Effects of exposure to ambient fine particulate matter on the heart of diet -induced obesity mouse model

Effects of exposure to ambient fine particulate matter on the heart of diet -induced obesity mouse model
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环境细颗粒物暴露对饮食诱导肥胖小鼠模型心脏的影响

DOI:
10.1016/j.scitotenv.2020.139304
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发表时间:
2020-08-25
影响因子:
9.8
通讯作者:
Cai, Zongwei
Cai, Zongwei
中科院分区:
环境科学与生态学1区
文献类型:
--
作者:
Song, Yuanyuan;Qi, Zenghua;Cai, Zongwei

文献摘要

被引文献

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暴露于细颗粒物(PM2.5)与心脏功能下降有关,特别是在肥胖等高危人群中。本研究采用饮食诱导的肥胖小鼠模型,研究PM2.5暴露对心功能的影响。小鼠喂普通饲料或高脂饲料(HFD)四周,然后通过气管内滴注磷酸盐缓冲液或太原冬季PM2.5(0.25 mg/kg体重/天)再暴露四周。在记录的生理指标中,肥胖小鼠心脏暴露于PM2.5后心率和血压升高。代谢组学和脂质组学被应用于探索响应于PM2.5和HFD的共同处理的分子改变。我们的结果表明,这既对心脏功能产生直接影响,也对其他器官的损伤产生间接影响。肺和下丘脑的炎症可能是导致血清中苯丙氨酸代谢及其下游产物肾上腺素和去甲肾上腺素升高的原因,其中儿茶酚胺参与调节心脏系统。在心内系统,联合治疗导致能量代谢失衡,氧化应激和炎症反应。与葡萄糖和脂肪酸摄取和CoA合成的上调相反,ATP,乙酰CoA和糖酵解途径中间产物的水平在心脏中降低。提示能量代谢紊乱可能是HFD与PM2.5联合治疗的不良反应更为严重的重要因素之一。
Exposure to fine particulate matter (PM2.5) is associated with decreased cardiac function, especially in high risk populations such as obese ones. In this study, impacts of PM2.5 exposure on cardiac function were investigated by using the diet-induced obesity mice model. Mice were fed with normal diet or high-fat diet (HFD) for four weeks and then exposed to phosphate-buffered solution or Taiyuan winter PM2.5 (0.25 mg/kg body/day) through intratracheal instillation for another four weeks. Among physiological indices recorded, heart rate and blood pressure were increased after PM2.5 exposure in the heart of the obese mice. Metabolomics and lipidomics were applied to explore molecular alterations in response to the co-treatment of PM2.5 and HFD. Our results demonstrated both direct impacts on cardiac function and indirect effects resulted from the injury of other organs. Inflammation of lung and hypothalamus may be responsible for the elevation of phenylalanine metabolism in serum and its downstream products: epinephrine and norepinephrine, the catecholamines involves in regulating cardiac system. In intracardiac system, the co-treatment led to imbalance of energy metabolism, in addition to oxidative stress and inflammation. In contrast to the upregulation of glucose and fatty acids uptake and CoA synthesis, levels of ATP, acetyl-CoA and the intermediates in glycolysis pathway decreased in the heart. The results indicated that energy metabolism disorder was possibly one of the important contributing factors to the more severe adverse effects of the combined treatment of HFD and PM2.5.