ABSTRACT
Obesity not only increases the risk of asthma, but also, contributes significantly to its clinical heterogeneity. Obese asthmatics exhibit a distinct clinical phenotype characterized by diminished response to corticosteroids, increased hospitalization rates and decreased quality of life. Excess fat accumulation in the abdominal and thoracic cavities results in altered lung and chest wall mechanics contributing to the respiratory symptoms experienced by the obese subjects without asthma. However, altered lung mechanics due to visceral/truncal obesity does not fully explain the obese-asthma phenotype for the following reasons: (1) not all obese people tend to develop asthma, (2) metabolic dysregulation, a prominent feature of obesity, is frequently associated with asthma independent of body mass, and(3) maternal obesity, during pregnancy, has been shown to increase the risk of asthma incidence in offspring, independent of child’s own obesity. These findings suggest a role for intersecting molecular pathologies leading to either of the diseases. Emerging evidence suggests that mitochondrial dysfunction is a common denominator in both of these seemingly disparate diseases. This is not surprising given the critical role of mitochondria, apart from energy production, in metabolic regulation and adaptation, sensing nutrient stress, lipid handling, and cell survival/death decisions. In the present chapter, we examine the multiple lines of evidence suggesting mitochondrial dysfunction as a critical link connecting obesity and asthma. We further highlight the relevant mitochondrial health-centric strategies that could be considered for the clinical management of obese-asthma.
