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Am J Physiol Regul Integr Comp Physiol 293: R1102-R1109, 2007. First published July 18, 2007; doi:10.1152/ajpregu.00224.2007
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APPETITE, OBESITY, DIGESTION, AND METABOLISM

Effects of chronic spinal cord injury on body weight and body composition in rats fed a standard chow diet

Stefany D. Primeaux,1 Melissa Tong,2 and Gregory M. Holmes2

1Dietary Obesity Laboratory, Pennington Biomedical Research Center; and 2Neurotrauma and Nutrition Laboratory, Pennington Biomedical Research Center, Louisiana State University, Baton Rouge, Louisiana

Submitted 2 April 2007 ; accepted in final form 10 July 2007

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), we aimed 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 NMR. Despite lower body weight and fat mass, the cumulative consumption of standard laboratory chow (4.0 kcal/g) and mean energy intake (kcal·day–1·100 g body wt–1) 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 was significantly reduced after SCI and IBAT displayed significantly lower real-time PCR expression of UCP1 mRNA. The reduced fat mass and IBAT UCP1 mRNA expression are contraindicative of the cumulative caloric intake by the SCI rats. The prolonged postinjury 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.

metabolic syndrome; fat mass; lean body mass; weight loss; energy balance



Address for reprint requests and other correspondence: G. M. Holmes, Pennington Biomedical Research Center, 6400 Perkins Rd., Baton Rouge, LA 70808 (e-mail: HolmesGM{at}pbrc.edu)







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