Abstract
Background
Adipokines, such as resistin and adiponectin, modify inflammation and may contribute to increased asthma risk and severity in obese people.
Objective
To examine plasma resistin and resistin: adiponectin ratio: (1) in asthmatics compared to healthy controls, (2) according to asthma severity, obesity and gender (3) following weight loss in obese asthmatics.
Methods
In a cross-sectional observational study of asthmatic adults (n=96) and healthy controls (n=46), plasma resistin and adiponectin were measured. In a separate intervention study, obese asthmatic adults (n=27) completed a 10-week weight-loss intervention and plasma resistin and adiponectin concentrations were analysed.
Results
Plasma resistin and resistin: adiponectin ratio were higher in asthma compared to controls and were higher again in subjects with a severe versus mild to moderate asthma pattern. Amongst asthmatic subjects, resistin was not modified by gender or obesity, while adiponectin was lower in males and obese subjects. As a result, resistin: adiponectin ratio was higher in obese males, non-obese males and obese females, compared to non-obese females. In a logistic regression model, plasma resistin concentration was a predictor of asthma risk. In a multiple linear regression model, plasma resistin: adiponectin ratio was a negative predictor of FEV1 in asthma. Following weight loss, neither resistin, adiponectin nor resistin: adiponectin ratio were changed. However, the change (Δ) in %body fat was associated with Δ resistin: adiponectin ratio. Post intervention Δ resistin was negatively correlated with both ΔFRC and ΔRV.
Conclusion and clinical relevance
This study demonstrates that resistin and resistin: adiponectin ratio are higher in asthma and are higher again in subjects who have more severe disease. Resistin: adiponectin ratio is highest in obese male asthmatics. As resistin is a predictor of asthma risk and resistin:adiponectin is a predictor of FEV1 in asthma, these adipokines may be contributing to the obese-asthma phenotype, thus providing a potential therapeutic target for obese asthma.
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