Abstract: Clinical，experimental and genetic evidence suggested that polycystic ovary syndrome（PCOS）could have an fetal origin of adult disease. During fetal development，prenatal androgens excess may intervene the epigenome，such as the altered DNA methylation and genomic imprinting，which may increase the later risk of PCOS. Exposure to androgens in utero induces a permanent ■ phenotype characterized by hyperandrogenism, abnormal follicle development，luteinizing hormone hypersecretion from the reduced hypothalamic sensitivity to steroid negative feedback，and insulin resistance from the increased abdominal adiposity. The ability of prenatal androgens excess to alter the developmental trajectory of multiple organ systems could be one of early mechanisms of PCOS pathogenesis, which could be valuable for PCOS prevention in groups with high risks.

Key words: Polycystic ovary syndrome, Androgens, Environmental exposure, Epigenetics