Objective To establish a rat model of polycystic ovary syndrome (PCOS) with endometrial insulin resistance(IR) by combining dehydroepiandrosterone ( DHEA) with a high fat diet ( HFDs). And by detecting the expression levels of insulin resistance related proteins and PI3K/ AKT pathway-related proteins in the endometrium, we can observe whether there is insulin resistance in the endometrium and explore its possible mechanism. Methods Thirty-two 21-day-old SD female rats were randomly divided into a Model group (Model group, n= 24) and Control group (Control group, n= 8). The Model group was subcutaneously injected with 6 mg / 100 (g·d) DHEA on the back of the neck and fed the high fat diet. The Control group was subcutaneously injected with the same volume of corn oil for injection on the back of the neck and fed a normal diet. The experimental period was 30 days. In accordance with the result of vaginal smear and ovarian tissue staining, PCOS rats were screened. And PCOS with IR rats ( PCOS-IR) were screened by detecting fasting blood glucose (FBG), serum insulin level (FINS), and insulin resistance index (HOMA-IR). Then by detecting the differences in the expression of IR-related proteins (IRS1, GLUT-4) and PI3K/ AKT pathway-related proteins (PI3K, PI3K p110α, p-AKT, AKT) in the endometrium between the two groups to explore the possible mechanism. Results Smears from rats in the Control group showed regular estrus and a normal ovarian tissue structure, whereas those of rats in the Model group had disordered estrous cycles and the ovaries had polycystic ovary manifestations. Compared with the Control group, FBG (P> 0. 05), FINS (P> 0. 05), and HOMA-IR (P< 0. 01) of rats in the Model group were all increased, among which 11 PCOS rats and eight PCOS with IR rats were screened from the Model group. Additionally, western blotting of IR-related proteins in endometrial tissue showed that IRS1 and GLUT-4 expression in the PCOS-IR were decreased (P< 0. 01), suggesting the existence of IR in the endometrial tissue. Compared with the Control group, the PI3K expression level was increased in the PCOS-IR group (P< 0. 05), and the PI3K p110α(P< 0. 01), p-AKT (P< 0. 01), AKT (P> 0. 05) expression levels were decreased in the endometrial tissues, suggesting that it may be related to the down-regulation of PI3K/ AKT pathway-related protein expression in the endometrium. Conclusions Rats with PCOS and IR have characteristic polycystic ovary tissue and abnormal glucose metabolism, and their endometrium is mostly insulin resistant, and may be related to the downregulation of PI3K/ AKT pathway-related protein expression.