Objective:To investigate the therapeutic effects of Ping-tang Recipe(平糖方,PTR) on highfat diet(HFD)-induced insulin resistance and non-alcoholic fatty liver disease(NAFLD),and to elucidate the underlying mechanisms.Methods:Forty male SD rats were included in the study.Ten rats were fed on normal diet as normal control,and thirty rats were fed on HFD for 8 weeks to induce obesity,followed with low dose (0.42 g/kg) or high dose(0.84 g/kg) of PTR or vehicle for 8 weeks with 10 animals for each group.Glucose metabolism and insulin sensitivity were evaluated by oral glucose tolerance test and insulin tolerance test. Hepatic steatosis was measured by immunohistochemistry.Liver lipid metabolic genes were analyzed by quantitative real-time polymerase chain reaction,while AMP-activated protein kinase(AMPK) expression was examined by Western blot.Results:Rats fed on HFD developed abdominal obesity,insulin resistance and NAFLD.PTR treatment reduced visceral fat(peri-epididymal and peri-renal) accumulation,improved glucose metabolism,and attenuated hepatic steatosis.The expressions of the key lipolytic regulating genes,including peroxisome proliferators-activated receptorγco-activator 1α(PGC-1α),peroxisome proliferator-activated receptorγ(PRAR-γ) andα(PRAR-α),were up-regulated(P<0.05 or P<0.01),while the expressions of lipogenic genes such as sterol regulatory element-binding protein 1c(SREBP-1c),fatty acid synthase (FAS) and liver fatty acid-binding protein(L-FABP) were down-regulated(P<0.05 or P<0.01).In addition, PTR activated AMPK and promoted acetyl-CoA carboxylase phosphorylation in the liver.Conclusions:PTR improves insulin resistance and reverse hepatic steatosis in the rat model of HFD-induced obesity through promotion of lipolysis and reduction of lipogenesis,which involves the AMPK signaling pathway,thus representing a new therapeutic intervention for obesity related insulin resistance and NAFLD. Objective: To investigate the therapeutic effects of Ping-tang Recipe (PTR) on highfat diet (HFD) -induced insulin resistance and non-alcoholic fatty liver disease (NAFLD), and to elucidate the underlying mechanisms. Methods: Forty Male SD rats were fed on normal diet, and thirty rats were fed on HFD for 8 weeks to induce obesity, followed by low dose (0.42 g / kg) / kg) of PTR or vehicle for 8 weeks with 10 animals for each group. Glucose metabolism and insulin sensitivity were evaluated as oral glucose tolerance test and insulin tolerance test. Hepatic steatosis was measured by immunohistochemistry. Liver lipid metabolic genes were analyzed by quantitative real -time polymerase chain reaction, while AMP-activated protein kinase (AMPK) expression was examined by Western blot.Results: Rats fed on HFD developed abdominal obesity, insulin resistance and NAFLD.PTR treatment reduced visceral fat (peri-epididymal and peri-renal ) accumulation, improved glucose metabolism, and attenuated hepatic steatosis. These expressions of the key lipolytic regulating genes, including peroxisome proliferators-activated receptor gamma co-activator 1α (PGC-1α), peroxisome proliferator-activated receptor γ (PRAR- (P <0.05 or P <0.01), while the expressions of lipogenic genes such as sterol regulatory element-binding protein 1c (SREBP-1c), fatty acid synthase (FAS) and liver fatty acid-binding PTR activated insulin and reverse acetylcholinesterase in the liver. Conclusions: PTR improves insulin resistance and reverse hepatic steatosis in the rat (P <0.05 or P <0.01) model of HFD-induced obesity through promotion of lipolysis and reduction of lipogenesis, which involves the AMPK signaling pathway, representing a new therapeutic intervention for obesity related insulin resistance and NAFLD.