The inability to maintain body weight within prescribed ranges occurs in a significant portion of the human spinal cord injury (SCI) population. Using a rodent model of long-term high thoracic (spinal level T3) spinal cord transection (TX), our aim was to identify derangements in body weight, body composition, plasma insulin, glucose tolerance, and metabolic function as measured by uncoupling protein 1 (UCP1) expression in interscapular brown adipose tissue (IBAT). Sixteen weeks after SCI, body weights of injured female rats stabilized and were significantly lower than surgical control animals. At the same time point, SCI rats had a significantly lower whole body fat:lean tissue mass ratio than controls as measured indirectly by nuclear magnetic resonance. Despite lower body weight and fat mass, the cumulative consumption of standard laboratory chow (4.0 kcal/g) and mean energy intake (kcal/day/100g of body weight) of chronic SCI rats was significantly more than controls. Glucose tolerance tests indicated a significant enhancement in glucose handling in 16 wk SCI rats which were coupled with lower serum insulin levels. The post-mortem weight of gonadal and retroperitoneal fat-pads were significantly reduced after SCI and IBAT displayed significantly lower real time polymerase chain reaction (RT-PCR) expression of UCP1 mRNA. The reduced fat mass and IBAT UCP1 mRNA expression is contraindicative of the cumulative caloric intake by the SCI rats. The prolonged post-injury loss of body weight, including fat mass, is not due to hypophagia but possibly to permanent changes in gastrointestinal transit and absorption as well as whole body homeostatic mechanisms.