Document Detail


Role of fatty acids in the pathogenesis of obesity and fatty liver: impact of bariatric surgery.
MedLine Citation:
PMID:  18956297     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Elizabeth C Verna; Paul D Berk
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review     Date:  2008-10-27
Journal Detail:
Title:  Seminars in liver disease     Volume:  28     ISSN:  0272-8087     ISO Abbreviation:  Semin. Liver Dis.     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-10-28     Completed Date:  2009-01-22     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8110297     Medline TA:  Semin Liver Dis     Country:  United States    
Other Details:
Languages:  eng     Pagination:  407-26     Citation Subset:  IM    
Affiliation:
Department of Medicine, Division of Digestive and Liver Diseases, Columbia University Medical Center, New York, New York 10032, USA.
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MeSH Terms
Descriptor/Qualifier:
Abdominal Fat / 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:
DK-52401/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
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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