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Text
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URL Address
<a href="http://doi.org/10.1002/hep.28472" target="_blank" rel="noreferrer noopener">http://doi.org/10.1002/hep.28472</a>
Pages
1860–1874
Issue
6
Volume
63
Dublin Core
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Title
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Carboxylesterase 2 prevents liver steatosis by modulating lipolysis, endoplasmic reticulum stress, and lipogenesis and is regulated by hepatocyte nuclear factor 4 alpha in mice.
Publisher
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Hepatology (Baltimore, Md.)
Date
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2016
2016-06
Subject
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*Lipid Metabolism; Adiposity; Animals; Carboxylesterase/*metabolism; Carboxylic Ester Hydrolases/genetics/*metabolism; Diabetes Mellitus; Diet; Endoplasmic Reticulum Stress; Energy Metabolism; Experimental/enzymology; Gene Knockdown Techniques; Glucose Tolerance Test; Glucose/metabolism; Hepatocyte Nuclear Factor 4/*metabolism; High-Fat/adverse effects; Homeostasis; Humans; Inbred C57BL; Lipogenesis; Lipolysis; Liver/enzymology; Male; Mice; Non-alcoholic Fatty Liver Disease/*etiology/metabolism; Obesity/enzymology/etiology; Sterol Regulatory Element Binding Protein 1/metabolism
Creator
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Li Yuanyuan; Zalzala Munaf; Jadhav Kavita; Xu Yang; Kasumov Takhar; Yin Liya; Zhang Yanqiao
Description
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UNLABELLED: Nonalcoholic fatty liver disease (NAFLD) is a common liver disease that ranges from simple steatosis to nonalcoholic steatohepatitis (NASH). So far, the underlying mechanism remains poorly understood. Here, we show that hepatic carboxylesterase 2 (CES2) is markedly reduced in NASH patients, diabetic db/db mice, and high-fat diet (HFD)-fed mice. Restoration of hepatic CES2 expression in db/db or HFD-fed mice markedly ameliorates liver steatosis and insulin resistance. In contrast, knockdown of hepatic CES2 causes liver steatosis and damage in chow- or Western diet-fed C57BL/6 mice. Mechanistically, we demonstrate that CES2 has triglyceride hydrolase activity. As a result, gain of hepatic CES2 function increases fatty acid oxidation and inhibits lipogenesis, whereas loss of hepatic CES2 stimulates lipogenesis by inducing endoplasmic reticulum stress. We further show that loss of hepatic CES2 stimulates lipogenesis in a sterol regulatory element-binding protein 1 (SREBP-1)-dependent manner. Finally, we show that hepatocyte nuclear factor 4 alpha (HNF-4alpha) plays a key role in controlling hepatic CES2 expression in diabetes, obesity, or NASH. CONCLUSION: CES2 plays a protective role in development of NAFLD. Targeting the
Identifier
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<a href="http://doi.org/10.1002/hep.28472" target="_blank" rel="noreferrer noopener">10.1002/hep.28472</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
*Lipid Metabolism
2016
Adiposity
Animals
Carboxylesterase/*metabolism
Carboxylic Ester Hydrolases/genetics/*metabolism
Department of Integrative Medical Sciences
Department of Pharmaceutical Sciences
Diabetes Mellitus
Diet
Endoplasmic Reticulum Stress
Energy Metabolism
Experimental/enzymology
Gene Knockdown Techniques
Glucose Tolerance Test
Glucose/metabolism
Hepatocyte Nuclear Factor 4/*metabolism
Hepatology (Baltimore, Md.)
High-Fat/adverse effects
Homeostasis
Humans
Inbred C57BL
Jadhav Kavita
Kasumov Takhar
Li Yuanyuan
Lipogenesis
Lipolysis
Liver/enzymology
Male
Mice
NEOMED College of Medicine
NEOMED College of Pharmacy
Non-alcoholic Fatty Liver Disease/*etiology/metabolism
Obesity/enzymology/etiology
Sterol Regulatory Element Binding Protein 1/metabolism
Xu Yang
Yin Liya
Zalzala Munaf
Zhang Yanqiao