Neurotrophism and energy homeostasis: perfect together

Abstract

ENERGY HOMEOSTASIS DEPENDS upon the balance between anabolic and catabolic drives. Generally, anabolic neuropeptides such as neuropeptide Y (NPY) increase food intake and decrease thermogenesis (5), while catabolic ones such as melanocyte stimulating hormone (-MSH), which is released from proopiomelanocortin (POMC) neurons in the hypothalamic arcuate nucleus (Arc), reduce intake and increase energy expenditure (32). The companion papers published in this issue of the American Journal of Physiology-Regulatory, Integrative and Comparative Physiology by Wang et al. (62, 63) demonstrate that brain-derived neurotrophic factor (BDNF) acts as a prototypic catabolic factor when injected into the hypothalamic paraventricular nucleus (PVN). Food intake is decreased without provoking an aversive reaction, and resting energy expenditure is increased without affecting overall motor activity. These papers are important because they add to the growing body of data that demonstrate unequivocally that BDNF can act at a specific site as a relatively pure catabolic agent (4, 61). They also demonstrate that PVN BDNF injections act with different temporal patterns on energy expenditure and feeding. These findings support others (2) that demonstrate a divergence of neural pathways originating in the PVN by which energy intake and expenditure are regulated. On the other hand, these studies raise several questions about the regulation of energy homeostasis and the role of BDNF and other neurotrophic factors in this process.