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.
D000818:Animals; D002118:Calcium / Q000378:metabolism*; D002460:Cell Line; D002794:Choline / Q000494:pharmacology; D005947:Glucose / Q000494:pharmacology*; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007473:Ion Channels / Q000187:drug effects* / Q000378:metabolism; D007515:Islets of Langerhans / Q000187:drug effects* / Q000378:metabolism; D051379:Mice; D011188:Potassium / Q000378:metabolism; D051381:Rats; D012964:Sodium / Q000378:metabolism
D007328:Insulin; D007473:Ion Channels; D012964:Sodium; D005947:Glucose; D002794:Choline; D011188:Potassium; D002118:Calcium