Open AccessCa2+Transport in Pancreatic β-Cells during Glucose Stimulation of Insulin Secretion
Author(s) -
Bo Hellman,
Erik Gylfe,
Per Olof Berggren,
Tommy Andersson,
H Abrahamsson,
Patrik Rorsman,
Christer Betsholtz
Publication year - 1980
Publication title -
upsala journal of medical sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.808
H-Index - 41
eISSN - 2000-1967
pISSN - 0300-9734
DOI - 10.3109/03009738009179202
Subject(s) - medicine , endocrinology , stimulation , insulin , pancreatic islets , secretion , beta cell , cytoplasm , insulin oscillation , islet , microbiology and biotechnology , biology
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.