| First Author | Yuan Y | Year | 2023 |
| Journal | Nat Commun | Volume | 14 |
| Issue | 1 | Pages | 3982 |
| PubMed ID | 37414781 | Mgi Jnum | J:338037 |
| Mgi Id | MGI:7506389 | Doi | 10.1038/s41467-023-39713-w |
| Citation | Yuan Y, et al. (2023) Linker histone variant H1.2 is a brake on white adipose tissue browning. Nat Commun 14(1):3982 |
| abstractText | 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 Il10ralpha, which encodes an Il10 receptor, and positively regulates its expression to suppress thermogenesis in a beige cell autonomous manner. Il10ralpha 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 Il10ralpha overexpression abolishes these effects. Here, we show a metabolic function of H1.2-Il10ralpha axis in iWAT. |
