Wei Yongjie, Zhang Junfeng Jim, Li Zhigang, Gow Andrew, Chung Kian Fan, Hu Min, Sun Zhongsheng, Zeng Limin, Zhu Tong, Jia Guang, Li Xiaoqian, Duarte Marlyn, Tang Xiaoyan
State Key Joint Laboratory of Environmental Simulation and Pollution Control, College of Environmental Sciences and Engineering, Peking University, Beijing, China; State Key Laboratory of Environmental Criteria, and Risk Assessment and Environmental Standards Institute, Chinese Research Academy of Environmental Sciences, Beijing, China;
Nicholas School of the Environment and Duke Global Health Institute, Duke University, Durham, North Carolina, USA; Duke Kunshan University, Kunshan, China;
FASEB J. 2016 Jun;30(6):2115-22. doi: 10.1096/fj.201500142. Epub 2016 Feb 18.
Epidemiologic evidence suggests that air pollution is a risk factor for childhood obesity. Limited experimental data have shown that early-life exposure to ambient particles either increases susceptibility to diet-induced weight gain in adulthood or increases insulin resistance, adiposity, and inflammation. However, no data have directly supported a link between air pollution and non-diet-induced weight increases. In a rodent model, we found that breathing Beijing's highly polluted air resulted in weight gain and cardiorespiratory and metabolic dysfunction. Compared to those exposed to filtered air, pregnant rats exposed to unfiltered Beijing air were significantly heavier at the end of pregnancy. At 8 wk old, the offspring prenatally and postnatally exposed to unfiltered air were significantly heavier than those exposed to filtered air. In both rat dams and their offspring, after continuous exposure to unfiltered air we observed pronounced histologic evidence for both perivascular and peribronchial inflammation in the lungs, increased tissue and systemic oxidative stress, dyslipidemia, and an enhanced proinflammatory status of epididymal fat. Results suggest that TLR2/4-dependent inflammatory activation and lipid oxidation in the lung can spill over systemically, leading to metabolic dysfunction and weight gain.-Wei, Y., Zhang, J., Li, Z., Gow, A., Chung, K. F., Hu, M., Sun, Z., Zeng, L., Zhu, T., Jia, G., Li, X., Duarte, M., Tang, X. Chronic exposure to air pollution particles increases the risk of obesity and metabolic syndrome: findings from a natural experiment in Beijing.
流行病学证据表明，空气污染是儿童肥胖的一个风险因素。有限的实验数据表明，早年暴露于环境颗粒物中，要么会增加成年后饮食诱导体重增加的易感性，要么会增加胰岛素抵抗、肥胖和炎症。然而，尚无数据直接支持空气污染与非饮食诱导的体重增加之间的联系。在一个啮齿动物模型中，我们发现呼吸北京的高污染空气会导致体重增加以及心肺和代谢功能障碍。与暴露于过滤空气的大鼠相比，暴露于未过滤北京空气的怀孕大鼠在妊娠末期体重明显更重。在8周龄时，产前和产后暴露于未过滤空气的后代比暴露于过滤空气的后代体重明显更重。在大鼠母鼠及其后代中，持续暴露于未过滤空气后，我们观察到肺部血管周围和支气管周围炎症的明显组织学证据、组织和全身氧化应激增加、血脂异常以及附睾脂肪促炎状态增强。结果表明，肺中TLR2/4依赖性炎症激活和脂质氧化可全身扩散，导致代谢功能障碍和体重增加。——魏，Y.，张，J.，李，Z.，高，A.，钟，K.F.，胡，M.，孙，Z.，曾，L.，朱，T.，贾，G.，李，X.，杜阿尔特，M.，唐，X. 长期暴露于空气污染颗粒增加肥胖和代谢综合征风险：来自北京一项自然实验的结果
