GPRC5B a putative glutamate-receptor candidate is negative modulator of insulin secretion
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/4273138
- author
- Soni, Arvind LU ; Amisten, Stefan LU ; Rorsman, Patrik LU and Salehi, S Albert LU
- organization
- publishing date
- 2013
- 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
- pmid:24513213
- 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
- 2016-04-01 10:31:49
- date last changed
- 2022-04-27 22:58:43
@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 (<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.}}, author = {{Soni, Arvind and Amisten, Stefan and Rorsman, Patrik and Salehi, S Albert}}, issn = {{1090-2104}}, keywords = {{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}}, doi = {{10.1016/j.bbrc.2013.10.099}}, volume = {{441}}, year = {{2013}}, }