TY - JOUR
T1 - Chronic exposure to air pollution particles increases the risk of obesity and metabolic syndrome
T2 - Findings from a natural experiment in Beijing
AU - Wei, Yongjie
AU - Zhang, Junfeng
AU - Li, Zhigang
AU - Gow, Andrew
AU - Chung, Kian Fan
AU - Hu, Min
AU - Sun, Zhongsheng
AU - Zeng, Limin
AU - Zhu, Tong
AU - Jia, Guang
AU - Li, Xiaoqian
AU - Duarte, Marlyn
AU - Tang, Xiaoyan
N1 - Funding Information:
This work was supported in part by grants from the National Natural Science Foundation of China (21190051, 21477119), the Open Fund of the State Key Joint Laboratory of Environment Simulation and Pollution Control (13K03ESPCP), and the China Postdoctoral Science Foundation (201003010).
Publisher Copyright:
© FASEB.
PY - 2016/6
Y1 - 2016/6
N2 - 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.
AB - 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.
KW - Chronic inflammation
KW - Metabolic dysfunction
KW - Particulate matter
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U2 - 10.1096/fj.201500142
DO - 10.1096/fj.201500142
M3 - Article
C2 - 26891735
AN - SCOPUS:84971590282
SN - 0892-6638
VL - 30
SP - 2115
EP - 2122
JO - FASEB Journal
JF - FASEB Journal
IS - 6
ER -