Figure 5.
Model representing the POMC/BMPR1A-KO mice. Deletion of BMPR1A in POMC neurons led to a hyperphagic phenotype of hypothalamic neuropeptide expression, a compensatory increase of BMPR1A in the hypothalamus as a whole, and increased sympathetic activation of BAT, leading to increased thermogenesis and energy expenditure and protection from diet-induced obesity.