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Background: PCOS, the most common female endocrine disorder of unknown etiology is characterized by reproductive abnormalities and associated metabolic conditions comprising insulin resistance, Type 2 diabetes mellitus and dyslipidemia. We previously reported that transgenic overexpression of NGF, a marker of sympathetic hyperactivity, directed to the ovary by the mouse 17alpha-hydroxylase promoter (17NF mice), results in ovarian abnormalities similar to that seen in PCOS women (Dissen et al, 2009). Objective and hypotheses: In the present study we sought to investigate the metabolic profile exhibited by these transgenic mice. Method(s): We studied 17NF mice and its wild type littermate at 10, 15 and 20 weeks of age. We determined glucose homeostasis by glucose tolerance test (GTT) and body composition and bone mineral density (BMD) by Dexa scan. We also measured interscapular brown adipose tissue temperature (iBAT-T) and UCP1 expression as a marker of sympathetic nerve activity Results: We found that at 10 weeks of age 17NF mice display glucose intolerance (p< 0.01). This occurred despite no difference in body weight or total body fat, although 17NF mice showed an increase in visceral fat (p< 0.05). This impairment in glucose tolerance was maintained to 15 and 20 weeks of age when 17NF mice also displayed significantly increased body weight, body fat and visceral fat compared with WT mice. Interestingly, 17NF mice also exhibited an increased BMD from 15 weeks of age compared with WT (p< 0.05). Twenty four hours iBAT-T was higher in 17NF mice than WT at 10 and 20 weeks of age and was significantly different when just the dark period was considered (p< 0.05) . Conclusion(s): These findings suggest an overexpression of NGF in the ovary may be sufficient to cause both reproductive and metabolic alterations that are characteristic of PCOS. Most importantly, this new animal model could therefore allow for the exploration of new treatments of PCOS.