Abstract
BackgroundThe obese-asthma phenotype is not well defined. The aim of this study was to examine both mechanical and inflammatory influences, by comparing lung function with body composition and airway inflammation in overweight and obese asthma.MethodsOverweight and obese (BMI 28-40 kg/m2) adults with asthma (n = 44) completed lung function assessment and underwent full-body dual energy x-ray absorptiometry. Venous blood samples and induced sputum were analysed for inflammatory markers.ResultsIn females, android and thoracic fat tissue and total body lean tissue were inversely correlated with expiratory reserve volume (ERV). Conversely in males, fat tissue was not correlated with lung function, however there was a positive association between android and thoracic lean tissue and ERV. Lower body (gynoid and leg) lean tissue was positively associated with sputum %neutrophils in females, while leptin was positively associated with android and thoracic fat tissue in males.ConclusionsThis study suggests that both body composition and inflammation independently affect lung function, with distinct differences between males and females. Lean tissue exacerbates the obese-asthma phenotype in females and the mechanism responsible for this finding warrants further investigation.
Highlights
The obese-asthma phenotype is not well defined
In conclusion, our data suggests that body composition and systemic and airway inflammation independently alter respiratory function and that these influences are sexually dimorphic in nature
We found android and upper body adiposity to be negatively associated with lung function in females, whilst lean mass in the android region was an important positive predictor of lung function in males
Summary
The aim of this study was to examine both mechanical and inflammatory influences, by comparing lung function with body composition and airway inflammation in overweight and obese asthma. Obesity and asthma are associated conditions, with obese asthmatics experiencing more severe asthma symptoms, reduced lung function and poorer asthmarelated quality of life, compared to asthmatics of a healthy weight [1,2]. These clinical characteristics are well described, the mechanisms responsible are not understood. The most recent evidence suggests that the obese-asthma phenotype has both mechanical [3] and inflammatory [4,5] influences, and that these differ between males and females. Previous authors have cited a relationship between asthma incidence and serum leptin in females but not males; and between serum adiponectin levels and poorer lung function [7]
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