Document Detail


Effects of long-term ethanol administration in a rat total enteral nutrition model of alcoholic liver disease.
MedLine Citation:
PMID:  21051528     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Male Sprague-Dawley rats were chronically fed a high-unsaturated-fat diet for 130 days by using total enteral nutrition (TEN), or the same diet in which ethanol (EtOH) isocalorically replaced carbohydrate calories. Additional groups were supplemented with the antioxidant N-acetylcysteine (NAC) at 1.7 g·kg(-1)·day(-1). Relative to an ad libitum chow-fed group, the high-fat-fed controls had three- to fourfold greater expression of fatty acid transporter CD36 mRNA and developed mild steatosis but little other hepatic pathology. NAC treatment resulted in increased somatic growth relative to controls (4.0 ± 0.1 vs. 3.1 ± 0.1 g/day) and increased hepatic steatosis score (3.5 ± 0.6 vs. 2.7 ± 1.2), associated with suppression of the triglyceride hydrolyzing protein adiponutrin, but produced no elevation in serum alanine aminotransferase (ALT). Chronic EtOH treatment increased expression of fatty acid transport protein FATP-2 mRNA twofold, resulting in marked hepatic steatosis, oxidative stress, and a twofold elevation in serum ALT. However, no changes in tumor necrosis factor-α or transforming growth factor-β expression were observed. Fibrosis, as measured by Masson's trichrome and picrosirius red staining, and a twofold increase in expression of type I and type III collagen mRNA, was only observed after EtOH treatment. Long-term EtOH treatment increased hepatocyte proliferation but did not modify the hepatic mRNAs for hedgehog pathway ligands or target genes or genes regulating epithelial-to-mesenchymal transition. Although the effects of NAC on EtOH-induced fibrosis could not be fully evaluated, NAC had additive effects on hepatocyte proliferation and prevented EtOH-induced oxidative stress and necrosis, despite a failure to reverse hepatic steatosis.
Authors:
Martin J J Ronis; Leah Hennings; Ben Stewart; Alexei G Basnakian; Eugene O Apostolov; Emanuele Albano; Thomas M Badger; Dennis R Petersen
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2010-11-04
Journal Detail:
Title:  American journal of physiology. Gastrointestinal and liver physiology     Volume:  300     ISSN:  1522-1547     ISO Abbreviation:  Am. J. Physiol. Gastrointest. Liver Physiol.     Publication Date:  2011 Jan 
Date Detail:
Created Date:  2010-12-30     Completed Date:  2011-02-01     Revised Date:  2012-01-02    
Medline Journal Info:
Nlm Unique ID:  100901227     Medline TA:  Am J Physiol Gastrointest Liver Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  G109-19     Citation Subset:  IM    
Affiliation:
epartment of Pharmacology and Toxicology, 2University of Arkansas for Medical Sciences and Arkansas Children's Nutrition Center, Little Rock, Arkansas 72202, USA. RonisMartinJ@uams.edu
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MeSH Terms
Descriptor/Qualifier:
Acetylcysteine / pharmacology,  therapeutic use
Animals
Cell Proliferation / drug effects
Cytochrome P-450 Enzyme System / metabolism
Dietary Fats / administration & dosage
Enteral Nutrition
Ethanol / pharmacology,  toxicity*
Fatty Liver / etiology*,  pathology
Hedgehog Proteins / metabolism
Lipid Metabolism / drug effects
Liver / drug effects*,  pathology
Liver Diseases, Alcoholic / metabolism*,  pathology
Liver Regeneration / drug effects
Male
Oxidative Stress / drug effects
Rats
Grant Support
ID/Acronym/Agency:
R01 AA009300/AA/NIAAA NIH HHS; R01 AA08645/AA/NIAAA NIH HHS; R01 AA18282/AA/NIAAA NIH HHS; R01 DK078908/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Dietary Fats; 0/Hedgehog Proteins; 616-91-1/Acetylcysteine; 64-17-5/Ethanol; 9035-51-2/Cytochrome P-450 Enzyme System; EC 1.-/Cyp2f2 protein, rat

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


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