The Expression of GPR109A, NF-kB and IL-1β in Peripheral Blood Leukocytes from Patients with Type 2 Diabetes

This study was designed to explore the association between the G protein-coupled receptor 109A (GPR109A) expression in peripheral blood leukocytes (PBLs) and type 2 diabetes (T2DM) and to discuss the regulation of inflammatory factors by GPR109A signaling. GPR109A signaling has been confirmed to be associated with homeostasis of glucose/lipid metabolism, but the role of signaling in T2DM is still poorly understood. Peripheral blood samples and biochemical data were collected from healthy individuals (normal controls) and T2DM patients. Immunocytochemical staining was used to detect the expression of GPR109A in PBLs. Reverse transcription polymerase chain reaction (RT-PCR) was used to measure mRNA levels of GPR109A, NF-kappa B, and IL-1 beta in PBLs. Immunocytochemical staining showed that the GPR109A protein is localized in the nucleus and cytoplasm of granulocytes, monocytes, and lymphocytes. RT-PCR showed that mRNA levels of GPR109A, NF-kappa B, and IL-1 beta were higher in the T2DM group than in the control group (P<0.05). Correlation analysis showed a positive correlation both between GPR109A/NF-kappa B (r=0.376, P<0.05), and GPR109A/IL-1 beta (r=501, P<0.05) and between GPR109A and fasting plasma glucose (FPG) (r=0.179, P<0.05) and NF-kappa B /FPG (r=0.358, p<0.05). Our results suggest that GPR109A signaling is associated with T2DM, playing a role in regulation of the inflammatory cytokines.