EVIDENCE FOR GLUCOSE STIMULATION OF INTRACELLULAR BUFFERING OF CALCIUM IN THE PANCREATIC -CELL

¹ Department of Medical Cell Biology, Biomedicum, University of Uppsala, 5-751 23 Uppsala, Sweden

Glucose-induced movements of Ca²⁺ in pancreatic -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.

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