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1 Research services, VA Medical Center, Minneapolis, Minnesota, United States
2 Research Services, VA Medical Center, Minneapolis, Minnesota, United States
3 VA Medical Center, Minneapolis, Minnesota, United States; Minnesota Obesity Center, Minneapolis, Minnesota, United States
4 Research services, VA Medical Center, Minneapolis, Minnesota, United States; Department of Food Science and Nutrition, University of Minnesota, St. Paul, Minnesota, United States; Minnesota Obesity Center, Minneapolis, Minnesota, United States; Psychiatry, University of Minnesota, Minneapolis, Minnesota, United States
5 GeriatricResearch, Education and Clinical Center (11G), Veterans Affairs Medical Center, One Veterans Drive, Minneapolis, Minnesota, United States; Graduate Program in Neuroscience4, University of Minnesota, United States; Minnesota Obesity Center, Minneapolis, Minnesota, United States; Department of Food Science and Nutrition, University of Minnesota, St. Paul, Minnesota, United States
* To whom correspondence should be addressed. E-mail: cwang{at}umn.edu.
Brain-derived neurotrophic factor (BDNF) decreases food intake and body weight, but few central sites of action have been identified. The hypothalamic paraventricular nucleus (PVN) is important in energy metabolism regulation, and expresses both BDNF and its receptor. We tested three hypotheses: 1) PVN BDNF reduces feeding and increases energy expenditure (EE); 2) PVN BDNF-enhanced thermogenesis results from increased spontaneous physical activity (SPA) and resting metabolic rate (RMR); 3) PVN BDNF thermogenic effects are mediated in part by uncoupling protein 1 (UCP1) in brown adipose tissue (BAT). BDNF (0.5 µg) was injected into the PVN of Sprague Dawley rats, and oxygen consumption, carbon dioxide production, food intake and SPA were measured for 24 h in an indirect calorimeter. SPA was also measured in open field activity chambers for 48 h after BDNF injection. Animals were sacrificed 6 or 24 h after BDNF injection, and BAT UCP1 gene expression was measured with quantitative real-time polymerase chain reaction. BDNF significantly decreased food intake and body weight gain 24 h after injection. Heat production and RMR were significantly elevated for 7 h immediately after BDNF injection. BDNF had no effect on SPA, but increased UCP1 gene expression in BAT at 6 h, but not 24 h after injection. In conclusion, PVN BDNF reduces body weight by decreasing food intake and increasing EE consequent to increased RMR, which may be due in part to BAT UCP1 activity. These data suggest that the PVN is an important site of BDNF action to influence energy balance.
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