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. 2017 Oct 9;158(12):4233–4245. doi: 10.1210/en.2017-00212

Figure 5.

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.