Polycystic ovary syndrome (PCOS) is a heterogeneous group of disorders characterized by ovulation disorder, hyperandrogenism, and polycystic ovarian morphology (PCOM). Several diagnostic criteria suggest that hyperandrogenism is a core symptom of PCOS. Androgens are believed to cause preantral follicle growth and arrest the growth of antral follicles. This results in accumulation of small antral follicles in the ovaries, thus forming PCOM. Observational studies of patients with female-to-male transsexualism or congenital adrenal hyperplasia indicate that androgen administration to these patients does not produce typical PCOS-like features. However, endogenous androgen exposure in early life may lead to some traits of PCOS in adulthood. To reveal the association between the timing of excess androgen exposure and reproductive function, various animal models have been investigated using androgen administration. Rhesus monkeys exposed to excess androgen during the early fetal period show a PCOS-like phenotype, including metabolic and hypothalamic-pituitary characteristics. This finding implies that exposure to excess androgen during this critical period programs the hypothalamic-pituitary-ovary axis and metabolic organs. Although findings obtained in animal studies will not necessarily be replicated in humans, prenatal androgen excess is the dominant PCOS hypothesis.