Abstract
Obesity is a comorbidity that adversely affects asthma severity and control by mechanisms that are not fully understood. This review will discuss evidence supporting a role for nitric oxide (NO) as a potential mechanistic link between obesity and late-onset asthma (>12 years). Several studies have shown that there is an inverse association between increasing body mass index (BMI) and reduced exhaled NO. Newer evidence suggests that a potential explanation for this paradoxical relationship is related to nitric oxide synthase (NOS) uncoupling, which occurs due to an imbalance between L-arginine (NOS substrate) and its endogenous inhibitor, asymmetric di-methyl arginine (ADMA). The review will propose a theoretical framework to understand the relevance of this pathway and how it may differ between early and late-onset obese asthmatics. Finally, the paper will discuss potential new therapeutic approaches, based on these paradigms, for improving the respiratory health of obese subjects with asthma.
Highlights
Obesity is associated with less asthma control, greater risk of asthma exacerbations, and reduced inhaled corticosteroid efficacy, whether these conditions are causally related remains uncertain [1]
The inverse association between body mass index (BMI) and exhaled nitric oxide (eNO) [5] may be explained by an imbalance between L-arginine and one of its methylated products known as asymmetric dimethyl arginine (ADMA) [6, 7]
L-arginine is methylated to ADMA, which is an endogenous inhibitor of all nitric oxide synthase (NOS) isoforms [8]
Summary
Division of Pulmonary, Allergy & Critical Care, Asthma Institute, University of Pittsburgh, Pittsburgh, PA 15213, USA. Obesity is a comorbidity that adversely affects asthma severity and control by mechanisms that are not fully understood. This review will discuss evidence supporting a role for nitric oxide (NO) as a potential mechanistic link between obesity and late-onset asthma (>12 years). Newer evidence suggests that a potential explanation for this paradoxical relationship is related to nitric oxide synthase (NOS) uncoupling, which occurs due to an imbalance between L-arginine (NOS substrate) and its endogenous inhibitor, asymmetric di-methyl arginine (ADMA). The review will propose a theoretical framework to understand the relevance of this pathway and how it may differ between early and late-onset obese asthmatics. The paper will discuss potential new therapeutic approaches, based on these paradigms, for improving the respiratory health of obese subjects with asthma
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