徐仙, 韩瑞, 关素珍, 肖静, 连玉龙, 秦天悦, 朱怡华, 丁慧, 刘梦. 孕哺期大鼠全氟辛烷磺酸暴露对子代糖代谢的影响[J]. 环境与职业医学, 2015, 32(3): 222-226,232. DOI: 10.13213/j.cnki.jeom.2015.14442
引用本文: 徐仙, 韩瑞, 关素珍, 肖静, 连玉龙, 秦天悦, 朱怡华, 丁慧, 刘梦. 孕哺期大鼠全氟辛烷磺酸暴露对子代糖代谢的影响[J]. 环境与职业医学, 2015, 32(3): 222-226,232. DOI: 10.13213/j.cnki.jeom.2015.14442
XU Xian , HAN Rui , GUAN Su-zhen , XIAO Jing , LIAN Yu-long , QIN Tian-yue , ZHU Yi-hua , DING Hui , LIU Meng . Effects of Maternal PFOS Exposure during Pregnancy and Lactation on Glucose Metabolism of Rats Offspring[J]. Journal of Environmental and Occupational Medicine, 2015, 32(3): 222-226,232. DOI: 10.13213/j.cnki.jeom.2015.14442
Citation: XU Xian , HAN Rui , GUAN Su-zhen , XIAO Jing , LIAN Yu-long , QIN Tian-yue , ZHU Yi-hua , DING Hui , LIU Meng . Effects of Maternal PFOS Exposure during Pregnancy and Lactation on Glucose Metabolism of Rats Offspring[J]. Journal of Environmental and Occupational Medicine, 2015, 32(3): 222-226,232. DOI: 10.13213/j.cnki.jeom.2015.14442

孕哺期大鼠全氟辛烷磺酸暴露对子代糖代谢的影响

Effects of Maternal PFOS Exposure during Pregnancy and Lactation on Glucose Metabolism of Rats Offspring

  • 摘要: 目的 探讨孕哺期全氟辛烷磺酸(PFOS)暴露对子代大鼠糖代谢的影响。

    方法 将Wistar孕鼠自孕0天(GD0)随机分为对照组(0 mg/kg)、低剂量组(0.6 mg/kg)和高剂量组(2 mg/kg),每组10只; PFOS灌胃染毒至仔鼠出生后21天(PND21)断乳为止。采用高效液相/质谱法检测PND0、PND21时仔鼠血清PFOS含量;观察仔鼠体重变化趋势;比较9周龄和15周龄仔鼠空腹血糖、空腹胰岛素水平;检测仔鼠瘦素和抵抗素基因表达水平变化。

    结果 PND21时低剂量组和高剂量组仔鼠血清中PFOS浓度分别为(16.00& #177;1.27)mg/L和(80.54& #177;6.55)mg/L(P < 0.05)。低剂量组雌性仔鼠出生后8、9周龄和高剂量7~9周龄,低剂量组雄性仔鼠出生8~12周龄、高剂量7、8、10周龄的体重均明显低于对照组(均P < 0.05)。高剂量组9周龄和低剂量组15周龄雌性仔鼠的胰岛素水平分别为(10.85& #177;1.37)mU/L和(13.62& #177;1.87)mU/L,均高于对照组(P < 0.05);高剂量组9周龄雄性仔鼠的空腹血糖和胰岛素水平分别为(5.43& #177;0.77)mmol/L和(13.23& #177;1.81)mU/L, 15周龄雄性仔鼠低剂量组分别为(4.99& #177;0.54)mmol/L和(13.57& #177;1.22)mU/L, 15周龄高剂量组分别为(5.71& #177;0.56)mmol/L和(13.44& #177;2.97)mU/L,均高于对照组(P < 0.05)。高剂量组15周龄雄性仔鼠的抵抗素基因表达上调1.25& #177;0.03(P < 0.05),瘦素基因表达下调0.67& #177;0.08(P < 0.05)。

    结论 PFOS孕哺期暴露可能引起子代大鼠糖代谢异常,增加糖尿病患病风险。

     

    Abstract: Objective To examine effects of maternal exposure to perfluorooctane sulfonate (PFOS) during pregnancy and lactation on glucose metabolism of rats offspring.

    Methods Pregnant Wistar rats were exposed to PFOS with doses of 0 (control), 0.6 (low), and 2 (high) mg/kg PFOS through gavage from gestation day 0 (GD0) to postnatal day 21 (PND21). We applied high performance liquid chromatography-mass spectrometry to detect serum PFOS concentrations on PND0 and PND21; analyzed the trend of offspring's body weight variation; compared fasting blood glucose and fasting serum insulin levels of offspring at 9 weeks and 15 weeks; measured the expression of leptin and resistin genes.

    Results The serum PFOS concentrations increased to (16.00& #177;1.27)mg/L in the lowdose group and (80.54& #177;6.55)mg/L in the high-dose group on PND21 (P < 0.05), respectively. Compared with the control group, the body weight was significantly lower in female offspring at 8-9 weeks in the low-dose group and 7-9 weeks in the high-dose group, and similar tendency was observed in the male offspring at 8-12 weeks in the low-dose group and at 7, 8, 10 weeks in the high-dose group (all P < 0.05). The serum insulin of female offspring was (10.85& #177;1.37)mU/L at 9 weeks of the low-dose group and (13.62& #177;1.87)mU/L at 15 weeks of the high-dose group, both higher than that of the control group (P < 0.05). For the male offspring of the high-dose group at 9 weeks, the fasting plasma glucose and the serum insulin were (5.43& #177;0.77)mmol/L and (13.23& #177;1.81)mU/L respectively; for the male offpring of the low-dose group at 15 weeks were (4.99& #177;0.54)mmol/L and (13.57& #177;1.22)mU/L respectively; for the male offspring of the high-dose group at 15 weeks were (5.71& #177;0.56)mmol/L and (13.44& #177;2.97)mU/L respectively, all higher than those of the control offspring (P < 0.05). Gene expression of glucose metabolism-related adipokine resistin were significantly up-regulated to 1.25& #177;0.03 (P < 0.05) and that of leptin were significantly down-regulated to 0.67& #177;0.08 (P < 0.05).

    Conclusion Prenatal exposure to PFOS could disturb glucose homeostasis of rat pups and increase the risk of diabetes.

     

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