Ca2+ transport in pancreatic βcells during glucose stimulation of insulin secretion

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

Research output: Contribution to journalArticle

2 Scopus citations

Abstract

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

Original languageEnglish (US)
Pages (from-to)321-329
Number of pages9
JournalUpsala Journal of Medical Sciences
Volume85
Issue number3
DOIs
StatePublished - Jan 1 1980

ASJC Scopus subject areas

  • Medicine(all)

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    Hellman, B., Gylfe, E., Berggren, P. O., Andersson, T., Abrahamsson, H., Rorsman, P., & Betsholtz, C. (1980). Ca2+ transport in pancreatic βcells during glucose stimulation of insulin secretion. Upsala Journal of Medical Sciences, 85(3), 321-329. https://doi.org/10.3109/03009738009179202