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Thorax 2008;63:1110-1117 doi:10.1136/thx.2007.086827
  • Review series

Obesity and the lung: 5 · Obesity and COPD

  1. F M E Franssen1,
  2. D E O’Donnell2,
  3. G H Goossens3,
  4. E E Blaak3,
  5. A M W J Schols1
  1. 1
    Department of Respiratory Medicine, University Hospital Maastricht, Maastricht, The Netherlands
  2. 2
    Division of Respiratory and Critical Care Medicine, Department of Medicine, Queens University, Kingston, Ontario, Canada
  3. 3
    Department of Human Biology, Nutrition and Toxicology Research Institute (NUTRIM), Maastricht University, Maastricht, The Netherlands
  1. Dr A M W J Schols, NUTRIM School for Nutrition, Toxicology and Metabolism, Department of Respiratory Medicine, University Hospital Maastricht, P O Box 5800, 6202 AZ Maastricht, The Netherlands; a.schols{at}pul.unimaas.nl
  • Received 15 February 2008
  • Accepted 30 April 2008

Abstract

Chronic obstructive pulmonary disease (COPD) and obesity are common and disabling chronic health conditions with increasing prevalence worldwide. A relationship between COPD and obesity is increasingly recognised, although the nature of this association remains unknown. This review focuses on the epidemiology of obesity in COPD and the impact of excessive fat mass on lung function, exercise capacity and prognosis. The evidence for altered adipose tissue functions in obesity—including reduced lipid storage capacity, altered expression and secretion of inflammatory factors, adipose tissue hypoxia and macrophage infiltration in adipose tissue—is also reviewed. The interrelationship between these factors and their contribution to the development of insulin resistance in obesity is considered. It is proposed that, in patients with COPD, reduced oxidative capacity and systemic hypoxia may amplify these disturbances, not only in obese patients but also in subjects with hidden loss of fat-free mass. The potential interaction between abnormal adipose tissue function, systemic inflammation and COPD may provide more insight into the pathogenesis and reversibility of systemic pathology in this disease.

Footnotes

  • Competing interests: None.

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