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1 Neurology Service, VA Medical Center, E. Orange, NJ, USA; Neurology and Neurosciences, New Jersey Medical School, Newark, NJ, USA
* To whom correspondence should be addressed. E-mail: levin{at}umdnj.edu.
The effects of running wheel exercise and caloric restriction on the regulation of body weight, adiposity and hypothalamic neuropeptide expression were compared in diet-induced obese male rats over 6wk. Compared to sedentary controls, exercising rats had reduced body weight gain (24%), visceral (4 fat pads; 36%) and carcass (leptin; 35%) adiposity but not insulin levels. Arcuate nucleus (ARC) proopiomelanocortin (POMC) mRNA expression was 25% lower but ARC neuropeptide Y (NPY), agouti-related peptide, dorsomedial nucleus (DMN) NPY and paraventricular nucleus (PVN) corticotrophin releasing hormone (CRH) expression was comparable to controls. Sedentary rats, calorically restricted to 85% of control body weight reduced their visceral adiposity (24%), leptin (64%) and insulin (21%) levels. ARC NPY (23%) and DMN NPY (60%) were increased, while ARC POMC (40%) and PVN CRH (14%) were decreased. Calorically restricted exercising rats ran half as much as ad lib-fed exercising rats and had less visceral obesity than comparably restricted sedentary rats. When sedentary restricted rats were re-fed after 4wk, they increased intake and regained the weight gain and adiposity of sedentary controls. While re-fed exercising rats and sedentary rats ate comparable amounts, re-fed exercising rats regained weight and adiposity only to the level of ad lib-fed exercising rats. Thus, exercise lowers the defended level of weight gain and adiposity without a compensatory increase in intake and with a very different profile of hypothalamic neuropeptide expression from calorically restricted rats. This may be due to exercise-related factors other than plasma insulin and leptin.
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