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首页> 外文期刊>Toxicology Letters: An International Journal Providing a Forum for Original and Pertinent Contributions in Toxicology Research >Chronic exposure of mice to environmental endocrine-disrupting chemicals disturbs their energy metabolism
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Chronic exposure of mice to environmental endocrine-disrupting chemicals disturbs their energy metabolism

机译:小鼠长期暴露于破坏环境的内分泌化学物质中会干扰其能量代谢

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摘要

We evaluated the effects of a 20-week chronic exposure of mice to a low dose of cypermethrin (CYP), atrazine (ATZ) and 17α-ethynyestradiol (EE2) on energy metabolism. Here, male mice were exposed to 50. μg/kg BW/day CYP, 100. μg/kg BW/day ATZ or 1. μg/kg BW/day EE2 supplied in their drinking water for 20 weeks. During the exposure, mice were fed a high energy diet (HD). The bodyweights were not significantly affected by chronic exposure to EDCs, while the serum-free fatty acids (FFA) levels, hepatic lipid accumulation and triacylglycerol (TG) contents increased significantly in the ATZ- and CYP-HD groups. To determine the mechanism involved, we determined the expression levels of the genes in the glucose and fat metabolism pathways in the liver and adipose tissue. The results showed that chronic exposure to ATZ and CYP increased the mRNA levels of a number of key genes involved in both the de novo FFA synthesis pathway and the transport of FFA from blood. The increased amount of FFA was partially consumed as energy through β-oxidation in the mitochondria. Some of the FFA was used to synthesize TG in the liver by up-regulating primary genes, which resulted in increased TG levels and lipid accumulation. The results indicate that chronic exposure to EDCs has the potential to cause energy metabolic dysregulation and hepatotoxicity in mice.
机译:我们评估了低剂量的氯氰菊酯(CYP),阿特拉津(ATZ)和17α-乙炔雌二醇(EE2)对小鼠进行20周慢性暴露对能量代谢的影响。在这里,雄性小鼠暴露于其饮用水中提供的50.μg/ kg BW /天CYP,100。μg/ kg BW /天ATZ或1.μg/ kg BW /天EE2中,持续20周。在暴露期间,给小鼠喂食高能量饮食(HD)。长期暴露于EDCs对体重没有显着影响,而ATZ和CYP-HD组的无血清脂肪酸(FFA)水平,肝脂质蓄积和三酰甘油(TG)含量显着增加。为了确定涉及的机制,我们确定了肝脏和脂肪组织中葡萄糖和脂肪代谢途径中基因的表达水平。结果表明,长期暴露于ATZ和CYP会增加涉及从头FFA合成途径和FFA从血液转运的许多关键基因的mRNA水平。通过线粒体中的β氧化,FFA的增加量被部分消耗为能量。一些FFA用于通过上调主要基因来合成肝脏中的TG,从而导致TG水平和脂质积累增加。结果表明,长期暴露于EDCs可能导致小鼠体内能量代谢失调和肝毒性。

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