Abstract: Objective: Observing the effects of polysaccharide from red kidney beans (PRK) combined with exercise (E) to improve the diet induced obese mice metabolic disorders, and analyzing its mechanism. Methods: C57BL/6 mice were randomly divided into 5 groups: Control group (normal diet), model group (high fat diet), PRK group (400 mg/kg PRK), E group (exercise), PRK+E group (400 mg/kg PRK+exercise). After continuous intervention for 12 weeks, oral glucose tolerance test (OGTT) was performed, and blood glucose, insulin, total cholesterol (TC), triglyceride (TG), low density lipoprotein (LDL), high density lipoprotein (HDL) were measured by biochemical analyzer. TC, TG, superoxide dismutase (SOD), malondialdehyde (MDA) and glutathione peroxidase (GSH-Px) were analyzed in liver. The contents of insulin, tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-1β were determined by enzyme-linked immunoassay kit. The levels of PPARα, FASN, Nrf2, NQO1 and HO-1 were detected by western blot. Results: Compared with the control group, the body weight and liver weight of model group were significantly increased (P<0.01). Compared with the model group, PRK combined with exercise significantly decreased the body weight, lipid, blood glucose and insulin levels in obese mice (P<0.01). Compared with model group, PRK combined exercise significantly decreased the contents of TG, TC and LDL in serum, significantly increased HDL, significantly decreased the levels of TNF-α, IL-6 and IL-1β in liver, significantly decreased the levels of TG and TC in liver, significantly increased the level of PPARα in liver and significantly decreased the level of FASN (P<0.01). Compared with model group, PRK, E or PRK+E combined intervention extremely significantly increased liver GSH-Px and SOD levels, extremely significantly decreased MDA content, and extremely significantly increased Nrf2, NQO1 and HO-1 protein levels, especially PRK+E combined intervention (P<0.01). Conclusion: PRK combined exercise could reduce lipid accumulation, inhibit inflammation and oxidative stress to improve metabolic disorders caused by obesity, and its mechanism was related to the regulation of PGC-1α, FASN, Nrf2/NQO1/HO-1 signaling pathways.