Polycystic ovary syndrome (PCOS) is associated with endothelial dysfunction; whether this is attributable to co-morbid hyperandrogenism and/or obesity remains to be established. Therefore, we (1) compared endothelial function between lean and overweight/obese (OW/OB) women with and without androgen excess (AE)-PCOS and (2) examined androgens as potential modulators of endothelial function in these women. The flow-mediated dilation (FMD) test was applied in 14 women with AE-PCOS (lean: n=7; OW/OB: n=7) and 14 controls (CTRL; lean: n=7, OW/OB: n=7) at baseline (BSL) and following 7-days of ethinyl estradiol supplementation (EE; 30mg/day) in order to assess the effect of a vasodilatory therapeutic on endothelial function; at each time point we assessed peak increases in diameter during reactive hyperemia (%FMD), shear rate, and low flow-mediated constriction (%LFMC). BSL %FMD was attenuated in lean AE-PCOS vs both lean CTRL (5.2±1.5 vs 10.3±2.6%, P<0.01) and OW/OB AE-PCOS (5.2±1.5 vs 6.6±0.9%, P=0.048). A negative correlation between BSL %FMD and free testosterone was observed in lean AE-PCOS only (R2=0.68, P=0.02). EE increased %FMD in both OW/OB groups (CTRL: 7.6±0.6 vs 10.4±2.5%, AE-PCOS: 6.6±0.9 vs 9.6±1.7%, P<0.01), had no impact on %FMD in lean AE-PCOS (5.17±1.5 vs 5.17±1.1%, P=0.99), and reduced %FMD in lean CTRL (10.3±2.6 vs 7.6±1.2%, P=0.03). Collectively, these data indicate that lean women with AE-PCOS exhibit more severe endothelial dysfunction than their OW/OB counterparts. Furthermore, endothelial dysfunction appears to be mediated by circulating androgens in lean but not in OW/OB AE-PCOS, suggesting a difference in the endothelial pathophysiology of AE-PCOS between these phenotypes.