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全氟辛烷磺酸通过抑制低密度脂蛋白排泄诱导BALB/c小鼠脂质代谢紊乱。

PFOS induced lipid metabolism disturbances in BALB/c mice through inhibition of low density lipoproteins excretion.

作者信息

Wang Ling, Wang Yu, Liang Yong, Li Jia, Liu Yuchen, Zhang Jie, Zhang Aiqian, Fu Jianjie, Jiang Guibin

机构信息

1] State Key Laboratory of Environmental Chemistry and Ecotoxicology, Research Center for Eco-Environmental Sciences, Chinese Academy of Sciences, P. O. Box 2871, Beijing 100085, P. R. China [2] Key Laboratory of Subtropical Agriculture and Environment, Ministry of Agriculture, Huazhong Agricultural University, Wuhan 430070, P. R. China.

1] Key Laboratory of Subtropical Agriculture and Environment, Ministry of Agriculture, Huazhong Agricultural University, Wuhan 430070, P. R. China [2] Department of Environmental Science and Technology, Dalian University of Technology, Dalian 116024, P. R. China.

出版信息

Sci Rep. 2014 Apr 3;4:4582. doi: 10.1038/srep04582.

Abstract

Male BALB/c mice fed with either a regular or high fat diet were exposed to 0, 5 or 20 mg/kg perfluorooctane sulfonate (PFOS) for 14 days. Increased body weight, serum glucose, cholesterol and lipoprotein levels were observed in mice given a high fat diet. However, all PFOS-treated mice got reduced levels of serum lipid and lipoprotein. Decreasing liver glycogen content was also observed, accompanied by reduced serum glucose levels. Histological and ultrastructural examination detected more lipid droplets accumulated in hepatocytes after PFOS exposure. Moreover, transcripitonal activity of lipid metabolism related genes suggests that PFOS toxicity is probably unrelevant to PPARα's transcription. The present study demonstrates a lipid disturbance caused by PFOS and thus point to its role in inhibiting the secretion and normal function of low density lipoproteins.

摘要

给雄性BALB/c小鼠分别喂食常规饮食或高脂饮食,并使其暴露于0、5或20毫克/千克的全氟辛烷磺酸(PFOS)中14天。喂食高脂饮食的小鼠体重、血清葡萄糖、胆固醇和脂蛋白水平升高。然而,所有经PFOS处理的小鼠血清脂质和脂蛋白水平均降低。还观察到肝糖原含量降低,同时血清葡萄糖水平也降低。组织学和超微结构检查发现,PFOS暴露后肝细胞中积累了更多脂滴。此外,脂质代谢相关基因的转录活性表明,PFOS毒性可能与PPARα的转录无关。本研究证明了PFOS引起的脂质紊乱,从而指出其在抑制低密度脂蛋白分泌和正常功能中的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/3a3e/3974142/b1efea8af6ca/srep04582-f1.jpg

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