Sheep exposed to testosterone during early-mid gestation exhibit reproductive defects that include hypergonadotropism, functional hyperandrogenism, polycystic ovaries and anovulatory infertility; perturbations similar to those observed in women with polycystic ovary syndrome Obesity increases the severity of the phenotype in women with polycystic ovary syndrome. To determine if prepubertal weight gain would exaggerate the reproductive disruptions in prenatal testosterone-treated sheep, pregnant sheep were injected with 100 mg testosterone propionate (1.2 mg/kg) im twice-weekly, from days 30–90 of gestation. Beginning 14 weeks after birth a subset of control and prenatal testosterone-treated females were overfed to increase body weight to 25% above that of controls. Twice-weekly progesterone measurements found no differences in timing of puberty but overfed prenatal testosterone-treated females stooped cycling earlier. Detailed characterization of periovulatory hormonal dynamics following estrus synchronization with prostaglandin F_2a found 100% of controls, 71% overfed controls, 43% prenatal testosterone-treated, and 14% overfed prenatal testosterone-treated females had definable LH surges. Only 1 of 7 overfed prenatal testosterone-treated female versus 100% of control, 100% of overfed control and 7 of 8 prenatal testosterone-treated females exhibited luteal progesteroneincrease. Assessment of LH pulse characteristics during the anestrous season found both overfeeding and prenatal testosterone excess increased LH pulse frequency without an interaction between these two variables. These findings agree with the increased prevalence of anovulation observed in obese women with polycystic ovary syndrome and indicate that excess postnatal weight gain amplifies reproductive disruptions caused by prenatal testosterone excess.