Glucose and lipid homeostasis in adult rat is impaired by early-life exposure to perfluorooctane sulfonate
Glucose and lipid homeostasis in adult rat is impaired by early-life exposure to perfluorooctane sulfonate
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成年大鼠的葡萄糖和脂质稳态因生命早期接触全氟辛烷磺酸而受损
DOI：
10.1002/tox.20747
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发表时间：
2013-09-01
影响因子：
4.5
通讯作者：
Xu, Shunqing
中科院分区：
文献类型：
--
作者：
Lv, Ziquan;Li, Gengqi;Xu, Shunqing
全氟辛烷磺酸（PFOS）属于许多全氟化合物的降解产物，被列入持久性有机污染物（POPs）清单，目前在野生动物和人类中都检测到。本研究在大鼠中研究了妊娠期和哺乳期全氟辛烷磺酸暴露对子代糖尿病前期效应的影响。母鼠从妊娠第0天至出生后第21天，分别给药0.5 mg/kg/d或1.5 mg/kg/d的PFOS。研究了糖脂代谢对后代成年期的影响。妊娠期和哺乳期暴露于全氟辛烷磺酸导致婴儿从出生到断奶体重过低，并诱发糖尿病前期症状，空腹血清胰岛素和瘦素水平升高，糖耐量下降，尽管空腹血清葡萄糖和糖基化血清蛋白水平正常。肝脏脂肪变性和性腺脂肪垫重量增加也可观察到异常的脂质稳态。然而，空腹循环血清甘油三酯水平和胆固醇水平与对照组没有差异。我们的研究结果表明，发育暴露于全氟辛烷磺酸可能导致成年期糖脂代谢紊乱。(c) 2011 Wiley期刊公司环境科学学报，2013,31(2):532-542。
Perfluorooctane sulfonate (PFOS), which belongs to the degradation product of many perfluorinated compounds, is on the list of persistent organic pollutants (POPs) and is currently detected in both wildlife and humans. The consequence of gestational and lactational exposure to PFOS on prediabetes effect in offspring was investigated in rats in the present study. Maternal rats were treated with vehicle, 0.5 mg/kg/day or 1.5 mg/kg/day PFOS respectively from gestation day 0 to postnatal day 21. The glucose and lipid metabolism effects were investigated on the offspring in adulthood. The gestational and lactational exposure to PFOS led to low body weight from birth to weaning, and evoked signs of a prediabetic state, with elevated fasting serum insulin and leptin level, impaired glucose tolerance, though the fasting serum glucose and glycosylated serum protein level were normal. Abnormal lipid homeostasis was also observed by the phenomenon of hepatic steatosis and increased gonadal fat pad weight. However, the circulating serum level of fasting triglyceride and cholesterol level were no different from controls. Our results suggested that developmental exposure to PFOS may contribute to glucose and lipid metabolic disorder in adulthood. (c) 2011 Wiley Periodicals, Inc. Environ Toxicol 28: 532-542, 2013.