β-Cell cytoplasmic Ca2+ balance as a determinant for glucose-stimulated insulin release

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Abstract
The introduction of new techniques and the access to clonal lines of insulin-secreting cells have enabled re-evaluation of glucose effects on Ca2+ movements in pancreatic β cells. It became evident that glucose, in addition to stimulating the entry of Ca2+ also promotes active sequestration of the ion in intracellular stores and its extrusion from the β cells. The balance between these processes will determine the activity of Ca2+ in the cytoplasm and consequently the rate of insulin release. With the demonstration that glucose can not only increase but also lower cytoplasmic Ca2+, it follows that exposure to the sugar under certain conditions results in a paradoxical inhibition of insulin release. In diabetic patients this may be manifest as prompt reduction of circulating concentrations of insulin and C-peptide after an intravenous injection of glucose. The concept of the dual action of glucose might aid in explaining a number of poorly understood phenomena, such as the induction of rhythmic oscillations of the membrane potential of β cells and the fact that their secretory response is improved by prolonged exposure to glucose and after priming with the sugar.