Document Detail


Quantitative lipid metabolomic changes in alcoholic micropigs with fatty liver disease.
MedLine Citation:
PMID:  19170661     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND: Chronic ethanol consumption coupled with folate deficiency leads to rapid liver fat accumulation and progression to alcoholic steatohepatitis (ASH). However, the specific effects of alcohol on key liver lipid metabolic pathways involved in fat accumulation are unknown. It is unclear whether lipid synthesis, lipid export, or a combination of both is contributing to hepatic steatosis in ASH. METHODS: In this study we estimated the flux of fatty acids (FA) through the stearoyl-CoA desaturase (SCD), phosphatidylethanolamine-N-methyltransferase (PEMT), and FA elongation pathways in relation to liver triacylglycerol (TG) content in Yucatan micropigs fed a 40% ethanol folate-deficient diet with or without supplementation with S-adenosyl methionine (SAM) compared with controls. Flux through the SCD and PEMT pathways was used to assess the contribution of lipid synthesis and lipid export respectively on the accumulation of fat in the liver. Liver FA composition within TG, cholesterol ester (CE), phosphatidylethanolamine, and phosphatidylcholine classes was quantified by gas chromatography. RESULTS: Alcoholic pigs had increased liver TG content relative to controls, accompanied by increased flux through the SCD pathway as indicated by increases in the ratios of 16:1n7 to 16:0 and 18:1n9 to 18:0. Conversely, flux through the elongation and PEMT pathways was suppressed by alcohol, as indicated by multiple metabolite ratios. SAM supplementation attenuated the TG accumulation associated with alcohol. CONCLUSIONS: These data provide an in vivo examination of liver lipid metabolic pathways confirming that both increased de novo lipogenesis (e.g., lipid synthesis) and altered phospholipid metabolism (e.g., lipid export) contribute to the excessive accumulation of lipids in liver affected by ASH.
Authors:
Angela M Zivkovic; J Bruce German; Farah Esfandiari; Charles H Halsted
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't     Date:  2009-01-21
Journal Detail:
Title:  Alcoholism, clinical and experimental research     Volume:  33     ISSN:  1530-0277     ISO Abbreviation:  Alcohol. Clin. Exp. Res.     Publication Date:  2009 Apr 
Date Detail:
Created Date:  2009-04-01     Completed Date:  2009-07-07     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  7707242     Medline TA:  Alcohol Clin Exp Res     Country:  England    
Other Details:
Languages:  eng     Pagination:  751-8     Citation Subset:  IM    
Affiliation:
Department of Entomology, University of California Davis, Davis, California 95616, USA. amzivkovic@ucdavis.edu
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Descriptor/Qualifier:
Alcoholism / metabolism*
Animals
Cholesterol Esters / metabolism
Disease Models, Animal
Ethanol / metabolism
Fatty Acids / metabolism
Fatty Liver / metabolism*
Fatty Liver, Alcoholic / metabolism*
Lipid Metabolism / physiology*
Male
Metabolomics*
Phosphatidylcholines / metabolism
Phosphatidylethanolamine N-Methyltransferase / metabolism
Phosphatidylethanolamines / metabolism
Stearoyl-CoA Desaturase / metabolism
Swine
Swine, Miniature
Triglycerides / metabolism
Grant Support
ID/Acronym/Agency:
AA RO-114545/AA/NIAAA NIH HHS; P01 ES11269/ES/NIEHS NIH HHS; P42 ES04699/ES/NIEHS NIH HHS
Chemical
Reg. No./Substance:
0/Cholesterol Esters; 0/Fatty Acids; 0/Phosphatidylcholines; 0/Phosphatidylethanolamines; 0/Triglycerides; 39382-08-6/phosphatidylethanolamine; 64-17-5/Ethanol; EC 1.14.19.1/Stearoyl-CoA Desaturase; EC 2.1.1.17/Phosphatidylethanolamine N-Methyltransferase

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


Previous Document:  Effect of proton pump inhibition on the gastric volume: assessed by magnetic resonance imaging.
Next Document:  Altered impulse control in alcohol dependence: neural measures of stop signal performance.