The key factor for development of obesity is a positive energy balance, in which excess energy is stored in white adipose tissue. Accumulated lipids are burned by brown adipose tissue (BAT) in the process of thermogenesis. Bone morphogenetic proteins (BMP’s) are known to have an important role in the development of adipose tissue, where BMP’s 2 and 4 contribute to white adipogenesis (1) and BMP7 induces commitment of preadipocytes into a brown adipocyte lineage (2). The ventromedial hypothalamic nucleus (VMH) is involved in the control of energy homeostasis, where it has been shown that activation of AMP-activated protein kinase (AMPK) and fatty acid metabolism promotes energy conservation and control of BAT activation (3). The aim of our study was to investigate the role of hypothalamic Bmp8b on energy balance and thermogenesis in BAT. To perform the experiments female C57Bl6/J mice and Sprague-Dawley rats were used. Surgical procedures were performed with mice and rats under tribromoethanol (480 mg/kg) and ketamine (100mg/kg)/xylazine (15mg/kg) anaesthesia (IP), respectively. Animals were implanted in the lateral ventricle with intracerebroventricular (ICV) cannulae as previously described (3, 4), and received an ICV injection of Bmp8b or vehicle. Before Bmp8b treatment rats were treated with AMPKα dominant-negative (DN) or constitutively active (CA) expressing isoforms, or GFP as a control, targeted to the VMH using stereotaxic adenoviral delivery (3, 4). After Bmp8b treatment body temperature was recorded with a rectal probe and BAT skin temperature was recorded with an infrared thermal camera. Hypothalamic protein levels were analyzed by western blot using specific antibodies (3). Neuronal activation in specific nuclei was measured by immunohistochemistry (3). Compared to vehicle, mice treated with Bmp8b showed an increase in core body temperature and increased phosphorylation of hypothalamic AMPKα and ACCα. Also, these animals displayed augmented neuronal activation in VMH and lateral hypothalamic area and in raphe pallidus and inferior olive nuclei, which coordinate sympathetic tone to BAT. Bmp8b’s effect on core temperature was increased in presence of AMPKα-DN and was completely inhibited by expression of AMPKα-CA in comparison to vehicle treated animals. BAT’s relative activation after Bmp8b ICV treatment, measured by thermal imaging, correlated extremely well with changes in body temperature in a given animal. Our data show that central Bmp8b induces thermogenesis in BAT through neuronal activation in hypothalamic regulatory nuclei and medulla oblongata. Also, we suggest that AMPK in the hypothalamus acts in opposition to Bmp8b creating a conterregulatory mechanism that modulates thermogenesis in BAT to control energy balance (5). Thus, modulation of central Bmp8b action could offer new strategies to counter obesity.