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

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Bibtex

@article{0abda3a54d7441118bf08252ee5448e5,
title = "GPRC5B a putative glutamate-receptor candidate is negative modulator of insulin secretion",
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.",
keywords = "Diabetes, Endocrinology, Pancreatic islet, Insulin secretion, Cell, viability",
author = "Arvind Soni and Stefan Amisten and Patrik Rorsman and Salehi, {S Albert}",
year = "2013",
doi = "10.1016/j.bbrc.2013.10.099",
language = "English",
volume = "441",
pages = "643--648",
journal = "Biochemical and Biophysical Research Communications",
issn = "1090-2104",
publisher = "Elsevier",
number = "3",

}