In oleic acid (OA)-induced insulin resistance HepG2 cells, SW attenuated hepatic glycemic load, lipid accumulation, reactive oxygen species (ROS), and insulin resistance by targeting AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor α (PPAR-α) and modulating fat metabolic enzymes, such as FAS, ACC1, phosphoenolpyruvate carboxykinase (PEPCK), and the expression levels of insulin signal proteins, such as ser-307 insulin receptor substrate 1 (IRS1), insulin receptor β-subunit (IR-β), phosphatidylinositol 3-kinase (PI(3)K), and phosphorylated AKT (p-AKT). The gene discussed is INS; the disease is Insulin resistance.