OBJECTIVE: To evaluate effects of metformin on endocrine, metabolic parameters and endometrial androgen receptor (AR) expression in polycystic ovary syndrome (PCOS). DESIGN: Prospective observational study. METHODS: We analyzed blood samples from 10 PCOS patients, of whom endometrium was also analyzed in five patients. Before and after three months of metformin treatment, endocrine, glucose metabolic parameters and the endometrial AR expressions were assessed. The relative expression levels of AR were examined by immunohistochemistry. MAIN OUTCOME MEASURES: The group post-treatment mean of homeostasis model assessment insulin resistance (HOMA-IR) for all patients was significantly lower than the pretreatment. Ovulation was restored in five out of 10 patients. The group post-treatment means of luteinizing hormone (LH) and HOMA-IR for the five ovulatory patients were significantly lower. The relative expression levels of endometrial AR were decreased in four out of the five patients as compared with pretreatment. In the four patients, one or more of the parameters, HOMA-IR, LH or free testosterone, decreased compared with pretreatment. CONCLUSION: Metformin was effective in decreasing HOMA-IR, LH, free testosterone and the relative expression levels of AR. Furthermore, metformin might improve the systemic and local environment of the uterus caused by hyperandrogenemia in PCOS patients with insulin resistance.
OBJECTIVE: To evaluate effects of metformin on endocrine, metabolic parameters and endometrial androgen receptor (AR) expression in polycystic ovary syndrome (PCOS). DESIGN: Prospective observational study. METHODS: We analyzed blood samples from 10 PCOSpatients, of whom endometrium was also analyzed in five patients. Before and after three months of metformin treatment, endocrine, glucose metabolic parameters and the endometrial AR expressions were assessed. The relative expression levels of AR were examined by immunohistochemistry. MAIN OUTCOME MEASURES: The group post-treatment mean of homeostasis model assessment insulin resistance (HOMA-IR) for all patients was significantly lower than the pretreatment. Ovulation was restored in five out of 10 patients. The group post-treatment means of luteinizing hormone (LH) and HOMA-IR for the five ovulatory patients were significantly lower. The relative expression levels of endometrial AR were decreased in four out of the five patients as compared with pretreatment. In the four patients, one or more of the parameters, HOMA-IR, LH or free testosterone, decreased compared with pretreatment. CONCLUSION:Metformin was effective in decreasing HOMA-IR, LH, free testosterone and the relative expression levels of AR. Furthermore, metformin might improve the systemic and local environment of the uterus caused by hyperandrogenemia in PCOSpatients with insulin resistance.