a member of the family of neurotrophins, is essential for the survival and maintenance of peripheral sensory neurons (1, 2). Because most Bdnf �/ � mutants die during the second postnatal week, less is known about the in vivo role of this neurotrophin in the postnatal brain. Previous findings implicated BDNF in weight regulation as exogenous BDNF treatment was demonstrated to cause a reduction in weight and Bdnf �/ � animals show an age-related increase in body weight (3, 4). However, the mode of action of BDNF in weight regulation remains elusive. Through the generation and characterization of several mouse genetic obesity models, a number of central and peripheral factors and their mechanism of action in food intake and metabolic function have been identified. Central regulation of food intake is generally associated with the hypothalamus, where orexigenic factors such as NPY, agouti related protein (AGRP), orexin, and melanin concentrating hormone (MCH) and anorexigenic factors such as cocaine and amphetamine-related transcript, serotonin, TRH, and �-MSH are present (5–12). BDNF and its receptor, Tr
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