Transgenic (TG) female mice, expressing a chimeric bovine luteinizing hormone (LH) -subunit/human chorionic gonadotropin (hCG) -subunit C-terminal extension (bLH-CTP) gene, produce high levels of circulating LH and serve as a model for functional ovarian hyperandrogenism and follicular cysts. We report here that obesity is a typical feature of the bLH-CTP female mice and present so of its endocrine and metabolic correlates. The mean body weight of the bLH-CTP females was significantly higher (p < 0.01) than in controls at and beyond 5 weeks of age, and at 5 months, it was 32% higher than in controls (p < 0.01). At this age, the amount of white adipose tissue in the bLH-CTP females was significantly increased, as reflected by the weight difference of the retroperitoneal fat pad; 162 ± 18 vs. 64 ± 25 mg in controls (p < 0.01). In addition, the expression of leptin mRNA in white adipose tissue of the TG females was about 2-fold elevated (p < 0.05). Serum leptin and insulin levels were also significantly increased in the bLH-CTP females, and their basal glucose levels tended to be higher than in controls. Food intake of the bLH-CTP females was significantly increased (p < 0.05). Brown adipose tissue thermogenic activity, as measured by GDP binding to brown fat mitochondria, was reduced (p < 0.05). However, the bLH-CTP mice were able to maintain normal body temperature when exposed to +4 °C. Ovariectomy at the age of 3 weeks totally prevented the development of obesity. As expected the treatment of the gonadectomized bLH-CTP females with dihydrotestosterone increased the body weight, while estradiol had an opposite effect. In summary, the present results shows that intact female bLH-CTP mice are obese and have increased food consumption and reduced brown adipose tissue thermogenic activity. The weight gain can be partly explained by elevated androgens, but it is probably also contributed to the increased adrenal glucocorticoid production. As was found with the increased adrenal glucocorticoid production. As was previosly found with the increased adrenal steroidogenesis, obesity was dependent on the presence of ovaries, apparently through estrogen stimulated prolactin secretion. Hence, the bLH-CTP mice provide a useful model for studying obesity related to elevated LH secretion, with consequent alterations in ovarian and adrenal function.