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

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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.


Research areas and keywords

Subject classification (UKÄ) – MANDATORY

  • Endocrinology and Diabetes
Original languageEnglish
Pages (from-to)453-U171
JournalNature Cell Biology
Issue number4
Publication statusPublished - 2007
Publication categoryResearch