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Chunchun Wei Department of Pathophysiology, Naval Medical University, Shanghai, China
Department of Physiology, Naval Medical University, Shanghai, China

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Xianhua Ma Department of Pathophysiology, Naval Medical University, Shanghai, China

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Kai Su Department of Pathophysiology, Naval Medical University, Shanghai, China

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Shasha Qi Department of Pathophysiology, Naval Medical University, Shanghai, China

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Yuangang Zhu The State Key Laboratory of Membrane Biology, Center for Life Sciences and Institute of Molecular Medicine, Peking University, Beijing, China

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Junjian Lin Department of Pathophysiology, Naval Medical University, Shanghai, China

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Chenxin Wang The State Key Laboratory of Membrane Biology, Center for Life Sciences and Institute of Molecular Medicine, Peking University, Beijing, China

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Rui Yang Department of Pathophysiology, Naval Medical University, Shanghai, China

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Xiaowei Chen The State Key Laboratory of Membrane Biology, Center for Life Sciences and Institute of Molecular Medicine, Peking University, Beijing, China

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Weizhong Wang Department of Physiology, Naval Medical University, Shanghai, China

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Weiping J Zhang Department of Pathophysiology, Naval Medical University, Shanghai, China
NHC Key Laboratory of Hormones and Development, Tianjin Key Laboratory of Metabolic Diseases, Tianjin Medical University Chu Hsien-I Memorial Hospital and Tianjin Institute of Endocrinology, Tianjin, China

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Brown adipose tissue (BAT) plays a critical role in energy expenditure by uncoupling protein 1 (UCP1)-mediated thermogenesis. Carbohydrate response element-binding protein (ChREBP) is one of the key transcription factors regulating de novo lipogenesis (DNL). As a constitutively active form, ChREBP-β is expressed at extremely low levels. Up to date, its functional relevance in BAT remains unclear. In this study, we show that ChREBP-β inhibits BAT thermogenesis. BAT ChREBP-β mRNA levels were elevated upon cold exposure, which prompted us to generate a mouse model overexpressing ChREBP-β specifically in BAT using the Cre/LoxP approach. ChREBP-β overexpression led to a whitening phenotype of BAT at room temperature, as evidenced by increased lipid droplet size and decreased mitochondrion content. Moreover, BAT thermogenesis was inhibited upon acute cold exposure, and its metabolic remodeling induced by long-term cold adaptation was significantly impaired by ChREBP-β overexpression. Mechanistically, ChREBP-β overexpression downregulated expression of genes involved in mitochondrial biogenesis, autophagy, and respiration. Furthermore, thermogenic gene expression (e.g. Dio2, UCP1) was markedly inhibited in BAT by the overexpressed ChREBP-β. Put together, our work points to ChREBP-β as a negative regulator of thermogenesis in brown adipocytes.

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