CDK6 inhibits white to beige fat transition by suppressing RUNX1

Xiaoli Hou, Yongzhao Zhang, Wei Li, Alexander J. Hu, Chi Luo, Wenhui Zhou, Jamie K. Hu, Stefano G. Daniele, Jinfeng Wang, Jinghao Sheng, Yongsheng Fan, Andrew S. Greenberg, Stephen R. Farmer and Miaofen G. Hu ()
Additional contact information
Xiaoli Hou: Tufts Medical Center
Yongzhao Zhang: Tufts Medical Center
Wei Li: Tufts Medical Center
Alexander J. Hu: Tufts Medical Center
Chi Luo: Harvard Medical School
Wenhui Zhou: Tufts Medical Center
Jamie K. Hu: Tufts Medical Center
Stefano G. Daniele: MD program for Jamie K. Hu, MD-PhD Program for Stefano G. Daniele
Jinfeng Wang: Tufts Medical Center
Jinghao Sheng: Tufts Medical Center
Yongsheng Fan: Center for Analysis and Testing
Andrew S. Greenberg: JM-USDA Human Nutrition Research Center
Stephen R. Farmer: Department of Biochemistry
Miaofen G. Hu: Tufts Medical Center

Nature Communications, 2018, vol. 9, issue 1, 1-14

Abstract: Abstract Whereas white adipose tissue depots contribute to the development of metabolic diseases, brown and beige adipose tissue has beneficial metabolic effects. Here we show that CDK6 regulates beige adipocyte formation. We demonstrate that mice lacking the CDK6 protein or its kinase domain (K43M) exhibit significant increases beige cell formation, enhanced energy expenditure, better glucose tolerance, and improved insulin sensitivity, and are more resistant to high-fat diet-induced obesity. Re-expression of CDK6 in Cdk6 −/− mature or precursor cells, or ablation of RUNX1 in K43M mature or precursor cells, reverses these phenotypes. Furthermore, RUNX1 positively regulates the expression of Ucp-1 and Pgc1α by binding to proximal promoter regions. Our findings indicate that CDK6 kinase activity negatively regulates the conversion of fat-storing cells into fat-burning cells by suppressing RUNX1, and suggest that CDK6 may be a therapeutic target for the treatment of obesity and related metabolic diseases.

Date: 2018
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DOI: 10.1038/s41467-018-03451-1

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