有氧运动抑制肥胖引起的呼吸表型。

Aerobic exercise inhibits obesity-induced respiratory phenotype.

机构信息

Nove de Julho University, Rua Vergueiro 235/249, São Paulo, SP 01504-001, Brazil.

Brazilian Institute of Teaching and Research in Pulmonary and Exercise Immunology (IBEPIPE), Rua Pedro Ernesto 240, Sao José dos Campos, SP 12245-520, Brazil.

出版信息

Cytokine. 2018 Apr;104:46-52. doi: 10.1016/j.cyto.2017.12.025. Epub 2018 Feb 15.

DOI:10.1016/j.cyto.2017.12.025

PMID:29454302

Abstract

PURPOSE

Obesity results in decreased lung function and increased inflammation. Moderate aerobic exercise (AE) reduced lung inflammation and remodeling in a variety of respiratory disease models. Therefore, this study investigated whether AE can attenuate a diet-induced obesity respiratory phenotype; including airway hyper-responsiveness (AHR), remodeling and inflammation.

METHODS

Sixty C57Bl/6 male mice were distributed into four groups: control lean (CL), exercise lean (EL), obese (O) and obese exercise (OE) groups (2 sets of 7 and 8 mice per group; n = 15). A classical model of diet-induced obesity (DIO) over 12 weeks was used. AE was performed 60 min/day, 5 days/week for 5 weeks. Airway hyperresponsiveness (AHR), lung inflammation and remodeling, adipokines and cytokines in bronchoalveolar lavage (BAL) was determined.

RESULTS

A high fat diet over 18 weeks significantly increased body weight (p < .0001). Five weeks of AE significantly reduced both AHR and pulmonary inflammation. AHR in obese mice that exercised was reduced at the basal level (p < .05), vehicle (PBS) (p < .05), 6.25 MCh mg/mL (p < .05), 12.5 MCh mg/mL (p < .01), 25 MCh mg/mL (p < .01) and 50 MCh mg/mL (p < .05). Collagen (p < .001) and elastic (p < .001) fiber deposition in airway wall and also smooth muscle thickness (p < .001) were reduced. The number of neutrophils (p < .001), macrophages (p < .001) and lymphocytes (p < .01) were reduced in the peribronchial space as well as in the BAL: lymphocytes (p < .01), macrophages (p < .01), neutrophils (p < .001). AE reduced obesity markers leptin (p < .001), IGF-1 (p < .01) and VEGF (p < .001), while increased adiponectin (p < .01) in BAL. AE also reduced pro-inflammatory cytokines in the BAL: IL-1β (p < .001), IL-12p40 (p < .001), IL-13 (p < .01), IL-17 (p < .001, IL-23 (p < .05) and TNF-alpha (p < .05), and increased anti-inflammatory cytokine IL-10 (p < .05).

CONCLUSIONS

Aerobic exercise reduces high fat diet-induced obese lung phenotype (AHR, pulmonary remodeling and inflammation), involving anti-inflammatory cytokine IL-10 and adiponectin.

摘要

目的

肥胖会导致肺功能下降和炎症增加。中等强度的有氧运动（AE）可减少多种呼吸系统疾病模型中的肺炎症和重塑。因此，本研究旨在探讨 AE 是否可以减轻饮食诱导的肥胖呼吸表型，包括气道高反应性（AHR）、重塑和炎症。

方法

将 60 只 C57Bl/6 雄性小鼠分为四组：对照瘦（CL）、运动瘦（EL）、肥胖（O）和肥胖运动（OE）组（每组 7 到 8 只小鼠；n=15）。使用经典的饮食诱导肥胖（DIO）模型 12 周。AE 每天进行 60 分钟，每周 5 天，持续 5 周。测定气道高反应性（AHR）、肺炎症和重塑、支气管肺泡灌洗液（BAL）中的脂肪因子和细胞因子。

结果

高脂肪饮食 18 周显著增加体重（p<0.0001）。5 周的 AE 显著降低了 AHR 和肺部炎症。肥胖小鼠的基础水平（p<0.05）、载体（PBS）（p<0.05）、6.25 MCh mg/mL（p<0.05）、12.5 MCh mg/mL（p<0.01）、25 MCh mg/mL（p<0.01）和 50 MCh mg/mL（p<0.05）的 AHR 均降低。气道壁胶原（p<0.001）和弹性（p<0.001）纤维沉积以及平滑肌厚度（p<0.001）均减少。周细胞（p<0.001）、巨噬细胞（p<0.001）和淋巴细胞（p<0.01）在支气管周围空间和 BAL 中的数量减少：淋巴细胞（p<0.01）、巨噬细胞（p<0.01）、中性粒细胞（p<0.001）。AE 降低了肥胖标志物瘦素（p<0.001）、IGF-1（p<0.01）和 VEGF（p<0.001），同时增加了 BAL 中的脂联素（p<0.01）。AE 还降低了 BAL 中的促炎细胞因子：IL-1β（p<0.001）、IL-12p40（p<0.001）、IL-13（p<0.01）、IL-17（p<0.001）、IL-23（p<0.05）和 TNF-α（p<0.05），并增加了抗炎细胞因子 IL-10（p<0.05）。