| Activation of peroxisome proliferator-activated receptor-γ by rosiglitazone improves lipid homeostasis at the adipose tissue-liver axis in ethanol-fed mice. | |
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MedLine Citation:
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PMID: 22173916 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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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:
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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:
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Created Date: 2012-02-22 Completed Date: 2012-04-16 Revised Date: 2013-04-15 |
Medline Journal Info:
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Nlm Unique ID: 100901227 Medline TA: Am J Physiol Gastrointest Liver Physiol Country: United States |
Other Details:
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Languages: eng Pagination: G548-57 Citation Subset: IM |
Affiliation:
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Department of Nutrition, University of North Carolina at Greensboro, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acyl-CoA Oxidase
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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:
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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:
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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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