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

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

Research output: Contribution to journalArticlepeer-review

74 Scopus citations


Pancreatic islets have a central role in blood glucose homeostasis. In addition to insulin-producing β-cells and glucagon-secreting α-cells, the islets contain somatostatin-releasing δ-cells. Somatostatin is a powerful inhibitor of insulin and glucagon secretion. It is normally secreted in response to glucose and there is evidence suggesting its release becomes perturbed in diabetes. Little is known about the control of somatostatin release. Closure of ATP-regulated K+-channels (KATP-channels) and a depolarization-evoked increase in cytoplasmic free Ca2+ concentration ([Ca2+]6-8) have been proposed to be essential. Here, we report that somatostatin release evoked by high glucose (≥10 mM) is unaffected by the KATP-channel activator diazoxide and proceeds normally in KATP-channel-deficient islets. Glucose-induced somatostatin secretion is instead primarily dependent on Ca2+-induced Ca2+-release (CICR). This constitutes a novel mechanism for KATP-channel-independent metabolic control of pancreatic hormone secretion.

Original languageEnglish (US)
Pages (from-to)453-460
Number of pages8
JournalNature Cell Biology
Issue number4
StatePublished - Apr 2007

ASJC Scopus subject areas

  • Cell Biology


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