Abstract

Abstract Objective To explore G protein-coupled receptor 120 (GPR120)'s role in mediating saturated and unsaturated long-chain fatty acid on adipocyte inflammation, ER stress and insulin signaling pathway. Methods Omental adipose tissue from 5 patients undergoing elective gallstone removal surgery was collected and the primary adipocytes were isolated and cultured. In the first experiment, cells were divided into the following four groups: (1) Control group; (2): Docosahexaenoic acid (DHA) group; (3)DHA+10 μmol/L GW9508 group; and (4) DHA+20 μmol/L GW9508 group. In the second experiment, cells were divided into the following four groups:(1) Control group; (2) Palmic acid (PA) group; (3) PA+10 μmol/L GW9508 group; and (4) PA+20 μmol/L GW9508 group. Real time PCR and western blot were used to evaluate the gene and protein expression of GPR120, FABP4, inflammatory factors and ER stress markers. Results (1) Under the stimulation of DHA and PA, the expression of GPR and FABP4 were increased. But with inhibition of GPR120, the expression of GPR120and FABP4 decreased in both DHA and PA treatment groups.(2) DHA treatment could decrease TNF-alpha expression and inflammation factor mRNA levels in primary adipocytes. Production of these factors increased with inhibition of GPR120. PA treatment could increase TNF-alpha expression and inflammation factor mRNA levels in primary adipocytes. They were further increased by inhibition of GPR120. (3) DHA treatment could decrease ER stress in primary adipocytes. GPR120 inhibition could promote ER stress. PA treatment could increase ER stress in primary adipocytes. Again, GPR120 inhibition further increased ER stress. Conclusion GPR120 mediated long-chain fatty acid-related inflammation and ER stress regulation, and balanced the function of saturated and unsaturated long-chain fatty acid in adipose tissue.

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