BATF relieves hepatic steatosis by inhibiting PD1 and promoting energy metabolism

Author:

Zhang Zhiwang1,Liao Qichao1,Pan Tingli1,Yu Lin1,Luo Zupeng1,Su Songtao1,Liu Shi1,Hou Menglong1,Li Yixing2,Damba Turtushikh3,Liang Yunxiao1,Zhou Lei1ORCID

Affiliation:

1. Institute of Digestive Disease, Guangxi Academy of Medical Sciences, the People's Hospital of Guangxi Zhuang Autonomous Region

2. College of Animal Science and Technology, Guangxi University

3. School of Pharmacy, Mongolian National University of Medical Sciences

Abstract

The rising prevalence of nonalcoholic fatty liver disease (NAFLD) has become a global health threat that needs to be addressed urgently. Basic leucine zipper ATF-like transcription factor (BATF) is commonly thought to be involved in immunity, but its effect on lipid metabolism is not clear. Here, we investigated the function of BATF in hepatic lipid metabolism. BATF alleviated high-fat diet (HFD)-induced hepatic steatosis and inhibited elevated programmed cell death protein (PD)1 expression induced by HFD. A mechanistic study confirmed that BATF regulated fat accumulation by inhibiting PD1 expression and promoting energy metabolism. PD1 antibodies alleviated hepatic lipid deposition. In conclusion, we identified the regulatory role of BATF in hepatic lipid metabolism and that PD1 is a target for alleviation of NAFLD. This study provides new insights into the relationship between BATF, PD1, and NAFLD.

Funder

National Natural Science Foundation of China

Guangxi Science Foundation for Distinguished Young Scholars

Guangxi Natural Science Foundation

Guangxi Academy of Medical Sciences high-level Talents Foundation

Publisher

eLife Sciences Publications, Ltd

Subject

General Immunology and Microbiology,General Biochemistry, Genetics and Molecular Biology,General Medicine,General Neuroscience

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