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

PFOS induced lipid metabolism disturbances in BALB/c mice through inhibition of low density lipoproteins excretion.
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PFOS通过抑制低密度脂蛋白排泄诱导BALB/c小鼠脂质代谢紊乱

DOI:
10.1038/srep04582
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发表时间:
2014-04-03
期刊:
影响因子:
4.6
通讯作者:
Jiang G
Jiang G
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Wang L;Wang Y;Liang Y;Li J;Liu Y;Zhang J;Zhang A;Fu J;Jiang G

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将常规或高脂肪饮食喂养的雄性 BALB/c 小鼠暴露于 0、5 或 20mg/kg 全氟辛烷磺酸 (PFOS) 中 14 天。在给予高脂肪饮食的小鼠中观察到体重、血清葡萄糖、胆固醇和脂蛋白水平增加。然而,所有 PFOS 治疗的小鼠的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降低。组织学和超微结构检查发现,接触全氟辛烷磺酸后,肝细胞中积累了更多的脂滴。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。本研究证明全氟辛烷磺酸会引起脂质紊乱,从而指出其在抑制低密度脂蛋白的分泌和正常功能中的作用。
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.
DOI: 10.1016/s0045-6535(02)00304-1
发表时间: 2002-10-01
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