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Erik Renström

Erik Renström

Vice-chancellor

Erik Renström

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

Author

  • 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

Summary, in English

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.

Department/s

  • Islet cell physiology
  • Department of Clinical Sciences, Malmö

Publishing year

2007

Language

English

Pages

171-453

Publication/Series

Nature Cell Biology

Volume

9

Issue

4

Document type

Journal article

Publisher

Nature Publishing Group

Topic

  • Endocrinology and Diabetes

Status

Published

Research group

  • Islet cell physiology

ISBN/ISSN/Other

  • ISSN: 1465-7392