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We have recently shown that the G protein-coupled receptor 142 ( GPR142 ) is expressed in both rodent and human pancreatic β-cells. Herein, we investigated the cellular distribution of GPR142 within islets and the effects of selective agonists of GPR142 on glucose-stimulated insulin secretion (GSIS) in the mouse islets and INS-1832/13 cells. Double-immunostaining revealed that GPR142 immunoreactivity in islets mainly occurs in insulin-positive cells. Potentiation of GSIS by GPR142 activation was accompanied by increased cAMP content in INS-1832/13 cells. PKA/Epac inhibition markedly suppressed the effect of GPR142 activation on insulin release.  Gpr142  knockdown ( Gpr142 -KD) in islets was accompanied by elevated release of MCP-1, IFNγ, and TNFα during culture period and abolished the modulatory effect of GPR142 activation on the GSIS.  Gpr142 -KD had no effect on  Ffar1 ,  Ffar2 , or  Ffar3  mRNA while reducing  Gpr56  and increasing  Tlr5  and  Tlr7  mRNA expression.  Gpr142 -KD was associated with an increased expression of  Chrebp ,  Txnip ,  RhoA , and mitochondrial  Vdac1  concomitant with a reduced  Pdx1 ,  Pax6 , and mitochondrial  Vdac2  mRNA levels. Long-term exposure of INS-1832/13 cells to hyperglycemia reduced  Gpr142  and  Vdac2  while increased  Chrebp ,  Txnip , and  Vdac1  mRNA expression. GPR142 agonists or Bt 2 -cAMP counteracted this effect. Glucotoxicity-induced decrease of cell viability in  Gpr142 -KD INS-1 cells was not affected by GPR142-agonists while Bt 2 -cAMP prevented it. The results show the importance of Gpr142 in the maintenance of pancreatic β-cell function in rodents and that GPR142 agonists potentiate GSIS by an action, which most likely is due to increased cellular generation of second messenger molecule cAMP.

The functional impact of G protein-coupled receptor 142 (Gpr142) on pancreatic β-cell in rodent