From the Cardiovascular Research Center, Division of Massachusetts General Hospital, Boston, MA, USA; Pulmonary and Critical Care, Division of Massachusetts General Hospital, Boston, MA, USA.
From the Cardiovascular Research Center, Division of Massachusetts General Hospital, Boston, MA, USA; Cardiology Division of Massachusetts General Hospital, Boston, MA, USA.
Respir Med. 2021 Jul;183:106434. doi: 10.1016/j.rmed.2021.106434. Epub 2021 Apr 30.
Obesity has multifactorial effects on lung function and exercise capacity. The contributions of obesity-related inflammatory pathways to alterations in lung function remain unclear.
To examine the association of obesity-related inflammatory pathways with pulmonary function, exercise capacity, and pulmonary-specific contributors to exercise intolerance.
We examined 695 patients who underwent cardiopulmonary exercise testing (CPET) with invasive hemodynamic monitoring at Massachusetts General Hospital between December 2006-June 2017. We investigated the association of adiponectin, leptin, resistin, IL-6, CRP, and insulin resistance (HOMA-IR) with pulmonary function and exercise parameters using multivariable linear regression.
Obesity-related inflammatory pathways were associated with worse lung function. Specifically, higher CRP, IL-6, and HOMA-IR were associated with lower percent predicted FEV and FVC with a preserved FEV/FVC ratio suggesting a restrictive physiology pattern (P ≤ 0.001 for all). For example, a 1-SD higher natural-logged CRP level was associated with a nearly 5% lower percent predicted FEV and FVC (beta -4.8, s.e. 0.9 for FEV1; beta -4.9, s.e. 0.8 for FVC; P < 0.0001 for both). Obesity-related inflammatory pathways were associated with worse pulmonary vascular distensibility (adiponectin, IL-6, and CRP, P < 0.05 for all), as well as lower pulmonary artery compliance (IL-6 and CRP, P ≤ 0.01 for both).
Our findings highlight the importance of obesity-related inflammatory pathways including inflammation and insulin resistance on pulmonary spirometry and pulmonary vascular function. Specifically, systemic inflammation as ascertained by CRP, IL-6 and insulin resistance are associated with restrictive pulmonary physiology independent of BMI. In addition, inflammatory markers were associated with lower exercise capacity and pulmonary vascular dysfunction.
肥胖对肺功能和运动能力有多种影响。肥胖相关的炎症途径对肺功能变化的贡献尚不清楚。
研究肥胖相关炎症途径与肺功能、运动能力以及导致运动不耐受的肺部特定因素之间的关系。
我们对 2006 年 12 月至 2017 年 6 月期间在马萨诸塞州总医院接受心肺运动测试（CPET）和有创血流动力学监测的 695 例患者进行了研究。我们使用多变量线性回归来研究脂联素、瘦素、抵抗素、IL-6、CRP 和胰岛素抵抗（HOMA-IR）与肺功能和运动参数的关系。
肥胖相关的炎症途径与较差的肺功能相关。具体而言，较高的 CRP、IL-6 和 HOMA-IR 与较低的 FEV 和 FVC 百分比预测值相关，而 FEV/FVC 比值保持不变，提示存在限制性生理学模式（所有 P 值均≤0.001）。例如，1-SD 更高的自然对数 CRP 水平与 FEV 和 FVC 的百分比预测值降低近 5%（FEV1 的β值为-4.8，s.e. 0.9；FVC 的β值为-4.9，s.e. 0.8；两者均 P＜0.0001）。肥胖相关的炎症途径与较差的肺血管可扩张性（脂联素、IL-6 和 CRP，所有 P 值均＜0.05）以及较低的肺动脉顺应性（IL-6 和 CRP，两者均 P≤0.01）相关。
我们的研究结果强调了肥胖相关的炎症途径（包括炎症和胰岛素抵抗）对肺功能和肺血管功能的重要性。具体而言，CRP、IL-6 和胰岛素抵抗等全身炎症与 BMI 无关，与限制性肺生理学有关。此外，炎症标志物与运动能力下降和肺血管功能障碍相关。
