| Effects of farnesoid X receptor on the expression of the fatty acid synthetase and hepatic lipase. | |
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MedLine Citation:
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PMID: 20373033 Owner: NLM Status: In-Process |
Abstract/OtherAbstract:
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The farnesoid X receptor (FXR) is a nuclear receptor that regulates gene expression in response to bile acids (BAs). FXR plays an important role in the homeostasis of bile acid, cholesterol, lipoprotein and triglyceride. In this report, we identified fatty acid synthase (FAS) and hepatic lipase (HL) genes as novel target genes of FXR. Human hepatoma HepG2 cells were treated with chenodeoxycholic acid, the natural FXR ligand, and the messenger RNA and protein levels of FAS and HL were determined by RT-PCR and Western blot analysis, respectively. Chenodeoxycholic acid (CDCA) down-regulated the expression of FAS and HL genes in a dose and time-dependent manner in human hepatoma HepG2 cells. In addition, treatment of mice with CDCA significantly decreased the expression of FAS and HL in mouse liver and the activity of HL. These results demonstrated that FAS and HL might be FXR-regulated genes in liver cells. In view of the role of FAS and HL in lipogenesis and plasma lipoprotein metabolism, our results further support the central role of FXR in the homeostasis of fatty acid and lipid. |
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Authors:
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Li-Li Shen; Hong Liu; Jiahe Peng; Lin Gan; Li Lu; Qian Zhang; Liangpeng Li; Fengtian He; Yu Jiang |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-04-07 |
Journal Detail:
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Title: Molecular biology reports Volume: 38 ISSN: 1573-4978 ISO Abbreviation: Mol. Biol. Rep. Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2010-12-02 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0403234 Medline TA: Mol Biol Rep Country: Netherlands |
Other Details:
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Languages: eng Pagination: 553-9 Citation Subset: IM |
Affiliation:
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Department of Biochemistry and Molecular Biology, The Third Military Medical University, Chongqing, 400038, China. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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