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[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±1.27)mg/L和(80.54±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±1.37)m U/L和(13.62±1.87)m U/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±0.77)mmol/L和(13.23±1.81)m U/L,15周龄雄性仔鼠低剂量组分别为(4.99±0.54)mmol/L和(13.57±1.22)m U/L,15周龄高剂量组分别为(5.71±0.56)mmol/L和(13.44±2.97)m U/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±0.03(P<0.05),瘦素基因表达下调0.67±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。
[Objective] To investigate the effect of PFOS exposure on glucose metabolism in offsprings of rats during pregnancy and lactation. [Methods] Wistar pregnant rats were randomly divided into control (0 mg / kg), low dose (0.6 mg / kg) and high dose (2 mg / kg) ; PFOS intragastric administration to the pups born after 21 days (PND21) weaning so far. The levels of serum PFOS in PND0 and PND21 were detected by high performance liquid chromatography / mass spectrometry (LC-MS / MS). The body weight of the pups were observed. The fasting blood glucose and fasting insulin levels of the pups at 9 weeks and 15 weeks were compared. The levels of leptin and resistin Gene expression changes. [Results] The concentrations of PFOS in PND21 low dose group and high dose group were (16.00 ± 1.27) mg / L and (80.54 ± 6.55) mg / L, respectively (P <0.05). At 8, 9 weeks of age and 7-9 weeks of age, the male offspring of low dose group were 8-12 weeks of age at birth, and the body weights of male offspring at 7, 8 and 10 weeks of high dose were significantly lower Control group (all P <0.05). The insulin levels in high dose group and low dose group were (10.85 ± 1.37) mU / L and (13.62 ± 1.87) mU / L, respectively, all higher than those in control group (P <0.05 ). The fasting blood glucose and insulin levels in high dose group were (5.43 ± 0.77) mmol / L and (13.23 ± 1.81) m U / L respectively in male offspring of 9 weeks old group, 4.99 ± 0.54mmol / L and 13.57 ± 1.22mU / L, respectively, and were significantly higher in the 15-week-old high-dose group than in the control group (5.71 ± 0.56mmol / L and 13.44 ± 2.97mU / L, (P <0.05). The resistin gene expression in high-dose 15-week-old male offspring rats was increased by 1.25 ± 0.03 (P <0.05) and leptin gene expression was decreased by 0.67 ± 0.08 (P <0.05). [Conclusion] Exposure to PFOS during pregnancy and lactation may cause abnormal glucose metabolism in offspring rats and increase the risk of diabetes.