R-type Ca2+-channel-evoked CICR regulates glucose-induced somatostatin secretion

Quan Zhang, Martin Bengtsson, Chris Partridge, S Albert Salehi, Matthias Braun, Roger Cox, Lena Eliasson, Paul R. V. Johnson, Erik Renström, Toni Schneider, Per-Olof Berggren, Sven Gopel, Frances M. Ashcroft, Patrik Rorsman

Research output: Contribution to journalArticlepeer-review

Abstract

Pancreatic islets have a central role in blood glucose homeostasis. In addition to insulin-producing beta-cells and glucagon-secreting alpha-cells, the islets contain somatostatin-releasing delta-cells(1). Somatostatin is a powerful inhibitor of insulin and glucagon secretion(2). It is normally secreted in response to glucose(3) and there is evidence suggesting its release becomes perturbed in diabetes(4). Little is known about the control of somatostatin release. Closure of ATP-regulated K+-channels (K-ATP-channels)(5) and a depolarization-evoked increase in cytoplasmic free Ca2+ concentration ([Ca2+](i))(6-8) have been proposed to be essential. Here, we report that somatostatin release evoked by high glucose (>= 10 mM) is unaffected by the K-ATP-channel activator diazoxide and proceeds normally in K-ATP-channel-deficient islets. Glucose-induced somatostatin secretion is instead primarily dependent on Ca2+-induced Ca2+-release (CICR). This constitutes a novel mechanism for K-ATP-channel-independent metabolic control of pancreatic hormone secretion.
Original languageEnglish
Pages (from-to)453-U171
JournalNature Cell Biology
Volume9
Issue number4
DOIs
Publication statusPublished - 2007

Subject classification (UKÄ)

  • Endocrinology and Diabetes

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