Source: Annual Congress 2002 - Cell biology and genetics of COPD and emphysema
Disease area: Airway diseases

Abstract

Loss of oxidative capacity in peripheral skeletal muscle occurs in COPD and glucose homeostasis is probably altered in these patients. A role of uncoupling protein 3 (UCP3) in the regulation of substrate metabolism and glucose homeostatis has been shown (Clapham et al, Nature 2000). Biopsies from the vastus lateralis of 16 COPD patients (age 67 ±] 2 yrs; BMI 24 ±] 1 kg/m²; FEV₁ 42 ±] 4%) and 15 healthy age-matched control subjects (age 64 ±] 1 yrs; BMI 24 ±] 1 kg/m²; FEV₁ 108 ±] 5%) were taken. UCP3 and cytochrome c (as a marker for mitochondrial content) were measured by Western blotting. Muscle fiber types and metabolic profile were examined histochemically as described previously (Gosker et al, Eur Respir J 2002). We showed, for the first time, that protein levels of UCP3 in skeletal muscle were markedly decreased in COPD compared to controls (48 ±] 8 vs 95 ±] 13 AU, p<0.01). In addition, there was a positive correlation between UCP3 contents and the FEV₁ (r=0.66; p=0.008) in patients. There were no correlations between UCP3 and other muscular data such as fiber types, markers of oxidative/glycolytic energy metabolism, or cytochrome c. There was no relation between UCP3 and BMI. We conclude that UCP3 content is decreased in skeletal muscle of patients with COPD and is related to disease severity. The low UCP3 content is independent of the loss of oxidative capacity observed in these patients. Further studies are needed to examine whether low UCP3 plays a role in abnormal glucose homeostasis in COPD. Supported by the Netherlands Asthma Foundation.

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H. R. Gosker, P. Schrauwen, M. K. C. Hesselink, G. Schaart, G. J. van der Vusse, E. F. M. Wouters, A. M. W. J. Schols (Maastricht, The Netherlands). Uncoupling protein 3 content is decreased in skeletal muscle of patients with COPD. Eur Respir J 2002; 20: Suppl. 38, 639

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