[Activation and significance of the PI3K/Akt pathway in endometrium with polycystic ovary syndrome patients].

OBJECTIVE: To investigate activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway in the endometrium of women with polycystic ovary syndrome (PCOS) and its role in endometrium hyperplasia and carcinogenesis, and the factors affecting the activation of the PI3K/Akt pathway. METHODS: From Jan 2007 to Jun 2008, 52 patients with PCOS who underwent dilatation and curettage were selected as experimental group matched with 32 non-PCOS patients as control group. Serous hormonal parameters, fasting blood glucose and insulin, body mass index (BMI), and endometrium pathology were measured and evaluated in all patients. The PCOS patients were divided into insulin resistance and non-insulin resistance group according to homeostasis model assessment-insulin resistance index (HOMA-IR). Meanwhile, the PCOS patients were grouped as normal, endometrial hyperplasia and carcinoma depending on outcome of pathology. The expression of Akt and phosphorylated Akt (p-Akt) were determined by western blot. RESULTS: (1) The expression of p-Akt was significantly higher in PCOS group [(46 ± 18)%] than that in control [(33 ± 9)%, P < 0.01)]. (2) The expression of p-Akt was significantly higher in group of endometrial hyperplasia and carcinoma [(56 ± 19)%] when compared with those in normal endometria group [(31 ± 12)%, P < 0.05]; the expression of p-Akt was significantly higher in group of insulin resistance [(50 ± 19)%] compared with that in non-insulin resistance group [(34 ± 10)%, P < 0.01]. (3) There was a positive correlation between the expression level of p-Akt in endometrium with PCOS and HOMA-IR and BMI respectively (r = 0.400, 0.326, both P < 0.05). CONCLUSIONS: The PI3K/Akt pathway was over activated in endometrium with PCOS which may be associated with the formation of endometrial hyperplasia and carcinoma in PCOS patients. Insulin resistance and obesity may be high risk factors for over-activation of the PI3K/Akt pathway in endometrium with PCOS.