Ca2+ transport in pancreatic beta-cells during glucose stimulation of insulin secretion.
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.
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D002118:Calcium / Q000378:metabolism*; D000242:Cyclic AMP / Q000378:metabolism; D003594:Cytoplasmic Granules / Q000378:metabolism; D007328:Insulin / Q000097:blood*; D007473:Ion Channels / Q000378:metabolism; D007515:Islets of Langerhans / Q000378:metabolism*; D008564:Membrane Potentials; D051379:Mice; D008928:Mitochondria / Q000378:metabolism; D012636:Secretory Rate; D013347:Subcellular Fractions / Q000378:metabolism
D001786:Blood Glucose; D007328:Insulin; D007473:Ion Channels; D000255:Adenosine Triphosphate; D000242:Cyclic AMP; D002118:Calcium