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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 (1 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 b-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.

Type

Journal article

Journal

Biochem Biophys Res Commun

Publication Date

22/11/2013

Volume

441

Pages

643 - 648

Keywords

Adult, Aged, Animals, Apoptosis, Cell Proliferation, Cells, Cultured, Diabetes Mellitus, Type 2, Down-Regulation, Female, Humans, Insulin, Insulin-Secreting Cells, Islets of Langerhans, Male, Mice, Middle Aged, Receptors, G-Protein-Coupled, Receptors, Glutamate