Polycystic ovary syndrome (PCOS) is a common and complex endocrine disorder. Apart from the characteristic reproductive and endocrine traits, PCOS patients also suffer from metabolic features including obesity, insulin resistance, liver steatosis and type 2 diabetes. Although insulin sensitizer agents such as metformin are commonly administrated to ameliorate PCOS metabolic traits, the beneficial effects of metformin are still questionable. Nicotinamide adenine dinucleotide (NAD+) plays a key role in energy metabolism. Moreover, animal and human studies have shown that NAD+ precursors can have beneficial effects on insulin resistance and liver damage. Therefore, we aimed to assess the efficacy of nicotinamide mononucleotide (NMN), a precursor of NAD+, in treating features of PCOS in a dihydrotestosterone (DHT)-induced PCOS mice model. Prepubertal mice were implanted s.c with blank (n=14) or DHT (n=14) implants. After 12 weeks, control and PCOS mice (8/group) were treated with NMN in drinking water while the remaining mice received normal water (NW). All mice were collected 8 weeks after administration of NMN/NW. NMN treatment had no effect on reproductive traits of PCOS. However, oil red O absorption, a marker of liver steatosis, was significantly lower in NMN- versus NW-treated PCOS mice (PCOS+NW: 13.4±2.3; PCOS+NMN: 2.6±1.7; P<0.01). Fasting insulin levels and homeostatic model assessment of insulin resistance (HOMA-IR) were also decreased in PCOS+NMN mice compared to PCOS+NW mice (fasting insulin levels: PCOS+NW, 0.85±0.1ng/mL; PCOS+NMN, 0.52±0.1ng/mL; P<0.05. HOMA-IR: PCOS+NW, 10.6±1.9; PCOS+NMN, 6.9±0.5; P<0.05). While there was no significant difference in body weights, inguinal fat pad weights of PCOS+NMN mice were significantly decreased (PCOS+NW: 17.1±1mg/BW; PCOS+NMN: 12.7±1mg/BW; P<0.001). These findings suggest that boosting NAD+ may represent a novel therapeutic strategy to target metabolic features of PCOS.