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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
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

Abstract 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.


  • Endocrinology and Diabetes


  • Islet cell physiology
  • ISSN: 1465-7392
Erik Renström
E-mail: erik [dot] renstrom [at] med [dot] lu [dot] se

Deputy head of department

Department of Clinical Sciences, Malmö

+46 40 39 11 57

+46 40 39 11 57

Principal investigator

Islet patophysiology

+46 40 39 11 57

+46 40 39 11 57



Lund University Diabetes Centre, CRC, SUS Malmö, Entrance 72, House 91:12. SE-205 02 Malmö. Telephone: +46 40 39 10 00