脂肪生成
产热
内分泌学
生物
内科学
胰岛素抵抗
肥胖
白色脂肪组织
脂肪组织
医学
作者
Zhao Zhang,Yiao Jiang,Lijing Su,Sara Ludwig,Xuechun Zhang,Miao Tang,Xiaohong Li,Priscilla Anderton,Xiaoming Zhan,Mihwa Choi,Jamie L. Russell,Chun-Hui Bu,Stephen Lyon,Darui Xu,Sara Hildebrand,Lindsay Scott,Jiexia Quan,Rochelle Simpson,Qihua Sun,Baifang Qin
出处
期刊:Cell Metabolism
[Cell Press]
日期:2022-10-12
卷期号:34 (11): 1860-1874.e4
被引量:13
标识
DOI:10.1016/j.cmet.2022.09.018
摘要
Using random germline mutagenesis in mice, we identified a viable hypomorphic allele (boh) of the transcription-factor-encoding gene Ovol2 that resulted in obesity, which initially developed with normal food intake and physical activity but decreased energy expenditure. Fat weight was dramatically increased, while lean weight was reduced in 12-week-old boh homozygous mice, culminating by 24 weeks in massive obesity, hepatosteatosis, insulin resistance, and diabetes. The Ovol2boh/boh genotype augmented obesity in Lepob/ob mice, and pair-feeding failed to normalize obesity in Ovol2boh/boh mice. OVOL2-deficient mice were extremely cold intolerant. OVOL2 is essential for brown/beige adipose tissue-mediated thermogenesis. In white adipose tissues, OVOL2 limited adipogenesis by blocking C/EBPα engagement of its transcriptional targets. Overexpression of OVOL2 in adipocytes of mice fed with a high-fat diet reduced total body and liver fat and improved insulin sensitivity. Our data reveal that OVOL2 plays dual functions in thermogenesis and adipogenesis to maintain energy balance.
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