Maternal environmental influence on fetal epigenetic development is emerging as a potential cause of adult diseases. Polycystic Ovary Syndrome (PCOS) is a common endocrine disorder affecting up to 10% of reproductive age women, and associated with reproductive, endocrine and metabolic abnormalities. The aetiology of PCOS remains unknown but fetal origins have been proposed. As hyperandrogenism is a hallmark of PCOS, we aimed to examine the potential role of prenatal hyperandrogenism and the androgen receptor (AR) in the development of PCOS traits later in life. Wildtype (WT) and AR knockout (ARKO) mice were subcutaneously injected with DHT (250μg; sesame oil vehicle) daily on days 16-18 of gestation. WT mice prenatally exposed to DHT when studied at 13 weeks of age displayed irregular estrous cycles (DHT 0.58 ± 0.19 cycles/14 days vs. control 2.50 ± 0.19 cycles/14 days; p < 0.01), fewer corpora lutea, indicative of reduced ovulation (5.0 ± 0.2 vs. 9.8 ± 1.8; p < 0.05), and they all had ovarian cysts and exhibited significantly more unhealthy small and large preantral follicles (20.3 ± 3.9 % & 20.3 ± 3.2 %, respectively, vs. 1.6 ± 1.1 % & 6.0 ± 1.3 %; p < 0.01 for both). DHT treated WT mice had no significant changes in body weight but had an increase in parametrial adipocyte area (2195.7 ± 467.7 μm2 vs. 1353.3 ± 132.4 μm2, p = 0.05). DHT treated WT mice showed no significant difference in cholesterol, triglyceride and adiponectin serum levels. In contrast, ARKO mice exposed to DHT prenatally had normal estrous cycles without either ovarian cysts or altered adipocyte size. Hence we conclude that prenatal hyperandrogenism induces PCOS traits in adult life by a mechanism mediated via the AR.