Document Detail


Activation of peroxisome proliferator-activated receptor-γ by rosiglitazone improves lipid homeostasis at the adipose tissue-liver axis in ethanol-fed mice.
MedLine Citation:
PMID:  22173916     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The development of alcohol-induced fatty liver is associated with a reduction of white adipose tissue (WAT). Peroxisome proliferator-activated receptor (PPAR)-γ prominently distributes in the WAT and plays a crucial role in maintaining adiposity. The present study investigated the effects of PPAR-γ activation by rosiglitazone on lipid homeostasis at the adipose tissue-liver axis. Adult C57BL/6 male mice were pair fed liquid diet containing ethanol or isocaloric maltose dextrin for 8 wk with or without rosiglitazone supplementation to ethanol-fed mice for the last 3 wk. Ethanol exposure downregulated adipose PPAR-γ gene and reduced the WAT mass in association with induction of inflammation, which was attenuated by rosiglitazone. Ethanol exposure stimulated lipolysis but reduced fatty acid uptake capacity in association with dysregulation of lipid metabolism genes. Rosiglitazone normalized adipose gene expression and corrected ethanol-induced lipid dyshomeostasis. Ethanol exposure induced steatosis and upregulated inflammatory genes in the liver, which were attenuated by rosiglitazone. Hepatic peroxisomal fatty acid β-oxidation was suppressed by ethanol in associated with inhibition of acyl-coenzyme A oxidase 1. Rosiglitazone elevated plasma adiponectin level and normalized peroxisomal fatty acid β-oxidation rate. However, rosiglitazone did not affect ethanol-reduced very low-density lipoprotein secretion from the liver. These results demonstrated that activation of PPAR-γ by rosiglitazone reverses ethanol-induced adipose dysfunction and lipid dyshomeostasis at the WAT-liver axis, thereby abrogating alcoholic fatty liver.
Authors:
Xiuhua Sun; Yunan Tang; Xiaobing Tan; Qiong Li; Wei Zhong; Xinguo Sun; Wei Jia; Craig J McClain; Zhanxiang Zhou
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2011-12-15
Journal Detail:
Title:  American journal of physiology. Gastrointestinal and liver physiology     Volume:  302     ISSN:  1522-1547     ISO Abbreviation:  Am. J. Physiol. Gastrointest. Liver Physiol.     Publication Date:  2012 Mar 
Date Detail:
Created Date:  2012-02-22     Completed Date:  2012-04-16     Revised Date:  2013-06-27    
Medline Journal Info:
Nlm Unique ID:  100901227     Medline TA:  Am J Physiol Gastrointest Liver Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  G548-57     Citation Subset:  IM    
Affiliation:
Department of Nutrition, University of North Carolina at Greensboro, USA.
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MeSH Terms
Descriptor/Qualifier:
Acyl-CoA Oxidase / metabolism
Adiponectin / blood
Adipose Tissue, White / drug effects,  metabolism*,  physiopathology
Animals
Ethanol / pharmacology*
Fatty Liver, Alcoholic / metabolism
Lipid Metabolism / drug effects*
Lipoproteins, VLDL / metabolism
Liver / drug effects*,  metabolism
Male
Mice
Mice, Inbred C57BL
PPAR gamma / drug effects,  physiology*
Thiazolidinediones / pharmacology*
Grant Support
ID/Acronym/Agency:
P01AA017103/AA/NIAAA NIH HHS; P30AA019360/AA/NIAAA NIH HHS; R01 AA018016/AA/NIAAA NIH HHS; R01 AA018869/AA/NIAAA NIH HHS; R01AA015970/AA/NIAAA NIH HHS; R01AA018844/AA/NIAAA NIH HHS; R01AA018869/AA/NIAAA NIH HHS; R01AA020212/AA/NIAAA NIH HHS; R37AA010762/AA/NIAAA NIH HHS; RC2AA019385/AA/NIAAA NIH HHS
Chemical
Reg. No./Substance:
0/Adiponectin; 0/Lipoproteins, VLDL; 0/PPAR gamma; 0/Thiazolidinediones; 122320-73-4/rosiglitazone; 64-17-5/Ethanol; EC 1.3.3.6/Acyl-CoA Oxidase
Comments/Corrections

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


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