| New insights from rodent models of Fatty liver disease. | |
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MedLine Citation:
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PMID: 21126212 Owner: NLM Status: In-Data-Review |
Abstract/OtherAbstract:
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Abstract Rodent models of fatty liver disease are essential research tools that provide a window into disease pathogenesis and a testing ground for prevention and treatment. Models come in many varieties involving dietary and genetic manipulations, and sometimes both. High-energy diets that induce obesity do not uniformly cause fatty liver disease; this has prompted close scrutiny of specific macronutrients and nutrient combinations to determine which have the greatest potential for hepatotoxicity. At the same time, diets that do not cause obesity or the metabolic syndrome but do cause severe steatohepatitis have been exploited to study factors important to progressive liver injury, including cell death, oxidative stress, and immune activation. Rodents with a genetic predisposition to overeating offer yet another model in which to explore the evolution of fatty liver disease. In some animals that overeat, steatohepatitis can develop even without resorting to a high-energy diet. Importantly, these models and others have been used to document that aerobic exercise can prevent or reduce fatty liver disease. This review focuses primarily on lessons learned about steatohepatitis from manipulations of diet and eating behavior. Numerous additional insights about hepatic lipid metabolism, which have been gained from genetically engineered mice, are also mentioned. Antioxid. Redox Signal. 15, 535-550. |
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Authors:
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Jacquelyn J Maher |
Publication Detail:
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Type: Journal Article Date: 2011-04-26 |
Journal Detail:
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Title: Antioxidants & redox signaling Volume: 15 ISSN: 1557-7716 ISO Abbreviation: Antioxid. Redox Signal. Publication Date: 2011 Jul |
Date Detail:
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Created Date: 2011-06-21 Completed Date: - Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100888899 Medline TA: Antioxid Redox Signal Country: United States |
Other Details:
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Languages: eng Pagination: 535-50 Citation Subset: IM |
Affiliation:
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Liver Center and Department of Medicine, University of California , San Francisco San Francisco, California. |
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From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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