The major function of primary order neurons in the ARC of the hypothalamus is control of energy homeostasis. Among these neurons, POMC neurons play a significant role in controlling anorexigenic feeding behavior and upregulating energy expenditure. Additionally, TRPM2 is a well-established temperature sensor, but no evidence of regulation of BAT thermogenesis via POMCTRPM2 neurons in the ARC has been reported to date. We here investigated the role of ARC POMCTRPM2 in BAT thermogenesis. Through single-cell RT-PCR and IHC analyses, we confirmed that some POMC neurons express TRPM2. The specific stimulation of POMC neurons via chemogenetic modulation induced BAT thermogenesis, indicating their role in regulating BAT activity through neuronal connections. Adenosine diphosphoribose (ADPR), a TRPM2 agonist, elevated the membrane potential of POMC neurons. This effect was suppressed by TRP and TRPM2 antagonists. Additionally, icv injection of ADPR increased c-Fos expression of a subset of POMC neurons, BAT/core body temperature, and expression of IRF-4, but not uncoupling protein 1 (UCP1), in normal chow diet- and HFD-fed mice. TRPM2 antagonists blocked this increase. Our findings offer new insights into the physiological mechanism of UCP1-independent BAT thermogenesis, which is regulated by hypothalamic POMCTRPM2 neurons. Consequently, these approaches to promoting BAT thermogenesis can provide novel therapeutic strategies and precautions to combat metabolic disorders.