Urotensin II-induced insulin resistance is mediated by NADPH oxidase-derived reactive oxygen species in HepG2 cells

Figure 1 Urotensin II decreases glucose consumption and glycogen synthesis in HepG2 hepatocytes. HepG2 cells were cultured in the presence of 0, 1, 10, or 100 nmol/L urotensin II (UII) for 24 h prior to stimulation with insulin (100 nmol/L, 30 min). Glucose consumption decreased in a dose-dependent manner (A). There was no cytotoxic effect of UII after incubation for 24 h (B). Exposure of HepG2 cells to UII (100 nmol/L, 24 h) reduced the intracellular glycogen content (C). Data from at least three independent experiments are presented as mean ± SD. ^aP < 0.05, ^bP < 0.01 vs control group; ^cP < 0.05 vs insulin (Ins) treatment alone.