Ca2+ Transport in Pancreatic β-Cells during Glucose Stimulation of Insulin Secretion

Abstract

The role of Ca²⁺ in the regulation of insulin secretion was evaluated using β-cell-rich pancreatic islets isolated from ob/ob-mice. The glucose stimulation of the secretory activity is supposed to result from accumulation of Ca²⁺ in the submembrane cytoplasmic space. It is likely that this process reflects the balance between increased entry of Ca²⁺ into the β-cells and an enhanced sequestration of Ca²⁺ in the organelle sinks. The proposed model can explain the cAMP potentiation of glucose-stimulated insulin release with suppression of the mitochondrial Ca²⁺ uptake. Furthermore, differences in the Ca²⁺ buffering capacity of the secretory granules may account for other characteristic features of glucose-stimulated insulin release, in particular its biphasic nature and sensitivity to suppression on withdrawal of nutrients.