Research Article

Fas-Associated Factor 1 Promotes Hepatic Insulin Resistance via JNK Signaling Pathway

Figure 3

Overexpression and knockdown of FAF1 regulated glycogen synthesis, glucose uptake, ROS production, and lipid accumulation. (a, e) Knockdown of FAF1 increased insulin-stimulated glycogen synthesis, and overexpression of FAF1 decreased insulin-stimulated glycogen synthesis in HepG2 and SK-HEP-1 cells. (b, f) Knockdown of FAF1 promoted insulin-stimulated glucose uptake, and overexpression of FAF1 inhibited insulin-stimulated glucose uptake in HepG2 and SK-HEP-1 cells. (c, g) Knockdown of FAF1 reduced the ROS production, and overexpression of FAF1 increased the ROS production in HepG2 and SK-HEP-1 cells. (d, h) Knockdown of FAF1 ameliorated PA-induced lipid accumulation, and overexpression of FAF1 aggravated PA-induced lipid accumulation in HepG2 and SK-HEP-1 cells. Data represent ( independent experiments). , , and .