Abstract: Polycystic ovary syndrome（PCOS） is a common reproductive endocrine and metabolic disorder. On the basis of experimental observations in the prenatally androgenized sheep and rhesus monkey，and supported by data from human studies. We therefore conclude that although PCOS is a complex，heterogeneous disorder，most if not all of the clinical and biochemical features can be explained on the basis of a developmental disorder of ovarian androgen production. This fetal （and/or prepubertal） androgen excess “programmes” the hypothalamic-pituitary control of LH，enhances visceral fat distribution （thus predisposing to insulin resistance and anovulation） and causes the clinical manifestations of hyperandrogenism in adulthood. Other secondary genetic and environmental （particularly dietary） factors may interact with this underlying linear process to modify the final phenotype and produce the heterogeneous nature of the syndrome.

Key words: Polycystic ovary syndrome, Hyperandrogenism, Macaca mulatta, Fetus, Luteinizing hormone