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36 reviewsSUMMARYGiven the evolutionary instinct for caloric intake and frequent weight rebound after diet or drug cessation,increasing energy expenditure emerges as an alternative obesity treatment. Environmental cues such ascold and seasonal light prompt the brain to adjust energy expenditure, yet the coordinating neural mechanisms remain poorly understood. Here, we identify a hypothalamic GABAergic neuronal subtype, markedby Crabp1, that targets multiple nuclei to regulate energy expenditure in mice. Silencing Crabp1 neurons reduces physical activity, body temperature, and adaptive thermogenesis, leading to obesity, whereas activation increases energy expenditure and mitigates diet-induced obesity. Structural and functional analysesreveal that Crabp1 neurons promote energy metabolism through a ‘‘one-to-many’’ projection pattern. WhileCrabp1 neurons are activated by cold exposure and physical activity, prolonged light exposure abrogatestheir firing, which mediates light-induced metabolic disorder. Together, we reveal a neural basis that integrates various physiological and environmental stimuli to control energy expenditure and body weight.
