Objective:To investigate the effects and mechanisms of apigenin on lipid metabolism disorder in mice with type 2 diabetes combined with nonalcoholic fatty liver disease (NAFLD). Methods8-week old male db/db mice were randomly divided into the model group and apigenin group (50 mg·kg-1·d-1). Male C57BL/6J mice were taken as the normal control group. After drug treatment for 8 weeks, the body weight, fasting blood glucose (FBG), total cholesterol (CHO), triglyceride (TG), free fatty acid (FFA), aspartate aminotransferase (AST), fibroblast growth factor-19 (FGF-19), fasting insulin (Fins) and homeostasis model assessment of insulin resistance (HOMA-IR) of mice were detected. HE staining was performed in liver tissue to observe the lipid deposition in hepatocytes. The mRNA expressions of SREBP1c, FAS, Sirt1, PGC1α and CPT1 were detected by RT-PCR and the protein expression of PPARα was detected by Western blot.  Results:Compared with the model group, the body weight and levels of FBG, CHO, TG and FFA in the apigenin group were decreased significantly (P<0.05, P<0.01), and the FGF-19 level was increased significantly (P<0.01). HE staining showed that the degree of lipid deposition in hepatocytes was alleviated, the number of intracellular lipid droplets was reduced and the cells arranged regularly in the apigenin group. The mRNA expressions of SREBP1c and FAS in liver were decreased (P<0.05, P<0.01), the mRNA expressions of Sirt1, PGC1α and CPT1α were significantly increased (P<0.05), and the protein expression of PPARα was significantly increased (P<0.01) in the apigenin group.  Conclusion:Apigenin can improve the liver lipid metabolism disorder in mice with diabetes combined with NAFLD, which may be accomplished by down-regulating the mRNA expressions of SREBP1c and FAS and up-regulating the expressions of Sirt1, PGC1α, CPT1α and PPARα in liver.