| Hepatic steatosis and peroxisomal fatty acid beta-oxidation. | |
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MedLine Citation:
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PMID: 22978396 Owner: NLM Status: Publisher |
Abstract/OtherAbstract:
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Three subhepatocellular compartments concur for fatty acids degradation including β-oxidation in endoplasmic reticulum and β-oxidation in both mitochondria and peroxisomes. Deficits affecting the peroxisomal physiology may be associated with multiple metabolic disturbances. Nowadays, a growing body of evidence underlines the key role of peroxisomal β-oxidation in the sensing of lipid metabolism through the production/degradation of some essential metabolites. Lessons from several mice models strengthen the link between fatty acid β-oxidation in peroxisomes and the nuclear hormone receptor Peroxisome Proliferator-Activated Receptor (PPAR)-α with an additional level of coregualtor complexity, which couples regulation of body energetic balance and hepatic caloric flux to functional peroxisome status. Here, we review key determinants of disrupted peroxisomal β-oxidation pathway, which in liver promotes hepatic steatosis and hepatocarcinogenesis. |
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Authors:
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Mustapha Cherkaoui; Sailesh Surapureddi; Hammam El Hajj; Joseph Vamecq; Pierre Andreoletti |
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Publication Detail:
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Type: JOURNAL ARTICLE Date: 2012-9-04 |
Journal Detail:
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Title: Current drug metabolism Volume: - ISSN: 1875-5453 ISO Abbreviation: Curr. Drug Metab. Publication Date: 2012 Sep |
Date Detail:
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Created Date: 2012-9-17 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100960533 Medline TA: Curr Drug Metab Country: - |
Other Details:
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Languages: ENG Pagination: - Citation Subset: - |
Affiliation:
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Bio-PeroxIL, EA 7270, Université de Bourgogne, 6 Bd Gabriel Dijon F-21000, France. malki@u-bourgogne.fr. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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