Regulation of hepatic lipogenesis by the zinc finger protein Zbtb20

Gan Liu, Luting Zhou, Hai Zhang, Rong Chen, Ye Zhang, Ling Li, Jun-Yu Lu, Hui Jiang, Dong Liu, Shasha Qi, Ying-Ming Jiang, Kai Yin, Zhifang Xie, Yuguang Shi, Yong Liu, Xuetao Cao, Yu-Xia Chen, Dajin Zou and Weiping J. Zhang ()
Additional contact information
Gan Liu: Second Military Medical University
Luting Zhou: Second Military Medical University
Hai Zhang: Second Military Medical University
Rong Chen: Second Military Medical University
Ye Zhang: Second Military Medical University
Ling Li: Second Military Medical University
Jun-Yu Lu: Second Military Medical University
Hui Jiang: Second Military Medical University
Dong Liu: Second Military Medical University
Shasha Qi: Second Military Medical University
Ying-Ming Jiang: National Key Laboratory of Medical Immunology, Second Military Medical University
Kai Yin: Obesity & Diabetes Research Center, Second Military Medical University
Zhifang Xie: Second Military Medical University
Yuguang Shi: Barshop Institute for Longevity and Aging Studies, University of Texas Health Science Center at San Antonio
Yong Liu: Institute of Nutritional Sciences, Shanghai Institute of Biological Sciences, Chinese Academy of Science
Xuetao Cao: National Key Laboratory of Medical Immunology, Second Military Medical University
Yu-Xia Chen: Second Military Medical University
Dajin Zou: Obesity & Diabetes Research Center, Second Military Medical University
Weiping J. Zhang: Second Military Medical University

Nature Communications, 2017, vol. 8, issue 1, 1-13

Abstract: Abstract Hepatic de novo lipogenesis (DNL) converts carbohydrates into triglycerides and is known to influence systemic lipid homoeostasis. Here, we demonstrate that the zinc finger protein Zbtb20 is required for DNL. Mice lacking Zbtb20 in the liver exhibit hypolipidemia and reduced levels of liver triglycerides, along with impaired hepatic lipogenesis. The expression of genes involved in glycolysis and DNL, including that of two ChREBP isoforms, is decreased in livers of knockout mice. Zbtb20 binds to and enhances the activity of the ChREBP-α promoter, suggesting that altered metabolic gene expression is mainly driven by ChREBP. In addition, ChREBP-β overexpression largely restores hepatic expression of genes involved in glucose and lipid metabolism, and increases plasma and liver triglyceride levels in knockout mice. Finally, we show that Zbtb20 ablation protects from diet-induced liver steatosis and improves hepatic insulin resistance. We suggest ZBTB20 is an essential regulator of hepatic lipogenesis and may be a therapeutic target for the treatment of fatty liver disease.

Date: 2017
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DOI: 10.1038/ncomms14824

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