Linker histone variant H1.2 is a brake on white adipose tissue browning

Yangmian Yuan, Yu Fan, Yihao Zhou, Rong Qiu, Wei Kang, Yu Liu, Yuchen Chen, Chenyu Wang, Jiajian Shi, Chengyu Liu, Yangkai Li, Min Wu, Kun Huang, Yong Liu and Ling Zheng ()
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Yangmian Yuan: Wuhan University
Yu Fan: Wuhan University
Yihao Zhou: Wuhan University
Rong Qiu: Wuhan University
Wei Kang: Wuhan University
Yu Liu: Wuhan University
Yuchen Chen: Huazhong University of Science and Technology
Chenyu Wang: Wuhan University
Jiajian Shi: Huazhong University of Science and Technology
Chengyu Liu: Huazhong University of Science and Technology
Yangkai Li: Huazhong University of Science and Technology
Min Wu: Wuhan University
Kun Huang: Huazhong University of Science and Technology
Yong Liu: Wuhan University
Ling Zheng: Wuhan University

Nature Communications, 2023, vol. 14, issue 1, 1-18

Abstract: Abstract Adipose-tissue is a central metabolic organ for whole-body energy homeostasis. Here, we find that highly expressed H1.2, a linker histone variant, senses thermogenic stimuli in beige and brown adipocytes. Adipocyte H1.2 regulates thermogenic genes in inguinal white-adipose-tissue (iWAT) and affects energy expenditure. Adipocyte H1.2 deletion (H1.2AKO) male mice show promoted iWAT browning and improved cold tolerance; while overexpressing H1.2 shows opposite effects. Mechanistically, H1.2 binds to the promoter of Il10rα, which encodes an Il10 receptor, and positively regulates its expression to suppress thermogenesis in a beige cell autonomous manner. Il10rα overexpression in iWAT negates cold-enhanced browning of H1.2AKO male mice. Increased H1.2 level is also found in WAT of obese humans and male mice. H1.2AKO male mice show alleviated fat accumulation and glucose intolerance in long-term normal chow-fed and high fat diet-fed conditions; while Il10rα overexpression abolishes these effects. Here, we show a metabolic function of H1.2-Il10rα axis in iWAT.

Date: 2023
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DOI: 10.1038/s41467-023-39713-w

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