| Acute moderate elevation of TNF-alpha does not affect systemic and skeletal muscle protein turnover in healthy humans. | |
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MedLine Citation:
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PMID: 18854397 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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CONTEXT: Skeletal muscle wasting has been associated with elevations in circulating inflammatory cytokines, in particular TNF-alpha. OBJECTIVE: In this study, we investigated whether TNF-alpha affects human systemic and skeletal muscle protein turnover via a 4-h recombinant human (rh) TNF-alpha infusion. We hypothesize that TNF-alpha increases human muscle protein breakdown and/or inhibits synthesis. SUBJECTS AND METHODS: Using a randomized, controlled, crossover design, postabsorptive healthy young males (n = 8) were studied 2 h under basal conditions followed by a 4-h infusion of either rhTNF-alpha (700 ng . m(-2) . h(-1)) or 20% human albumin (control), which was the vehicle of rhTNF-alpha. Systemic and skeletal muscle protein turnover was estimated by a combination of tracer dilution methodology (primed continuous infusion of l-[ring-(2)H(5)]phenylalanine and l-[(15)N-leucine], with prime of l-[ring-(2)H(4)]tyrosine) and femoral arterial-venous differences over the leg and muscle biopsies. RESULTS: Plasma TNF-alpha concentration rapidly increased from basal levels of approximately 0.7 to 17 pg . ml(-1) with rhTNF-alpha infusion. Whole body protein synthesis, breakdown, and net degradation were similar after the basal and infusion period of the control and rhTNF-alpha trials. Skeletal muscle, musculus vastus lateralis, protein fractional synthetic rate was not different over 4 h of control or rhTNF-alpha (rate of incorporation of (15)N-leucine). Muscle protein turnover determined with the phenylalanine three-compartment model showed similar muscle synthesis, breakdown, and net muscle degradation after 2-h basal and after 4-h control or rhTNF-alpha infusion. CONCLUSION: This study is the first to show in humans that TNF-alpha does not affect systemic and skeletal muscle protein turnover, when acutely elevated for 4 h to moderate levels not causing adverse effects. |
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Authors:
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Anne Marie Petersen; Peter Plomgaard; Christian P Fischer; Tobias Ibfelt; Bente Klarlund Pedersen; Gerrit van Hall |
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Publication Detail:
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Type: Journal Article; Randomized Controlled Trial; Research Support, Non-U.S. Gov't Date: 2008-10-14 |
Journal Detail:
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Title: The Journal of clinical endocrinology and metabolism Volume: 94 ISSN: 0021-972X ISO Abbreviation: J. Clin. Endocrinol. Metab. Publication Date: 2009 Jan |
Date Detail:
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Created Date: 2009-01-07 Completed Date: 2009-02-12 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 0375362 Medline TA: J Clin Endocrinol Metab Country: United States |
Other Details:
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Languages: eng Pagination: 294-9 Citation Subset: AIM; IM |
Affiliation:
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The Centre of Inflammation and Metabolism, Department of Infectious Diseases, Rigshospitalet, Faculty of Health Sciences, University of Copenhagen, DK2100 Copenhagen, Denmark. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adult Cross-Over Studies Humans Interleukin-6 / pharmacology Male Muscle Proteins / metabolism* Muscle, Skeletal / metabolism* Recombinant Proteins / pharmacology Tumor Necrosis Factor-alpha / blood, pharmacology* |
| Chemical | |
Reg. No./Substance:
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0/Interleukin-6; 0/Muscle Proteins; 0/Recombinant Proteins; 0/Tumor Necrosis Factor-alpha |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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