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肖静,连玉龙,马颖,赵健亚. 孕哺期全氟辛烷磺酸暴露对子代大鼠糖代谢的影响[J]. 生态毒理学报, 2013, 8(5): 678-686
孕哺期全氟辛烷磺酸暴露对子代大鼠糖代谢的影响
Effect of Perinatal PFOS Exposure on Glucose Homeostasis of Adult Rat Offspring
投稿时间:2013-04-23  修订日期:2013-05-24
DOI:10.7524/AJE.1673-5897.20130423001
中文关键词:  全氟辛烷磺酸(PFOS)  糖代谢  发育毒性
英文关键词:PFOS  glucose metabolism  developmental toxicity
基金项目:国家自然科学基金(81202228);南通市科技计划项目(HS2012012)
作者单位
肖静 南通大学公共卫生学院 职业卫生与环境毒理学教研室南通 226019 
连玉龙 南通大学公共卫生学院 职业卫生与环境毒理学教研室南通 226019 
马颖 中国科学院大连化学物理研究所 生物医用材料工程组大连 116023 
赵健亚 南通大学公共卫生学院 营养与食品卫生学教研室南通 226019 
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中文摘要:
      探讨孕哺期全氟辛烷磺酸(PFOS)暴露对子代大鼠成年后糖代谢稳态的影响。Wistar孕鼠随机分组,自孕0天(GD0)起分别以0 mg·kg-1(对照组)、4 mg·kg-1(低剂量组)和8 mg·kg-1 (高剂量组) PFOS(以饲料中PFOS计)经口染毒至仔鼠出生后21天(PND21)断乳为止。高效液相/质谱法检测PND1、PND21和PND42时仔鼠血清PFOS含量。检测仔鼠断乳后第8周和第18周时空腹血糖和胰岛素水平计算胰岛素抵抗指数(HOMA-IR);比较仔鼠口服糖耐量及肝脏糖代谢关键酶表达水平改变。结果显示:发育期
PFOS暴露导致仔鼠出现血清中PFOS蓄积,以PND21时浓度最高,在低剂量组和高剂量组中分别为(7.77±1.45) μg·mL-1和(5.09±0.57) μg·mL-1。与对照组相比,不同剂量组仔鼠在断乳前后均出现明显体重降低,并在成年后出现高胰岛素血症,但PFOS仅在雄性仔鼠中引起了血糖升高。18周龄时口服糖耐量结果显示,PFOS暴露使雄性仔鼠在该阶段出现糖耐量受损,同时造成过氧化物酶体增殖物活化受体γ协同刺激因子(PGC-1)、磷酸烯醇丙酮酸羧激酶(PEPCK)表达水平的显著增高以及葡萄糖-6-磷酸脱氢酶(G6P)表达水平的显著降低。以上结果说明PFOS孕哺期暴露可引起子代成年后糖代谢失调,有增加糖尿病患病风险可能。
           
AuthorAffiliation
Xiao JingDepartment of Occupational Medicine and Environmental Toxicology, School of Public Health, Nantong University, Nantong 226019, China
Lian YulongDepartment of Occupational Medicine and Environmental Toxicology, School of Public Health, Nantong University, Nantong 226019, China
Ma YingLaboratory of Biomedical Material Engineering, Dalian Institute of Chemical Physics, Chinese Academy of Sciences, Dalian 16023, China
Zhao JianyaDepartment of Nutrition ang Food Hygiene,School of Public Health,Nantong University,Nantong 226019,China
英文摘要:
      Effect of perinatal exposure to PFOS on glucose metabolism of adult rat offsprings was investigated. The pregnant rats were exposed to PFOS with doses of 0 mg·kg-1 PFOS (control), 4 mg·kg-1 PFOS (low) or 8 mg·kg-1 PFOS (high) through diet from gestation day 0 (GD 0) to postnatal day 21 (PND21). Serum PFOS concentrations were determined on PND1, PND21 and PND42 by HPLC-LC/MS. The rats' body weight was monitored during the experiments. Fasting blood glucose and fasting serum insulin level were measured at 8 and 18 weeks after weaning. Homeostasis model assessment insulin resistance index (HOMA-IR) was also calculated. Moreover, oral glucose tolerance test (OGTT) was performed on 18 weeks in male offspring after weaning and the area under curve was calculated. Besides, expression of glucose metabolism-related genes was measured using real-time PCR. The present study showed that serum PFOS concentration increased after exposure and the concentration was highest on PND 21, with (7.77±1.45) μg·mL-1 at 4 mg·kg-1 dose and (5.09±0.57) μg·mL-1 at 8 mg·kg-1 dose. Additionally, body weights of rat pups from PFOS exposure groups were significantly lower than control group. Though the fasting blood glucose levels were affected by PFOS only in male offspring, serum insulin levels were significantly elevated in all exposure groups. The degree of insulin resistance was also elevated and PFOS exposure could impair the glucose tolerance of male rat pups at 18 week. Furthermore, results from RT-PCR revealed that PFOS up-regulated the expression level of PGC-1 and PEPCK, while down-regulated the expression level of hypoglycemic gene G6P. In conclusion, developmental exposure to PFOS disturbed the glucose homeostasis of rat pups in the adulthood, led to insulin resistance and increased the risk of diabetes and metabolic disorder.
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