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Abstract Title:

A High-Fat Diet Attenuates Amp-Activated Protein Kinaseα1 in Adipocytes to Induce Exosome Shedding and Nonalcoholic Fatty Liver Development.

Abstract Source:

Diabetes. 2020 Dec 1. Epub 2020 Dec 1. PMID: 33262120

Abstract Author(s):

Chenghui Yan, Xiaoxiang Tian, Jiayin Li, Dan Liu, Ding Ye, Zhonglin Xie, Yaling Han, Ming-Hui Zou

Article Affiliation:

Chenghui Yan

Abstract:

Exosomes are important for intercellular communication, but the role of exosomes in the communication between adipose tissue (AT) and the liver remains unknown. The aim of this study is to determine the contribution of AT-derived exosomes in nonalcoholic fatty liver disease (NAFLD). Exosome components, liver fat content, and liver function were monitored in AT in mice fed a high-fat diet (HFD) or treated with metformin- or GW4869 and with AMP-activated protein kinase (AMPKα1) floxed/WT),, liver tissue-specific, or AT-specificmodification. In cultured adipocytes and white adipose tissue (WAT), the absence ofincreased exosome release and exosomal proteins by elevating tumor susceptibility gene 101 ()-mediated exosome biogenesis. In adipocytes treated with palmitic acid, TSG101 facilitated scavenger receptor class B (CD36) sorting into exosomes. CD36-containing exosomes were then endocytosed by hepatocytes to induce lipid accumulation and inflammation. Consistently, an HFD induced more severe lipid accumulation and cell death inand adipose tissue-specificmice than in WT and liver-specificmice. AMPK activation by metformin reduced adipocyte-mediated exosome release and mitigated fatty liver development in WT and liver specificmice. Moreover, administration of the exosome inhibitor GW4869 blocked exosome secretion and alleviated HFD-induced fatty livers inand adipocyte-specificmice. We conclude that HFD-mediated AMPKα1 inhibition promotes NAFLD by increasing numbers of AT CD36-containing exosomes.

Study Type : In Vitro Study

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