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Text
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Pages
G166-G174
Issue
2
Volume
320
ISSN
1931857
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<a href="http://neomed.idm.oclc.org/login?url=http://doi.org/10.1152/ajpgi.00315.2020" target="_blank" rel="noreferrer noopener">NEOMED Full-text Holding (if available) - Proxy DOI: 10.1152/ajpgi.00315.2020</a>
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Update Year & Number
March 2021 List
NEOMED College
NEOMED College of Medicine
NEOMED Department
Department of Integrative Medical Sciences
NEOMED Postdoc Publications
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Title
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Hepatocyte-specific expression of human carboxylesterase 2 attenuates nonalcoholic steatohepatitis in mice.
Publisher
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American Journal Of Physiology: Gastrointestinal & Liver Physiology
Date
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2021
2021-02
Subject
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steatohepatitis; LABORATORY mice; FATTY liver; lipotoxicity; CES2; fatty acid oxidation; lipolysis; FATTY acid oxidation; INSULIN sensitivity; STEROL regulatory element-binding proteins
Creator
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Xu Y;Pan X; Shuwei H;Zhu Y; Bawa FC;Li Y; Yin L; Zhang Y
Description
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Human carboxylesterase 2 (CES2) has triacylglycerol hydrolase (TGH) activities and plays an important role in lipolysis. In this study, we aim to determine the role of human CES2 in the progression or reversal of steatohepatitis in diet-induced or genetically obese mice. High-fat/high-cholesterol/high-fructose (HFCF) diet-fed C57BL/6 mice or db/db mice were intravenously injected with an adeno-associated virus expressing human CES2 under the control of an albumin promoter. Human CES2 protected against HFCF diet-induced nonalcoholic fatty liver disease (NAFLD) in C57BL/6J mice and reversed steatohepatitis in db/db mice. Human CES2 also improved glucose tolerance and insulin sensitivity. Mechanistically, human CES2 reduced hepatic triglyceride (T) and free fatty acid (FFA) levels by inducing lipolysis and fatty acid oxidation and inhibiting lipogenesis via suppression of sterol regulatory element-binding protein 1. Furthermore, human CES2 overexpression improved mitochondrial respiration and glycolytic function, and inhibited gluconeogenesis, lipid peroxidation, apoptosis, and inflammation. Our data suggest that hepatocyte-specific expression of human CES2 prevents and reverses steatohepatitis. Targeting hepatic CES2 may be an attractive strategy for treatment of NAFLD. NEW & NOTEWORTHY Human CES2 attenuates high-fat/cholesterol/fructose diet-induced steatohepatitis and reverses steatohepatitis in db/db mice. Mechanistically, human CES2 induces lipolysis, fatty acid and glucose oxidation, and inhibits hepatic glucose production, inflammation, lipid oxidation, and apoptosis. Our data suggest that human CES2 may be targeted for treatment of non-alcoholic steatohepatitis (NASH). [ABSTRACT FROM AUTHOR]
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<a href="http://doi.org/10.1152/ajpgi.00315.2020" target="_blank" rel="noreferrer noopener">10.1152/ajpgi.00315.2020</a>
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journalArticle
2021
American Journal Of Physiology: Gastrointestinal & Liver Physiology
Bawa FC
CES2
Department of Integrative Medical Sciences
Fatty acid oxidation
Fatty Liver
insulin sensitivity
journalArticle
LABORATORY mice
Li Y
Lipolysis
lipotoxicity
March 2021 List
NEOMED College of Medicine
NEOMED Postdoc Publications
Pan X
Shuwei H
steatohepatitis
STEROL regulatory element-binding proteins
Xu Y
Yin L
Zhang Y
Zhu Y