Lipid metabolic adaption to long-term ambient PM2.5 exposure in mice

被引:31
|
作者
Yang, Sijia [1 ]
Chen, Rucheng [1 ]
Zhang, Lu [1 ]
Sun, Qing [1 ]
Li, Ran [1 ]
Gu, Weijia [1 ]
Zhong, Mianhua [2 ]
Liu, Ying [3 ,4 ,5 ,6 ]
Chen, Lung-Chi [2 ]
Sun, Qinghua [7 ]
Liu, Cuiqing [1 ]
机构
[1] Zhejiang Chinese Med Univ, Joint China US Res Ctr Environm & Pulm Dis, Sch Basic Med Sci & Publ Hlth, Hangzhou, Peoples R China
[2] New York Univ, Dept Environm Med, Sch Med, New York, NY USA
[3] Natl Ctr Nanosci & Technol China, CAS Key Lab Biomed Effects Nanomat & Nanosafety, Beijing 100190, Peoples R China
[4] Natl Ctr Nanosci & Technol China, CAS Ctr Excellence Nanosci, Beijing 100190, Peoples R China
[5] Natl Ctr Nanosci & Technol China, Beijing Key Lab Ambient Particles Hlth Effects &, Beijing 100190, Peoples R China
[6] Univ Chinese Acad Sci, Beijing 100190, Peoples R China
[7] Ohio State Univ, Coll Publ Hlth, Columbus, OH USA
基金
中国国家自然科学基金;
关键词
Fine particulate matter; Exposure duration; Triglyceride; Free fatty acid; Lipid metabolism; FATTY LIVER-DISEASE; ADIPOSE TRIGLYCERIDE LIPASE; HORMONE-SENSITIVE LIPASE; AIR-POLLUTION; SUSCEPTIBILITY; GLUCOSE; TISSUE; ACIDS;
D O I
10.1016/j.envpol.2020.116193
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Emerging evidence has demonstrated that exposure to fine particulate matter (PM2.5) is a risk factor for lipid metabolic disorders in the liver. However, the effects of PM2.5 exposure time duration on hepatic lipid metabolism remain unknown. In this study, C57BL/6 mice were randomly divided into ambient PM2.5 (PM) or filtered air (FA) exposure chamber for short-term (4 weeks) or long-term (24 weeks) exposure via a whole body exposure system. We measured hepatic triglyceride and free fatty acid levels and analyzed the alteration of lipometabolism-related molecules in the liver. We found that triglyceride levels were significantly elevated in both short-term and long-term PM2.5-exposed mice and free fatty acid levels were increased after long-term PM2.5 exposure. Besides, enzymes for lipolysis and fatty acid oxidation in the liver were inhibited after short-term PM2.5 exposure but adaptively enhanced after long-term PM(2.5 )exposure. Furthermore, molecules for fatty acid uptake were down-regulated in the short-term PM2.5-exposed mice whereas molecules for lipid export were induced after long-term PM2.5 exposure. Therefore, ambient PM(2.5 )exposure disturbed hepatic lipid metabolism and the effects varied in different exposure duration. These findings in mice provide new insight into the biological basis of PM2.5-induced human metabolic dysfunction and specific strategies may be applied based on different exposure time periods. (C) 2020 Elsevier Ltd. All rights reserved.
引用
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页数:9
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