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The role of Ca2+ in the regulation of insulin secretion was evaluated using beta-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 beta-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.

Type

Journal article

Journal

Ups J Med Sci

Publication Date

1980

Volume

85

Pages

321 - 329

Keywords

Adenosine Triphosphate, Animals, Blood Glucose, Calcium, Cyclic AMP, Cytoplasmic Granules, Insulin, Ion Channels, Islets of Langerhans, Membrane Potentials, Mice, Mitochondria, Secretory Rate, Subcellular Fractions