Review Article

Arginine and Nitric Oxide Pathways in Obesity-Associated Asthma

Figure 1

Theoretical framework for the interaction of L-arginine-ADMA and NO in obesity and asthma. Among subjects with late onset (>12 years of age) asthma, reduced L-arginine/ADMA ratios uncouple airway NOS, leading to greater airway oxidative stress and reduced NO bioavailability. In turn, this impairs bronchodilation, worsening wheezing, dyspnea, and chest tightness. Several factors may contribute to having lower L-arginine/ADMA. Obesity and asthma both have been associated with decreased L-arginine bioavailability and increased L-arginine catabolism. Also, obesity has been associated with increased ADMA levels independently from asthma. This algorithm may not be present in those with early onset asthma (<12 years), either because obesity and asthma induce different effects on the L-arginine-ADMA metabolic pathway depending on the age of asthma onset or because other mechanistic pathways drive severity and changes in airway NO metabolism in the early onset asthmatics.
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