PT  - JOURNAL ARTICLE
AU  - A. H. Remels
AU  - P. Schrauwen
AU  - R. Broekhuizen
AU  - J. Willems
AU  - S. Kersten
AU  - H. R. Gosker
AU  - A. M. Schols
TI  - Peroxisome proliferator-activated receptor expression is reduced in skeletal muscle in COPD
AID  - 10.1183/09031936.00144106
DP  - 2007 Aug 01
TA  - European Respiratory Journal
PG  - 245--252
VI  - 30
IP  - 2
4099  - http://erj.ersjournals.com/content/30/2/245.short
4100  - http://erj.ersjournals.com/content/30/2/245.full
SO  - Eur Respir J2007 Aug 01; 30
AB  - Chronic obstructive pulmonary disease (COPD) is a multiorgan systemic disease. The systemic features are skeletal muscle weakness and cachexia, the latter being associated with systemic inflammation. The exact mechanisms underlying skeletal muscle dysfunction in COPD remain obscure. Recent evidence suggests involvement of the peroxisome proliferator-activated receptors (PPARs) and PPAR-γ coactivator (PGC)-1α in regulation of skeletal muscle morphology and metabolism, and mitochondrial transcription factor A (TFAM) has been implicated in the process of mitochondrial biogenesis. The aim of the present exploratory study was, therefore, to compare these factors in the skeletal muscle of nine healthy control subjects and 14 COPD patients stratified by cachexia. PPAR-γ, PPAR-δ and TFAM were measured at the mRNA and protein level by real-time quantitative PCR and Western blotting, respectively. PPAR-α and PGC-1α were meansured at the mRNA level. PPAR-δ and TFAM protein content, as well as PGC-1α mRNA levels, were decreased in the skeletal muscle of COPD patients compared with healthy controls. The cachectic COPD subgroup was further characterised by decreased PPAR-α mRNA expression and decreased TFAM protein and mRNA levels compared with noncachectic COPD patients. In addition, PPAR-α mRNA levels in skeletal muscle correlated negatively with inflammatory markers in plasma. Therefore, a disturbed expression of these regulatory factors may well underlie the disturbed skeletal muscle functioning in chronic obstructive pulmonary disease.