| Role of fatty acids in the pathogenesis of obesity and fatty liver: impact of bariatric surgery. | |
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MedLine Citation:
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PMID: 18956297 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Nonalcoholic fatty liver disease (NAFLD) spans a spectrum from simple steatosis to nonalcoholic steatohepatitis (NASH) to cirrhosis. Simple steatosis is the substrate upon which the more serious entities in the spectrum develop; it is the first "hit" in the multistep pathogenesis of NASH, which is considered the hepatic manifestation of the metabolic syndrome. Demonstration of the existence of regulatable fatty acid transport mechanisms has contributed to clarifying the role of fatty acid disposition in obesity, the various components of NAFLD, and the metabolic syndrome. Hepatic steatosis is closely linked to obesity. This linkage is based on the fact that obesity results in marked enlargement of the intraabdominal visceral fat depots. The eventual development of insulin resistance leads to continuous lipolysis within these depots, releasing fatty acids into the portal circulation, where they are rapidly translocated to the liver and reassembled into triglycerides. Reactive oxygen species, generated in the liver from oxidation of fatty acids, are precipitating factors in the cascade of events leading from simple steatosis to NASH. Dysregulation of fatty acid disposition, with ectopic lipid accumulation in other tissues, is a major contributing factor to other components of the metabolic syndrome. Bariatric surgery is an effective treatment for severe obesity, but its role in the management of the various forms of fatty liver disease is unclear. Our review of the literature that includes both initial and follow-up liver biopsies suggests that most obese patients with simple steatosis and NASH who undergo bariatric surgery will achieve improvement in hepatic histology, but that occasional patients, especially those who lose weight very rapidly, may show worsening of either fibrosis or steatohepatitis. |
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Authors:
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Elizabeth C Verna; Paul D Berk |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review Date: 2008-10-27 |
Journal Detail:
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Title: Seminars in liver disease Volume: 28 ISSN: 0272-8087 ISO Abbreviation: Semin. Liver Dis. Publication Date: 2008 Nov |
Date Detail:
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Created Date: 2008-10-28 Completed Date: 2009-01-22 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8110297 Medline TA: Semin Liver Dis Country: United States |
Other Details:
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Languages: eng Pagination: 407-26 Citation Subset: IM |
Affiliation:
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Department of Medicine, Division of Digestive and Liver Diseases, Columbia University Medical Center, New York, New York 10032, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Abdominal Fat
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metabolism Adipocytes / pathology Animals Bariatric Surgery* Comorbidity Diabetes Mellitus, Type 2 / epidemiology, metabolism Fatty Acids / metabolism* Fatty Liver / epidemiology, etiology*, metabolism, physiopathology Gastrointestinal Hormones / physiology Humans Insulin Resistance / physiology Leptin / metabolism Lipolysis Liver / metabolism Metabolic Syndrome X / physiopathology Obesity / epidemiology, etiology*, metabolism Obesity, Morbid / metabolism, surgery |
| Grant Support | |
ID/Acronym/Agency:
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DK-52401/DK/NIDDK NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Fatty Acids; 0/Gastrointestinal Hormones; 0/Leptin |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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