Orientin reduces the inhibitory effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin on adipogenic differentiation and insulin signaling pathway in murine 3T3-L1 adipocytes

2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) accumulates in human body, probably influencing adipocyte differentiation and causing various toxic effects, including wasting syndrome. Recently, orientin, a phenolic compound abundant in natural health products, has been shown to have antioxidant properties. We investigated the protective effects of orientin against TCDD-induced adipocyte dysfunction and its underlying mechanisms. In this study, orientin suppressed TCDD-induced loss of lipid accumulation. Orientin inhibited TCDD-driven decreases in the levels of peroxisome proliferator-activated receptor γ and adiponectin. Orientin also reduced TCDD-induced prostaglandin E2, and cytosolic phospholipase A2α levels, and increased TCDD-inhibited peroxisome proliferator-activated receptor gamma coactivator 1-alpha levels in 3T3-L1 adipocytes. TCDD reduced the levels of insulin receptor substrate 1 and glucose transporter 4, and decreased insulin-stimulated glucose uptake activity; however, orientin diminished these TCDD-induced effects. These results suggest that orientin may have beneficial effects on the prevention of TCDD-induced wasting syndrome and type II diabetes mellitus accompanied by insulin resistance. •Orientin suppressed TCDD-induced loss of lipid accumulation.•Orientin inhibited TCDD-driven decreases in the levels of PPARγ and adiponectin.•Orientin reduced TCDD-induced PGE2, and cPLA2α levels.•Orientin increased TCDD-inhibited PGC1-alpha levels.•Orientin increased TCDD-reduced IRS1, GLUT4 and insulin-stimulated glucose uptake.