Obesity-related asthma is a distinct pediatric asthma phenotype. It is associated with higher disease burden, lower pulmonary function, and suboptimal response to current asthma medications. Recent studies have made inroads into elucidating its pathophysiology. Systemic immune responses in obese children with asthma are skewed to a nonatopic T-helper cell type 1 (Th1) pattern that correlates with pulmonary function deficits. The prevalence of metabolic dysregulation is also higher among obese children with asthma than among normal-weight children with asthma. Insulin resistance and dyslipidemia, particularly low levels of high-density lipoprotein (HDL), are associated with lower airway obstruction and low expiratory reserve volume. These associations are independent of truncal and general adiposity and thereby suggest a direct association between metabolic abnormalities and pulmonary function. Furthermore, insulin resistance is associated with Th1 polarization, whereas low HDL is associated with monocyte activation. Although insulin resistance mediates the association of Th1 polarization with pulmonary function, HDL does not have a similar influence on the association of monocyte activation with pulmonary function. Together, these recent studies have paved the way to the understanding of obesity-related asthma as a distinct asthma phenotype and have begun to identify the complex relationships between metabolic dysregulation, systemic inflammation, and pulmonary function deficits in obese children with asthma. Studies are now needed to elucidate the mechanisms that link metabolic dysregulation and systemic immune responses to pulmonary function.