Document Detail


Exercise training restores uncoupling protein-3 content in limb muscles of patients with chronic obstructive pulmonary disease.
MedLine Citation:
PMID:  16352674     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Oxidative capacity and uncoupling protein-3 (UCP3) content are reduced in limb muscles of patients with chronic obstructive pulmonary disease (COPD). It has been hypothesized that the physiological role of UCP3 is to protect mitochondria against lipotoxicity in cases where fatty acid influx exceeds the capacity to oxidize them. Exercise training improves oxidative capacity and reduces UCP3 protein content in healthy subjects, but the response of UCP3 to training in COPD is unknown. We studied the effect of exercise training on UCP3 content in limb muscles of COPD patients. For this, seven healthy age-matched subjects and thirteen patients with COPD were studied. All patients were admitted to an 8-wk exercise training intervention. Exercise capacity was assessed by means of an incremental cycle ergometry test. Biopsies were taken from the vastus lateralis in which UCP3 and lipid peroxidation levels were determined by Western blotting. Citrate synthase and 3-hydroxyacyl-CoA dehydrogenase (HAD; an enzyme involved in fatty acid oxidation) were measured as indexes of muscle oxidative capacity. UCP3 in COPD was approximately 50% lower compared with healthy age-matched controls. In COPD, training induced upregulation of UCP3 [from 67.7 (SD 41.8) to 113.8 (SD 104.2) arbitrary units (AU), P = 0.062], especially in the patients who showed no increase in HAD activity [from 80.9 (SD 52.6) to 167.9 (SD 109.1) AU, P = 0.028], whereas lipid peroxidation levels remained unaltered. We conclude that exercise-training can restore muscle UCP3 protein level in COPD, and the nature of this response complies with the hypothesis that UCP3 may protect against lipotoxicity.
Authors:
Harry R Gosker; Patrick Schrauwen; Roelinka Broekhuizen; Matthijs K C Hesselink; Esther Moonen-Kornips; Kimberly A Ward; Frits M E Franssen; Emiel F M Wouters; Annemie M W J Schols
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Publication Detail:
Type:  Clinical Trial; Comparative Study; Journal Article; Research Support, Non-U.S. Gov't     Date:  2005-12-13
Journal Detail:
Title:  American journal of physiology. Endocrinology and metabolism     Volume:  290     ISSN:  0193-1849     ISO Abbreviation:  Am. J. Physiol. Endocrinol. Metab.     Publication Date:  2006 May 
Date Detail:
Created Date:  2006-04-10     Completed Date:  2006-06-19     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  100901226     Medline TA:  Am J Physiol Endocrinol Metab     Country:  United States    
Other Details:
Languages:  eng     Pagination:  E976-81     Citation Subset:  IM    
Affiliation:
Dept. of Respiratory Medicine, Maastricht Univ., Nutrition and Toxicology Research Institute Maastricht, P.O. Box 616, 6200 MD Maastricht, The Netherlands. H.Gosker@pul.unimaas.nl
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MeSH Terms
Descriptor/Qualifier:
3-Hydroxyacyl CoA Dehydrogenases / metabolism
Aged
Aldehydes / analysis,  metabolism
Carrier Proteins / metabolism*
Citrate (si)-Synthase / metabolism
Exercise / physiology*
Exercise Test
Female
Glycogen Phosphorylase / metabolism
Humans
Ion Channels
Male
Middle Aged
Mitochondrial Proteins
Myosin Heavy Chains / analysis
Phosphofructokinase-1 / metabolism
Protein Isoforms / analysis
Pulmonary Disease, Chronic Obstructive / metabolism*,  physiopathology,  therapy
Quadriceps Muscle / chemistry,  enzymology,  metabolism*
Up-Regulation
Chemical
Reg. No./Substance:
0/Aldehydes; 0/Carrier Proteins; 0/Ion Channels; 0/Mitochondrial Proteins; 0/Myosin Heavy Chains; 0/Protein Isoforms; 0/mitochondrial uncoupling protein 3; 29343-52-0/4-hydroxy-2-nonenal; EC 1.1.1.35/3-Hydroxyacyl CoA Dehydrogenases; EC 2.3.3.1/Citrate (si)-Synthase; EC 2.4.1.-/Glycogen Phosphorylase; EC 2.7.1.11/Phosphofructokinase-1; EC 2.7.1.56/1-phosphofructokinase

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