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1 Research Services, VA medical Center, Minneapolis, Minnesota, United States; Department of Food Science and Nutrition, University of Minnesota, St. Paul, Minnesota, United States
2 Research Services, VA medical Center, Minneapolis, Minnesota, United States
3 Department of Food Science and Nutrition, University of Minnesota, St. Paul, Minnesota, United States; Minnesota Obesity Center, Minneapolis, Minnesota, United States; Research Services, VA medical Center, Minneapolis, Minnesota, United States; Neuroscience, University of Minnesota, Minneapolis, Minnesota, United States
4 Metabolic Section (111G), Minneapolis VA Medical Center, Minneapolis,, Minnesota, United States; Minnesota Obesity Center, Minneapolis, Minnesota, United States
5 Geriatric Research, Education and Clinical Center (11G), Veterans Affairs 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; Graduate Program in Neuroscience, University of Minnesota, Minneapolis, Minnesota, United States
* To whom correspondence should be addressed. E-mail: cwang{at}umn.edu.
Recent studies show that brain-derived neurotrophic factor (BDNF) decreases feeding and body weight after peripheral and ventricular administration. BDNF mRNA and protein, and its receptor, TrkB, are widely distributed in the hypothalamus and other brain regions. However, there are few reports on specific brain sites of actions for BDNF. We evaluated the effect of BDNF, given into the ventromedial nucleus of the hypothalamus (VMH), on normal, deprivation- and NPY- induced feeding behavior and body weight. BDNF injected unilaterally or bilaterally into the VMH of food-deprived and non-deprived rats significantly decreased feeding and body weight gain within the 0-24 h and 24-48 h post-injection intervals. Doses effectively producing inhibition of feeding behavior did not establish a conditioned taste aversion. BDNF-induced feeding inhibition was attenuated by pretreatment of the TrkB-Fc fusion protein that blocks binding between BDNF and its receptor TrkB. VMH-injected BDNF significantly decreased VMH neuropeptide Y (NPY)-induced feeding at 1, 2 and 4 h following injection. In summary, BDNF in the VMH significantly decreases food intake and body weight gain, by TrkB receptor mediated actions. Furthermore, the anorectic effects of BDNF in this site appear to be mediated by NPY. These data suggest that the VMH is an important site of action for BDNF in its effects on energy metabolism.
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