Obesity and asthma: obesity causes and aggravates asthma across the entire type-2 inflammation spectrum.

This trend has important implications for asthma: individuals with obesity have a 30-50% higher risk of developing asthma, and obesity is highly prevalent among people with established disease.

这一趋势对哮喘有重要影响：肥胖个体患哮喘的风险比正常体重者高出30-50%，并且在已确诊疾病的人群中肥胖的患病率非常高。

Mean body mass index in clinical trials and registries of adults with asthma consistently ranges from 28 kg·m-2 to 30 kg·m-2, with up to 70% of patients being overweight or obese.

在成人哮喘的临床试验和登记研究中，平均体质指数（BMI）始终在28 kg·m-2到30 kg·m-2之间，多达70%的患者超重或肥胖。

These numbers highlight obesity as one of the most common comorbidities in asthma, consistently associated with poorer asthma control and a higher risk of exacerbations.

这些数据突显了肥胖是哮喘中最常见的合并症之一，它与哮喘控制较差和急性加重风险增加始终相关。

Although obesity-associated asthma is often described as type-2 (T2)-low phenotype, it is increasingly recognised as a heterogeneous condition not restricted to a single phenotype.

尽管肥胖相关的哮喘通常被描述为2型（T2）低表型，但越来越多地被认识到是一种不局限于单一表型的异质性疾病。

Excess adiposity influences asthma through multiple mechanisms, including dysregulated adipokine signalling, impaired innate lymphoid cells type 2 (ILC2)-eosinophil-macrophage cross-talk in adipose tissue, systemic low-grade inflammation, metabolic dysfunction, and mechanical effects on lung volumes.

过量的脂肪组织通过多种机制影响哮喘，包括失调的脂肪因子信号传导、脂肪组织中受损的先天性淋巴细胞类型2（ILC2）-嗜酸性粒细胞-巨噬细胞交叉谈话、全身性低度炎症、代谢功能障碍以及对肺容量的机械效应。

This diversity complicates diagnosis, endotyping, and treatment stratification.

这种多样性使得诊断、内型划分和治疗分层变得复杂。

Obesity should therefore be considered a treatable trait in asthma.

因此，肥胖应被视为哮喘中一种可治疗的特征。

Weight reduction (through lifestyle interventions, pharmacotherapy or bariatric surgery) improves symptoms, lung function, and exacerbation risk across both T2-high and T2-low asthma.

通过生活方式干预、药物治疗或减重手术减轻体重，可以改善T2高型和T2低型哮喘的症状、肺功能和急性加重风险。

Importantly, patients with obesity experience similar reductions in exacerbations with anti-T2 biologics as their lean counterparts, though improvements in symptoms and lung function are variable.

重要的是，肥胖患者使用抗T2生物制剂后，急性加重的减少与瘦型患者相似，尽管在症状和肺功能的改善方面存在差异。

Future research should prioritise randomised, placebo-controlledtrials evaluating glucagon-like peptide (GLP)-1 and dual GLP-1/glucose-dependent insulinotropic polypeptide (GIP)-agonist therapies specifically in patients with asthma and obesity, and elucidate how obesity modifies inflammatory endotypes and treatment responses.

未来的研究应优先考虑进行随机、安慰剂对照试验，专门评估胰高血糖素样肽（GLP）-1和双重GLP-1/葡萄糖依赖性胰岛素促进多肽（GIP）激动剂疗法，特别是在患有哮喘和肥胖症的患者中，并阐明肥胖如何改变炎症表型和治疗反应。