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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/668402
- author
- 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. (More)
- 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
; Schneider, Toni
; Berggren, Per-Olof
; Gopel, Sven
; Ashcroft, Frances M.
and Rorsman, Patrik
(Less)
- organization
- publishing date
- 2007
- 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
- pmid:17369816
- 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
- 2016-04-01 17:15:38
- date last changed
- 2022-04-07 21:52:46
@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}},
doi = {{10.1038/ncb1563}},
volume = {{9}},
year = {{2007}},
}