rate of insulin release.