Portal de Periódicos da CAPES

Ca 2+ Transport in Pancreatic β-Cells during Glucose Stimulation of Insulin Secretion

1980; Taylor & Francis; Volume: 85; Issue: 3 Linguagem: Inglês

10.3109/03009738009179202

2000-1967

Bo Hellman, Erik Gylfe, Per‐Olof Berggren, Tommy Andersson, Håkan Abrahamsson, Patrik Rorsman, Christer Betsholtz,

Diabetes and associated disorders

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.