Introduction: Excess visceral adipose tissue (VAT) is associated with poor metabolic health, including an increased risk of insulin resistance, type 2 diabetes, and hypertension. Excess VAT is also associated with increased systemic inflammation. Poor metabolic health and systemic inflammation have both been implicated in the development and severity of asthma. Therefore, this study aimed to determine whether excess VAT is associated with poorer asthma outcomes and inflammation in adults with asthma.
Methods: Participants were adults with stable physician-diagnosed asthma aged 18-55 years (n=45), recruited through Hunter Medical Research Institute, NSW, Australia. Body composition was assessed by dual-energy x-ray absorptiometry, with excess VAT mass classified according to Meredith-Jones1. Obesity was defined by body mass index (BMI). Lung function (spirometry) and airway inflammation (induced sputum eosinophil count) were measured. Systemic inflammation was assessed by measuring plasma interleukin (IL)-6 concentration via high-sensitivity ELISA.
Results: Compared to participants with a normal VAT mass, those with excess VAT had poorer lung function, indicated by a lower %predicted forced expiratory volume in 1 second (%FEV1; 79.1±17.0 vs 88.9±12.1%, p=0.029) and %predicted forced vital capacity (%FVC; 88.6±12.0 vs 97.1±9.9%, p=0.012). VAT mass was positively associated with eosinophilic airway inflammation (sputum eosinophils; rs=0.334, p=0.044) and systemic inflammation (IL-6; rs=0.434, p=0.003). Obesity, measured by BMI, was not associated with lung function or eosinophilic airway inflammation. However, participants with obesity had elevated systemic inflammation (IL-6) compared to participants without obesity [1.7 (1.5, 2.2) vs 1.0 (0.8, 1.3)pg/mL, p<0.001].
Conclusion: This study suggests that excess visceral adiposity, but not excess body mass, is associated with poorer asthma outcomes in adults with asthma, indicated by poorer lung function and increased eosinophilic airway inflammation.
Grant Support: This research was funded by an Asthma Australia Research Program Grant; TSANZ/National Asthma Council Australia Asthma and Airways Career Development Fellowship; and John Hunter Hospital Charitable Trust Grant.