GPR109A Expression in the Murine Min6 Pancreatic Beta Cell Line, and Its Relation with Glucose Metabolism and Inflammation.

Nicotinic acid has been used clinically to manage dyslipidemia for many years, and its receptor, GPR109A, is expressed in various tissues or cells. It is not known if GPR109A is also expressed in pancreatic beta cells or if it takes part in maintaining homeostasis of glucose metabolism.In this study, the expression of GPR109A was investigated in the murine Min6 pancreatic beta cell line. The anti-inflammatory role of GPR109A in MIN6 cells was also explored.RT-PCR, western blotting, and immunocytochemical staining were used to detect the expression of GPR109A in MIN6 cells. Real-Time RT-PCR was used to investigate GPR109A mRNA levels influenced by IFN-γ and glucose. Cell viability and cytoplasmic nitrite levels were measured colorimetrically.We have identified that MIN6 cell, a mouse pancreatic beta cell line, expresses GPR109A transcripts and protein. GPR109A protein is mainly located in the cell membrane and cytoplasm. GPR109A mRNA increased more than 9-fold in MIN6 cells incubated with IFN-γ. High glucose inhibited GPR109A mRNA expression. Nitric oxide accumulation, induced by IFN-γ/TNF-α, was inhibited by nicotinic acid and 3-hydroxy-butyrate.Our results suggest that the expression of GPR109A in pancreatic beta cells is not only influenced by inflammation and glucose, but also plays a protective role under inflammatory conditions. Moreover, the MIN6 cell line may serve as a cellular model for further investigation of GPR109A-mediated signal transduction in modulating metabolism and diabetes.