| Murine intramyocellular lipids quantified by NMR act as metabolic biomarkers in burn trauma. | |
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MedLine Citation:
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PMID: 18506378 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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It has been suggested that intramyocellular lipids (IMCLs) may serve as biomarkers of insulin resistance and mitochondrial dysfunction. Using a hind-limb mouse model of burn trauma, we tested the hypothesis that severe localized burn trauma involving 5% of the total body surface area causes a local increase in IMCLs in the leg skeletal muscle. We quantified IMCLs from ex vivo intact tissue specimens using High-Resolution Magic Angle Spinning (HRMAS) 1H NMR and characterized the accompanying gene expression patterns in burned versus control skeletal muscle specimens. We also quantified plasma-free fatty acids (FFAs) in burn versus control mice. Our results from HRMAS 1H NMR measurements indicated that IMCL levels were significantly increased in mice exposed to burn trauma. Furthermore, plasma FFA levels were also significantly increased, and gene expression of Glut4, insulin receptor substrate 1 (IRS1), glycolytic genes, and PGC-1beta was downregulated in these mice. Backward stepwise multiple linear regression analysis demonstrated that IMCL levels correlated significantly with FFA levels, which were a significant predictor of IRS1 and PGC-1beta gene expression. We conclude from these findings that IMCLs can serve as metabolic biomarkers in burn trauma and that FFAs and IMCLs may signal altered metabolic gene expression. This signaling may result in the observed burn-induced insulin resistance and skeletal muscle mitochondrial dysfunction. We believe that IMCLs may therefore be useful biomarkers in predicting the therapeutic effectiveness of hypolipidemic agents for patients with severe burns. |
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Authors:
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A Aria Tzika; Loukas G Astrakas; Haihui Cao; Dionyssios Mintzopoulos; Qunhao Zhang; Katie Padfield; Hongue Yu; Michael N Mindrinos; Laurence G Rahme; Ronald G Tompkins |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: International journal of molecular medicine Volume: 21 ISSN: 1107-3756 ISO Abbreviation: Int. J. Mol. Med. Publication Date: 2008 Jun |
Date Detail:
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Created Date: 2008-05-28 Completed Date: 2008-07-23 Revised Date: 2008-11-21 |
Medline Journal Info:
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Nlm Unique ID: 9810955 Medline TA: Int J Mol Med Country: Greece |
Other Details:
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Languages: eng Pagination: 825-32 Citation Subset: IM |
Affiliation:
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NMR Surgical Laboratory, Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. atzika@partners.org |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adaptor Proteins, Signal Transducing
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genetics,
metabolism Animals Biological Markers / analysis*, blood Body Surface Area Burns / genetics, metabolism*, pathology Fatty Acids, Nonesterified / analysis, blood, metabolism Gene Expression Profiling Glucose Transporter Type 4 / genetics, metabolism Glycolysis Hindlimb / metabolism, pathology Humans Insulin Receptor Substrate Proteins Insulin Resistance Lipid Metabolism Lipids / analysis* Magnetic Resonance Imaging Magnetic Resonance Spectroscopy Mice Mitochondria / metabolism Models, Biological Muscle Fibers, Skeletal / metabolism, pathology Muscle, Skeletal / metabolism*, pathology, ultrastructure Oligonucleotide Array Sequence Analysis Regression Analysis Trans-Activators / genetics, metabolism |
| Grant Support | |
ID/Acronym/Agency:
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P50GM021700/GM/NIGMS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Adaptor Proteins, Signal Transducing; 0/Biological Markers; 0/Fatty Acids, Nonesterified; 0/Glucose Transporter Type 4; 0/IRS1 protein, human; 0/Insulin Receptor Substrate Proteins; 0/Irs1 protein, mouse; 0/Lipids; 0/Ppargc1a protein, mouse; 0/Trans-Activators |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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