Liver governs adipose remodelling via extracellular vesicles in response to lipid overload
Yue Zhao,
Meng-Fei Zhao,
Shan Jiang,
Jing Wu,
Jia Liu,
Xian-Wen Yuan,
Di Shen,
Jing-Zi Zhang,
Nan Zhou,
Jian He,
Lei Fang (),
Xi-Tai Sun (),
Bin Xue () and
Chao-Jun Li ()
Additional contact information
Yue Zhao: Nanjing University
Meng-Fei Zhao: Nanjing University
Shan Jiang: Nanjing University
Jing Wu: Nanjing University
Jia Liu: Nanjing University
Xian-Wen Yuan: Nanjing University
Di Shen: Nanjing University
Jing-Zi Zhang: Nanjing University
Nan Zhou: Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School
Jian He: Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School
Lei Fang: Nanjing University
Xi-Tai Sun: Nanjing Drum Tower Hospital, The Affiliated Hospital of Nanjing University Medical School
Bin Xue: Nanjing Medical University
Chao-Jun Li: Nanjing University
Nature Communications, 2020, vol. 11, issue 1, 1-17
Abstract:
Abstract Lipid overload results in lipid redistribution among metabolic organs such as liver, adipose, and muscle; therefore, the interplay between liver and other organs is important to maintain lipid homeostasis. Here, we show that liver responds to lipid overload first and sends hepatocyte-derived extracellular vesicles (EVs) targeting adipocytes to regulate adipogenesis and lipogenesis. Geranylgeranyl diphosphate synthase (Ggpps) expression in liver is enhanced by lipid overload and regulates EV secretion through Rab27A geranylgeranylation. Consistently, liver-specific Ggpps deficient mice have reduced fat adipose deposition. The levels of several EV-derived miRNAs in the plasma of non-alcoholic fatty liver disease (NAFLD) patients are positively correlated with body mass index (BMI), and these miRNAs enhance adipocyte lipid accumulation. Thus, we highlight an inter-organ mechanism whereby the liver senses different metabolic states and sends corresponding signals to remodel adipose tissue to adapt to metabolic changes in response to lipid overload.
Date: 2020
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-14450-6
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DOI: 10.1038/s41467-020-14450-6
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