脂质代谢
甘油三酯
脂解
脂肪酸
脂肪肝
化学
新陈代谢
内分泌学
内科学
急性暴露
生物
生物化学
胆固醇
脂肪组织
医学
疾病
作者
Sijia Yang,Rucheng Chen,Lu Zhang,Qing Sun,Ran Li,Weijia Gu,Mianhua Zhong,Ying Liu,Lung‐Chi Chen,Qinghua Sun,Cuiqing Liu
标识
DOI:10.1016/j.envpol.2020.116193
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 PM2.5 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 PM2.5 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.
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