Document Detail


Nontriglyceride hepatic lipotoxicity: the new paradigm for the pathogenesis of NASH.
MedLine Citation:
PMID:  20425484     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Lipid droplet accumulation and oxidant stress, once thought to play essential roles in the pathogenesis of nonalcoholic steatohepatitis (NASH), may actually represent parallel epiphenomena. Emerging data now point to nontriglyceride lipotoxicity and complex mechanisms of hepatocyte injury and apoptosis as the major contributors to the disease phenotype currently recognized as NASH. Although specific mediators of hepatic lipotoxicity have not been identified with certainty, abundant evidence from animal studies and recent data in humans indicate that free fatty acids in the liver can serve as substrates for formation of nontriglyceride lipotoxic metabolites that cause liver injury. The accumulation of triglyceride in droplets may actually be protective, and thus therapeutic efforts directed at fat accumulation as a sole endpoint may be misguided. This review examines the new evidence supporting the role of nontriglyceride fatty acid metabolites in causing NASH and how adipose and muscle insulin resistance contribute to hepatic lipotoxicity.
Authors:
Brent A Neuschwander-Tetri
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Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Current gastroenterology reports     Volume:  12     ISSN:  1534-312X     ISO Abbreviation:  Curr Gastroenterol Rep     Publication Date:  2010 Feb 
Date Detail:
Created Date:  2010-04-28     Completed Date:  2010-09-16     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  100888896     Medline TA:  Curr Gastroenterol Rep     Country:  United States    
Other Details:
Languages:  eng     Pagination:  49-56     Citation Subset:  IM    
Affiliation:
Division of Gastroenterology and Hepatology, Saint Louis University School of Medicine, St. Louis, MO 63110, USA. tetriba@slu.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Biological Markers / metabolism*
Dicarboxylic Acids / metabolism
Fatty Acids / metabolism
Fatty Liver / etiology*
Humans
Lipogenesis / physiology
Lipolysis
Lysosomes / metabolism*
Triglycerides / biosynthesis*
Chemical
Reg. No./Substance:
0/Biological Markers; 0/Dicarboxylic Acids; 0/Fatty Acids; 0/Triglycerides

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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