Document Detail


Evolution of inflammation in nonalcoholic fatty liver disease: the multiple parallel hits hypothesis.
MedLine Citation:
PMID:  21038418     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Whereas in most cases a fatty liver remains free of inflammation, 10%-20% of patients who have fatty liver develop inflammation and fibrosis (nonalcoholic steatohepatitis [NASH]). Inflammation may precede steatosis in certain instances. Therefore, NASH could reflect a disease where inflammation is followed by steatosis. In contrast, NASH subsequent to simple steatosis may be the consequence of a failure of antilipotoxic protection. In both situations, many parallel hits derived from the gut and/or the adipose tissue may promote liver inflammation. Endoplasmic reticulum stress and related signaling networks, (adipo)cytokines, and innate immunity are emerging as central pathways that regulate key features of NASH.
Authors:
Herbert Tilg; Alexander R Moschen
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Hepatology (Baltimore, Md.)     Volume:  52     ISSN:  1527-3350     ISO Abbreviation:  Hepatology     Publication Date:  2010 Nov 
Date Detail:
Created Date:  2010-11-01     Completed Date:  2010-11-24     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8302946     Medline TA:  Hepatology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1836-46     Citation Subset:  IM    
Affiliation:
Christian Doppler Research Laboratory for Gut Inflammation, Medical University Innsbruck, Innsbruck, Austria. herbert.tilg@i-med.ac.at
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MeSH Terms
Descriptor/Qualifier:
Animals
Diet
Disease Progression
Fatty Liver / chemically induced,  etiology,  physiopathology*
Humans
Inflammation / complications,  physiopathology*
Interleukin-5 / adverse effects,  genetics
Leptin / adverse effects,  physiology
Metabolic Diseases / complications,  etiology,  physiopathology
Models, Biological
Obesity / complications
Trans Fatty Acids / adverse effects
Tumor Necrosis Factor-alpha / adverse effects,  genetics
Chemical
Reg. No./Substance:
0/Interleukin-5; 0/Leptin; 0/Trans Fatty Acids; 0/Tumor Necrosis Factor-alpha

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


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