PM_(2.5)暴露对子代小鼠糖脂代谢的影响  

Effects of PM_(2.5) exposure on glucose and lipid metabolism in offspring mice

作　　者：邵寒冰 胡文轩 褚修余 李思琦 赵新元 王晓珂[1,2] SHAO Han-bing;HU Wen-xuan;CHU Xiu-yu;LI Si-qi;ZHAO Xin-yuan;WANG Xiao-ke(School of Public Health,Nantong University,Nantong 226019,China;School of Medicine,University of Maryland)

机构地区：[1]南通大学公共卫生学院,南通226019 [2]美国马里兰大学医学院

出　　处：《环境卫生学杂志》2022年第5期326-331,共6页JOURNAL OF ENVIRONMENTAL HYGIENE

基　　金：江苏省自然科学基金项目(BK20201444);南通市科技局项目(JC2019016);江苏省青蓝工程优秀骨干教师(2020);江苏省大学生创新训练计划项目(202010304103Y);南通大学大学生创新训练计划(2020139)。

摘　　要：目的 探讨细颗粒物(fine particulate matter, PM_(2.5))暴露对子代小鼠糖脂代谢的影响。方法 将12只4周龄C57BL/6J雌性清洁级小鼠随机分为PM_(2.5)暴露组和清洁空气对照组(6 h/d, 5 d/周),实时暴露7周后,将雌鼠按雌雄2∶1的比例合笼并暴露至子鼠出生。子鼠断乳之后予高脂(总热能4.67 kcal/g,碳水化合物37.0%、蛋白质18.0%、脂肪45.0%)饲料,腹腔葡萄糖耐量实验(IPGTT)检测葡萄糖耐量;HE染色法检测病理变化;荧光实时定量PCR检测ERα和PPARγmRNA表达情况。结果 PM_(2.5)暴露显著降低子鼠的出生体重并导致雄性子鼠成年体重的增加和葡萄糖耐量的降低,而对雌性小鼠无显著影响,能够显著增加子代雄性小鼠的能量利用率,显著降低雄性子代小鼠的脂肪组织ERα和PPARγ基因表达。结论PM_(2.5)暴露可能通过程序性调控脂肪组织ERα和PPARγ基因的表达,诱导雄性成年期小鼠糖脂代谢紊乱的发生,而对雌性子代成年期小鼠无显著影响。Objective To explore the effect of prenatal PM_(2.5) exposure on the glucolipotoxicity of male and female mice under post weaning high fat diet.Methods Twelve four-week-old clean grade female C57 BL/6 J mice were randomly divided into PM_(2.5) exposure group and filter air(FA) control group. After real-time exposure for 7 weeks(6 h/d, 5 d/week), female mice in each group were caged with male mice(female∶male=2∶1), and continued to be exposed until the pups were born. The offspring were fed a high-fat diet(total energy 4.67 kcal/g: 37.0% carbohydrate, 20.00% protein and 45.0% fat) after weaning. Glucose tolerance was measured by the intraperitoneal glucose tolerance test. Pathological changes were observed with hematoxylin-eosin staining. Real-time PCR was used to measure the mRNA expression of estrogen receptor alpha(ERα) and peroxisome proliferator-activated receptor gamma(PPARγ).Results Prenatal exposure to PM_(2.5) significantly decreased the birth weight of offspring, and significantly increased the body weight and reduced the glucose intolerance of the adult male offspring, but with no significant changes in the adult female offspring. Compared with those in the control group, the adult male offspring with prenatal PM_(2.5) exposure had significantly increased energy efficiency and significantly reduced gene expression of ERα and PPARγ in the adipose tissue.Conclusion Prenatal exposure to PM_(2.5) may regulate the gene expression of ERα and PPARγ in the adipose tissue in a programmed way, to induce disturbances in glucose and lipid metabolism in adult male offspring, but have no significant implications for adult female offspring.

关 键 词：出生前暴露 细颗粒物(PM_(2.5)) 子代 糖脂毒性 

分 类 号：R12[医药卫生—环境卫生学]