Ca2+ Transport in Pancreatic β-Cells during Glucose Stimulation of Insulin Secretion

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

Abstract

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

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Published
1980-09-01
How to Cite
Hellman B., Gylfe E., Berggren P.-O., Andersson T., Abrahamsson H., Rorsman P., & Betsholtz C. (1980). Ca2+ Transport in Pancreatic β-Cells during Glucose Stimulation of Insulin Secretion. Upsala Journal of Medical Sciences, 85(3), 321-329. https://doi.org/10.3109/03009738009179202
Section
Original Articles

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