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GPRC5B a putative glutamate-receptor candidate is negative modulator of insulin secretion

Soni, Arvind LU ; Amisten, Stefan LU ; Rorsman, Patrik LU and Salehi, S Albert LU (2013) In Biochemical and Biophysical Research Communications 441(3). p.643-648
Abstract
GPRC5B is an orphan receptor belonging to the group C family of G protein-coupled receptors (GPCRs). GPRC5B is abundantly expressed in both human and mouse pancreatic islets, and both GPRC5B mRNA and protein are up-regulated 2.5-fold in islets from organ donors with type 2 diabetes. Expression of Gprc5b is 50% lower in islets isolated from newborn (<3 weeks) than in adult (>36 weeks) mice. Lentiviral shRNA-mediated down-regulation of Gprc5b in intact islets from 12 to 16 week-old mice strongly (2.5-fold) increased basal (I mmol/l) and moderately (40%) potentiated glucose (20 mmol/l) stimulated insulin secretion and also enhanced the potentiating effect of glutamate on insulin secretion. Downregulation of Gprc5b protected murine... (More)
GPRC5B is an orphan receptor belonging to the group C family of G protein-coupled receptors (GPCRs). GPRC5B is abundantly expressed in both human and mouse pancreatic islets, and both GPRC5B mRNA and protein are up-regulated 2.5-fold in islets from organ donors with type 2 diabetes. Expression of Gprc5b is 50% lower in islets isolated from newborn (<3 weeks) than in adult (>36 weeks) mice. Lentiviral shRNA-mediated down-regulation of Gprc5b in intact islets from 12 to 16 week-old mice strongly (2.5-fold) increased basal (I mmol/l) and moderately (40%) potentiated glucose (20 mmol/l) stimulated insulin secretion and also enhanced the potentiating effect of glutamate on insulin secretion. Downregulation of Gprc5b protected murine insulin-secreting clonal MIN6 cells against cytokine-induced apoptosis. We propose that increased expression of GPRC5B contributes to the reduced insulin secretion and beta-cell viability observed in type-2 diabetes. Thus, pharmacological targeting of GPRC5B might provide a novel means therapy for the treatment and prevention of type-2 diabetes. (C) 2013 Elsevier Inc. All rights reserved. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Diabetes, Endocrinology, Pancreatic islet, Insulin secretion, Cell, viability
in
Biochemical and Biophysical Research Communications
volume
441
issue
3
pages
643 - 648
publisher
Elsevier
external identifiers
  • wos:000327691100020
  • pmid:24513213
  • scopus:84888308286
ISSN
1090-2104
DOI
10.1016/j.bbrc.2013.10.099
language
English
LU publication?
yes
id
0abda3a5-4d74-4111-8bf0-8252ee5448e5 (old id 4273138)
alternative location
http://www.ncbi.nlm.nih.gov/pubmed/24513213?dopt=Abstract
date added to LUP
2014-02-10 12:24:38
date last changed
2019-01-06 04:19:30
@article{0abda3a5-4d74-4111-8bf0-8252ee5448e5,
  abstract     = {GPRC5B is an orphan receptor belonging to the group C family of G protein-coupled receptors (GPCRs). GPRC5B is abundantly expressed in both human and mouse pancreatic islets, and both GPRC5B mRNA and protein are up-regulated 2.5-fold in islets from organ donors with type 2 diabetes. Expression of Gprc5b is 50% lower in islets isolated from newborn (&lt;3 weeks) than in adult (&gt;36 weeks) mice. Lentiviral shRNA-mediated down-regulation of Gprc5b in intact islets from 12 to 16 week-old mice strongly (2.5-fold) increased basal (I mmol/l) and moderately (40%) potentiated glucose (20 mmol/l) stimulated insulin secretion and also enhanced the potentiating effect of glutamate on insulin secretion. Downregulation of Gprc5b protected murine insulin-secreting clonal MIN6 cells against cytokine-induced apoptosis. We propose that increased expression of GPRC5B contributes to the reduced insulin secretion and beta-cell viability observed in type-2 diabetes. Thus, pharmacological targeting of GPRC5B might provide a novel means therapy for the treatment and prevention of type-2 diabetes. (C) 2013 Elsevier Inc. All rights reserved.},
  author       = {Soni, Arvind and Amisten, Stefan and Rorsman, Patrik and Salehi, S Albert},
  issn         = {1090-2104},
  keyword      = {Diabetes,Endocrinology,Pancreatic islet,Insulin secretion,Cell,viability},
  language     = {eng},
  number       = {3},
  pages        = {643--648},
  publisher    = {Elsevier},
  series       = {Biochemical and Biophysical Research Communications},
  title        = {GPRC5B a putative glutamate-receptor candidate is negative modulator of insulin secretion},
  url          = {http://dx.doi.org/10.1016/j.bbrc.2013.10.099},
  volume       = {441},
  year         = {2013},
}