Objective:To observe the improvement effects of Shengmai Decoction on the insulin resistance in type 2 diabetes mellitus(T2DM) rats,and discuss its possible mechanisms. MethodsThe T2DM rat model with insulin resistance was established by intraperitoneal injection of low-dose streptozotocin combined with high sugar and fat diet. The rats were divided into the normal group,model group,metformin group and Shengmai Decoction groups with low-,middle- and high-dose,10 rats in each group. The metformin group was treated with 4.0 mg·kg-1 of metformin,the Shengmai Decoction groups with low-,middle- and high-dose were treated with Shengmai Decoction at doses of 50,0 and 400 mg·kg-1,respectively,the control group and the model group were treated with 0.9% NaCl solution at equivalent volume. After treatment for continuous 6 weeks,the serum levels of fasting blood glucose(FBG) and fasting insulin(FINS) were measured by kits and the insulin sensitivity index(ISI) was calculated. The serum levels of interleukin-6(IL-6) and tumor necrosis factor α(TNF-α) were detected by ELISA. The protein expressions of insulin receptor substrate -1(IRS-1),phosphatidylinositol -3- hydroxykinase p85 subunit(PI3Kp85) and glucose transporter(GLUT4) in skeletal muscle tissues were detected by Western blot. The Glut4 mRNA expression in skeletal muscle tissue was detected by RT-PCR.  Results:After treatment with Shengmai Decoction at different doses,the serum levels of FBG,FINS,TNF-α and IL-6 in diabetic rats were obviously decreased(P<0.05),the protein expressions of IRS-1 and PI3Kp85 were increased,and the protein and mRNA expressions of GLUT4 were up-regulated significantly in skeletal muscle tissues(P<0.05),in a dose-dependent manner. There were no statistically significant differences on the levels of TNF-α,IL-6,PI3Kp85 and GLUT4 between the metformin group and Shengmai Decoction group with high-dose.  Conclusion:Shengmai Decoction can significantly improve the insulin resistance in diabetic rats. Its mechanism may be associated with alleviating inflammatory responses and up-regulating the protein expressions of IRS-1,PI3Kp85 and GLUT4.