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

Zhang, Quan LU ; Bengtsson, Martin LU ; Partridge, Chris; Salehi, S Albert LU ; Braun, Matthias; Cox, Roger; Eliasson, Lena LU ; Johnson, Paul R. V.; Renström, Erik LU and Schneider, Toni, et al. (2007) In Nature Cell Biology 9(4). p.171-453
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... (More)
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. (Less)
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type
Contribution to journal
publication status
published
subject
in
Nature Cell Biology
volume
9
issue
4
pages
171 - 453
publisher
Nature Publishing Group
external identifiers
  • wos:000245359400017
  • scopus:34047136620
ISSN
1465-7392
DOI
10.1038/ncb1563
language
English
LU publication?
yes
id
319f6e85-7ec2-4544-ac11-f738a24f7163 (old id 668402)
date added to LUP
2007-12-19 10:37:39
date last changed
2017-10-29 04:26:41
@article{319f6e85-7ec2-4544-ac11-f738a24f7163,
  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.},
  author       = {Zhang, Quan and Bengtsson, Martin and Partridge, Chris and Salehi, S Albert and Braun, Matthias and Cox, Roger and Eliasson, Lena and Johnson, Paul R. V. and Renström, Erik and Schneider, Toni and Berggren, Per-Olof and Gopel, Sven and Ashcroft, Frances M. and Rorsman, Patrik},
  issn         = {1465-7392},
  language     = {eng},
  number       = {4},
  pages        = {171--453},
  publisher    = {Nature Publishing Group},
  series       = {Nature Cell Biology},
  title        = {R-type Ca2+-channel-evoked CICR regulates glucose-induced somatostatin secretion},
  url          = {http://dx.doi.org/10.1038/ncb1563},
  volume       = {9},
  year         = {2007},
}