| Amelioration of high fat diet induced liver lipogenesis and hepatic steatosis by interleukin-22. | |
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MedLine Citation:
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PMID: 20452699 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND & AIMS: Interleukin-22 (IL-22) is a Th17-related cytokine within the IL-10 family and plays an important role in host defense and inflammatory responses in orchestration with other Th17 cytokines. IL-22 exerts its functions in non-immune cells as its functional receptor IL-22R1 is restricted in peripheral tissues but not in immune cells. It was recently found that IL-22 serves as a protective molecule to counteract the destructive nature of the T cell-mediated immune response to liver damage. However, it is currently unknown whether IL-22 has an effect on lipid metabolism in the liver. METHODS: In this study, we demonstrate that IL-22 alleviates hepatic steatosis induced by high fat diet (HFD). RESULTS: Administration of recombinant murine IL-22 (rmIL-22) was able to stimulate STAT3 phosphorylation in HepG2 cells and mouse liver. The activation of STAT3 by rmIL-22 was reduced by the over-expression of a dominant negative IL-22R1. Within hours after rmIL-22 treatment, the expression of lipogenesis-related genes including critical transcription factors and enzymes for lipid synthesis in the liver was significantly down-regulated. The levels of triglyceride and cholesterol in the liver were significantly reduced by long-term treatment of rmIL-22 in C57BL/6 and ob/ob mice fed with HFD. The HFD-induced increases of ALT and AST in ob/ob mice were ameliorated by rmIL-22 treatment. In addition, the expression of fatty acid synthase and TNF-alpha in the liver was decreased by long-term rmIL-22 administration. CONCLUSIONS: Collectively, these data indicate that IL-22, in addition to its known functions in host defense and inflammation, has a protective role in HFD-induced hepatic steatosis via its regulation on lipid metabolism in the liver. |
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Authors:
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Ling Yang; Yixuan Zhang; Lingdi Wang; Fengjuan Fan; Lu Zhu; Zhigang Li; Xiangbo Ruan; Heng Huang; Zhenzhen Wang; Zhihua Huang; Yuliang Huang; Xiaoqiang Yan; Yan Chen |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-04-21 |
Journal Detail:
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Title: Journal of hepatology Volume: 53 ISSN: 1600-0641 ISO Abbreviation: J. Hepatol. Publication Date: 2010 Aug |
Date Detail:
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Created Date: 2010-07-06 Completed Date: 2010-11-02 Revised Date: 2012-08-24 |
Medline Journal Info:
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Nlm Unique ID: 8503886 Medline TA: J Hepatol Country: England |
Other Details:
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Languages: eng Pagination: 339-47 Citation Subset: IM |
Copyright Information:
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Copyright 2010 European Association for the Study of the Liver. Published by Elsevier B.V. All rights reserved. |
Affiliation:
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Key Laboratory of Nutrition and Metabolism, Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Graduate School of the Chinese Academy of Sciences, Shanghai 200031, China. |
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cholesterol / metabolism Dietary Fats / adverse effects, pharmacology* Disease Models, Animal Dose-Response Relationship, Drug Fatty Liver / chemically induced, metabolism, prevention & control* Interleukins / pharmacology*, therapeutic use* Lipid Metabolism / drug effects Lipogenesis / drug effects* Liver / drug effects, metabolism* Male Mice Mice, Inbred C57BL Phosphorylation / drug effects STAT3 Transcription Factor / metabolism Triglycerides / metabolism |
| Chemical | |
Reg. No./Substance:
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0/Dietary Fats; 0/Interleukins; 0/STAT3 Transcription Factor; 0/Stat3 protein, mouse; 0/Triglycerides; 0/interleukin-22; 57-88-5/Cholesterol |
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