Chronic exposure of mice to environmental endocrine-disrupting chemicals disturbs their energy metabolism

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• 作者：Yuanxiang Jin¹ ; Xiaojian Lin¹ ; Wenyu Miao ; Tao Wu ; Hangjie Shen ; Shan Chen ; Yanhong Li ; Qiaoqiao Pan ; Zhengwei Fu ; ^{azwfu@zjut.edu.cn" class="auth_mail} ; ^{azwfu2003@yahoo.com.cn" class="auth_mail}
• 关键词：Endocrine disruption chemicals ; Chronic exposure ; Fat metabolism ; Lipid accumulation ; Mice
• 刊名：Toxicology Letters
• 出版年：21 March, 2014
• 年：2014
• 卷：225
• 期：3
• 页码：392-400
• 全文大小：3353 K

文摘

We evaluated the effects of a 20-week chronic exposure of mice to a low dose of cypermethrin (CYP), atrazine (ATZ) and 17伪-ethynyestradiol (EE2) on energy metabolism. Here, male mice were exposed to 50 渭g/kg BW/day CYP, 100 渭g/kg BW/day ATZ or 1 渭g/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 尾-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.