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 journalArticle

61 Citations (Scopus)

Abstract

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
Pages (from-to)453-460
Number of pages8
JournalNature Cell Biology
Volume9
Issue number4
DOIs
StatePublished - Apr 1 2007
Externally publishedYes

Fingerprint

KATP Channels
Somatostatin
Glucose
Glucagon-Secreting Cells
Pancreatic Hormones
Insulin
Diazoxide
Somatostatin-Secreting Cells
Glucagon
Islets of Langerhans
Blood Glucose
Homeostasis
Adenosine Triphosphate

ASJC Scopus subject areas

  • Cell Biology

Cite this

Zhang, Q., Bengtsson, M., Partridge, C., Salehi, A., Braun, M., Cox, R., ... Rorsman, P. (2007). R-type Ca2+-channel-evoked CICR regulates glucose-induced somatostatin secretion. Nature Cell Biology, 9(4), 453-460. https://doi.org/10.1038/ncb1563

R-type Ca2+-channel-evoked CICR regulates glucose-induced somatostatin secretion. / Zhang, Quan; Bengtsson, Martin; Partridge, Chris; Salehi, Albert; Braun, Matthias; Cox, Roger; Eliasson, Lena; Johnson, Paul R V; Renström, Erik; Schneider, Toni; Berggren, Per Olof; Göpel, Sven; Ashcroft, Frances M.; Rorsman, Patrik.

In: Nature Cell Biology, Vol. 9, No. 4, 01.04.2007, p. 453-460.

Research output: Contribution to journalArticle

Zhang, Q, Bengtsson, M, Partridge, C, Salehi, A, Braun, M, Cox, R, Eliasson, L, Johnson, PRV, Renström, E, Schneider, T, Berggren, PO, Göpel, S, Ashcroft, FM & Rorsman, P 2007, 'R-type Ca2+-channel-evoked CICR regulates glucose-induced somatostatin secretion', Nature Cell Biology, vol. 9, no. 4, pp. 453-460. https://doi.org/10.1038/ncb1563
Zhang Q, Bengtsson M, Partridge C, Salehi A, Braun M, Cox R et al. R-type Ca2+-channel-evoked CICR regulates glucose-induced somatostatin secretion. Nature Cell Biology. 2007 Apr 1;9(4):453-460. https://doi.org/10.1038/ncb1563
Zhang, Quan ; Bengtsson, Martin ; Partridge, Chris ; Salehi, Albert ; Braun, Matthias ; Cox, Roger ; Eliasson, Lena ; Johnson, Paul R V ; Renström, Erik ; Schneider, Toni ; Berggren, Per Olof ; Göpel, Sven ; Ashcroft, Frances M. ; Rorsman, Patrik. / R-type Ca2+-channel-evoked CICR regulates glucose-induced somatostatin secretion. In: Nature Cell Biology. 2007 ; Vol. 9, No. 4. pp. 453-460.
@article{fe53c56060d541e48e47c5a2301d3999,
title = "R-type Ca2+-channel-evoked CICR regulates glucose-induced somatostatin secretion",
abstract = "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.",
author = "Quan Zhang and Martin Bengtsson and Chris Partridge and Albert Salehi and Matthias Braun and Roger Cox and Lena Eliasson and Johnson, {Paul R V} and Erik Renstr{\"o}m and Toni Schneider and Berggren, {Per Olof} and Sven G{\"o}pel and Ashcroft, {Frances M.} and Patrik Rorsman",
year = "2007",
month = "4",
day = "1",
doi = "10.1038/ncb1563",
language = "English",
volume = "9",
pages = "453--460",
journal = "Nature Cell Biology",
issn = "1465-7392",
publisher = "Nature Publishing Group",
number = "4",

}

TY - JOUR

T1 - R-type Ca2+-channel-evoked CICR regulates glucose-induced somatostatin secretion

AU - Zhang, Quan

AU - Bengtsson, Martin

AU - Partridge, Chris

AU - Salehi, Albert

AU - Braun, Matthias

AU - Cox, Roger

AU - Eliasson, Lena

AU - Johnson, Paul R V

AU - Renström, Erik

AU - Schneider, Toni

AU - Berggren, Per Olof

AU - Göpel, Sven

AU - Ashcroft, Frances M.

AU - Rorsman, Patrik

PY - 2007/4/1

Y1 - 2007/4/1

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=34047136620&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=34047136620&partnerID=8YFLogxK

U2 - 10.1038/ncb1563

DO - 10.1038/ncb1563

M3 - Article

C2 - 17369816

AN - SCOPUS:34047136620

VL - 9

SP - 453

EP - 460

JO - Nature Cell Biology

JF - Nature Cell Biology

SN - 1465-7392

IS - 4

ER -