Leptin, adiponectin, and asthma: findings from a population-based cohort study

Abstract

Obesity is thought to increase the risk of asthma, especially in women. It has been proposed that this association could be due to the immune-modulating effect of adipokines secreted by adipose tissue. To investigate whether aspects of the asthma phenotype are associated with higher levels of the proinflammatory adipokine leptin and lower levels of the anti-inflammatory adipokine adiponectin in a cross-sectional analysis of a group of young adults. Associations between leptin and adiponectin and a diagnosis of asthma, symptoms of wheeze, bronchodilator response, airflow obstruction, and exhaled nitric oxide were evaluated by logistic or linear regression in a population-based birth cohort of approximately 1,000 men and women aged 32 years. Further analyses adjusted for smoking and body fat. There were no significant associations between leptin and any of the markers of the asthma phenotype in either men or women. In men, higher levels of adiponectin were associated with lower levels of exhaled nitric oxide but an increased risk of bronchodilator responsiveness. The inverse association with exhaled nitric oxide remained significant after adjustment for body fat, but the association with bronchodilator responsiveness did not. Adiponectin levels were not associated with any markers of asthma in women. The inverse association between adiponectin and exhaled nitric oxide in men warrants further investigation. However, the findings indicate that levels of leptin and adiponectin are unlikely to mediate the previously observed association between obesity and asthma.