2025-09-23 中国科学院(CAS)
<関連情報>
- https://english.cas.cn/newsroom/research_news/life/202509/t20250923_1055233.shtml
- https://www.cell.com/neuron/abstract/S0896-6273(25)00630-0
マウス弓状視床下核におけるエネルギー消費の神経基盤の同定 Identification of a neural basis for energy expenditure in the mouse arcuate hypothalamus
Ting Wang ∙ Shuping Han ∙ Yaxin Wang ∙ … ∙ Hui Gong ∙ Peng Cao ∙ Qing-Feng Wu
Neuron Published:September 17, 2025
DOI:https://doi.org/10.1016/j.neuron.2025.08.021
Graphical abstract
Highlights
- Hypothalamic GABAergic Crabp1 neurons bidirectionally regulate energy expenditure
- Crabp1 neurons promote energy expenditure via a one-to-many projection pattern
- Crabp1 neurons are activated by cold and exercise but inhibited by long photoperiod
- Suppression of Crabp1 neurons underlies light-induced metabolic disorder
Summary
Given 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 as cold 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, marked by 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 analyses reveal that Crabp1 neurons promote energy metabolism through a “one-to-many” projection pattern. While Crabp1 neurons are activated by cold exposure and physical activity, prolonged light exposure abrogates their 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.
