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Lipopolysaccharide binding protein resists hepatic oxidative stress by regulating lipid droplet homeostasis

Qilun Zhang, Xuting Shen, Xin Yuan, Jing Huang, Yaling Zhu, Tengteng Zhu, Tao Zhang, Haibo Wu, Qian Wu, Yinguang Fan, Jing Ni, Leilei Meng, Anyuan He, Chaowei Shi, Hao Li, Qingsong Hu, Jian Wang, Cheng Chang, Fan Huang, Fang Li, Meng Chen, Anding Liu (), Shandong Ye (), Mao Zheng () and Haoshu Fang ()
Additional contact information
Qilun Zhang: University of Science and Technology of China
Xuting Shen: Anhui Medical University
Xin Yuan: Anhui Medical University
Jing Huang: Anhui Medical University
Yaling Zhu: Anhui Medical University
Tengteng Zhu: Anhui Medical University
Tao Zhang: Anhui Medical University
Haibo Wu: University of Science and Technology of China
Qian Wu: The First Affiliated Hospital of Anhui University of Chinese Medicine
Yinguang Fan: Anhui Medical University
Jing Ni: Anhui Medical University
Leilei Meng: Anhui Medical University
Anyuan He: Anhui Medical University
Chaowei Shi: University of Science and Technology of China
Hao Li: University of Science and Technology of China
Qingsong Hu: University of Science and Technology of China
Jian Wang: Beijing Institute of Lifeomics
Cheng Chang: Beijing Institute of Lifeomics
Fan Huang: First Affiliated Hospital of Anhui Medical University
Fang Li: First Affiliated Hospital of Anhui Medical University
Meng Chen: Graduate School of Bengbu Medical College
Anding Liu: Huazhong University of Science and Technology
Shandong Ye: University of Science and Technology of China
Mao Zheng: University of Science and Technology of China
Haoshu Fang: Anhui Medical University

Nature Communications, 2024, vol. 15, issue 1, 1-17

Abstract: Abstract Oxidative stress-induced lipid accumulation is mediated by lipid droplets (LDs) homeostasis, which sequester vulnerable unsaturated triglycerides into LDs to prevent further peroxidation. Here we identify the upregulation of lipopolysaccharide-binding protein (LBP) and its trafficking through LDs as a mechanism for modulating LD homeostasis in response to oxidative stress. Our results suggest that LBP induces lipid accumulation by controlling lipid-redox homeostasis through its lipid-capture activity, sorting unsaturated triglycerides into LDs. N-acetyl-L-cysteine treatment reduces LBP-mediated triglycerides accumulation by phospholipid/triglycerides competition and Peroxiredoxin 4, a redox state sensor of LBP that regulates the shuttle of LBP from LDs. Furthermore, chronic stress upregulates LBP expression, leading to insulin resistance and obesity. Our findings contribute to the understanding of the role of LBP in regulating LD homeostasis and against cellular peroxidative injury. These insights could inform the development of redox-based therapies for alleviating oxidative stress-induced metabolic dysfunction.

Date: 2024
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DOI: 10.1038/s41467-024-47553-5

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