Alterations in arginine metabolism and accelerated formation of advanced glycation end-products (AGEs), crucial mechanisms in obesity-related asthma, can be modulated by glucagon-like peptide 1 (GLP-1). l-arginine dysregulation in obesity promotes inflammation and bronchoconstriction. Prolonged hyperglycemia, dyslipidemia, and oxidative stress leads to production of AGEs, that bind to their receptor (RAGE) further potentiating inflammation. By binding to its widely distributed receptor, GLP-1 blunts the effects of RAGE activation and arginine dysregulation. The GLP-1 pathway, while comprehensively studied in the endocrine and cardiovascular literature, is under-recognized in pulmonary research. Insights into GLP-1 and the lung may lead to novel treatments for obesity-related asthma.

精氨酸代谢的改变和晚期糖基化终产物 (AGE) 的加速形成是肥胖相关哮喘的关键机制，可以通过胰高血糖素样肽 1 (GLP-1) 进行调节。肥胖中的L-精氨酸失调会促进炎症和支气管收缩。长期高血糖、血脂异常和氧化应激会导致 AGE 的产生，AGE 与其受体 (RAGE) 结合，进一步加剧炎症。通过与其广泛分布的受体结合，GLP-1 可以减弱 RAGE 激活和精氨酸失调的影响。 GLP-1 通路虽然在内分泌和心血管文献中得到了全面的研究，但在肺部研究中却未被充分认识。对 GLP-1 和肺部的深入了解可能会带来治疗肥胖相关哮喘的新疗法。