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围产期壬基酚暴露致子代成年雄性大鼠糖脂代谢紊乱及机制研究

发布时间:2018-05-09 09:29

  本文选题:围产期 + 壬基酚 ; 参考:《环境与健康杂志》2017年04期


【摘要】:目的探讨围产期壬基酚(nonylphenol,NP)暴露导致成年雄性仔鼠糖脂代谢紊乱及其机制。方法将32只健康成年SPF级SD妊娠大鼠随机分为普通饲料对照(玉米油)组、普通饲料+NP(200 mg/kg)组、高脂高糖饲料(15%猪油、20%白糖、65%普通饲料)对照组、高脂高糖饲料+NP(200 mg/kg)组,每组8只。母鼠从妊娠第6天至产后21 d(PND21,断乳)清晨空腹灌胃染毒NP,染毒容量为5 ml/kg,每天1次。每组随机选取10只雄性仔鼠,于出生70 d后检测胰腺组织中NP、血糖及血清中甘油三酯(triglycerides,TG)、总胆固醇(total cholesterol,TC)的水平,并检测胰腺糖代谢相关基因葡萄糖激酶(glucokinase,GCK)和葡萄糖转运蛋白-2(glucose transporter-2,GLUT-2)及脂肪细胞分化关键基因过氧化物酶体增殖物激活受体γ(peroxisome proliferator activated receptorγ,PPARγ)和脂肪酸合成酶(fatty acid sythase,FAS)的表达水平。结果与普通饲料对照组比较,第4、6周高脂高糖饲料对照组和高脂高糖饲料+NP组仔鼠的体重均大于普通饲料对照组,差异有统计学意义(P0.05)。第8周时,高脂高糖饲料+NP组仔鼠高脂高糖饲料对照组普通饲料对照组(P0.05),且高脂高糖饲料+NP组仔鼠高脂高糖饲料对照组普通饲料+NP组(P0.05)。与普通饲料对照组比较,普通饲料+NP组及高脂高糖饲料+NP组仔鼠的胰腺NP、血糖及血清TG、TC水平均增高,差异有统计学意义(P0.05)。高脂高糖饲料+NP组仔鼠的胰腺NP、血糖及血清TG、TC水平均高于普通饲料+NP组(P0.05)。各组仔鼠胰腺GCK、GLUT-2基因的表达水平依次为高脂高糖饲料+NP组普通饲料+NP组、高脂高糖饲料对照组普通饲料对照组,差异均有统计学意义(P0.05)。各组仔鼠脂肪细胞PPARγ、FAS基因的表达水平依次为高脂高糖饲料+NP组普通饲料+NP组高脂高糖饲料对照组普通饲料对照组,除普通饲料+NP组与高脂高糖饲料对照组比较的FAS基因外,差异均有统计学意义(P0.05)。结论围产期NP暴露可导致仔鼠糖脂代谢紊乱,其机制可能与NP促进胰腺糖代谢和脂肪细胞分化关键基因表达有关。
[Abstract]:Objective to investigate the metabolic disorder and mechanism of glycolipid metabolism in adult male offspring rats by perinatal nonylphenol (NP) exposure. Methods 32 healthy adult SPF grade SD pregnant rats were randomly divided into normal feed control (corn oil) group, ordinary feed +NP (200 mg/kg) group, high fat and high sugar diet (15% lard, 20% white sugar, 65% ordinary feed) control group, high fat diet. High glucose diet +NP (200 mg/kg) group, 8 mice in each group. From sixth days of pregnancy to 21 d postpartum (PND21, weaning), NP was administered to the stomach in the morning, the volume was 5 ml/kg, 1 times a day. 10 male offspring were randomly selected from each group. After the birth of 70 D, the blood glucose and serum triglyceride (triglycerides, TG), and total cholesterol (total Chol) were detected. The levels of esterol, TC) and the detection of glucokinase (glucokinase, GCK) and glucose transporter -2 (glucose transporter-2, GLUT-2) and the key genes for the differentiation of lipid cells and the peroxisome proliferator activated receptor gamma (peroxisome proliferator activated receptor gamma) and fatty acid synthetase. The expression level of acid sythase, FAS). Compared with the normal diet control group, the weight of the high fat and high sugar diet control group and the high fat and high sugar feed +NP group was higher than the normal diet control group at week 4,6, and the difference was statistically significant (P0.05). At the eighth week, the high fat high sugar diet + NP group of high fat and high sugar diet control group was compared with the normal diet control group Group (P0.05), and high fat and high sugar diet +NP group of high fat and high sugar diet control group +NP group (P0.05). Compared with the normal diet control group, the pancreas NP, blood sugar and serum TG, TC level in the +NP group and the high fat and high sugar diet +NP group were all higher, the difference was statistically significant (P0.05). P, blood glucose and serum TG, TC level were higher than that of normal diet +NP group (P0.05). The expression level of GLUT-2 gene in each group was in order of the +NP group of high fat and high sugar feed +NP common feed, and the control group of high fat and high sugar diet control group, the difference was statistically significant (P0.05). The expression of PPAR gamma, FAS gene expression in each group of adipocytes in each group The level of high fat and high sugar diet +NP group +NP high fat and high sugar diet control group common feed control group, except the common feed +NP group and high fat diet control group FAS gene, the difference was statistically significant (P0.05). Conclusion perinatal exposure to NP can lead to lipid metabolism disorder in offspring rats, the mechanism may be promoted with NP Glycometabolism and adipocyte differentiation are related to the expression of key genes in pancreas.

【作者单位】: 遵义医学院公共卫生学院;遵义医学院附属医院内分泌科;遵义医学院附属医院胃肠外科;
【基金】:国家自然科学基金(81360439;81560527) 贵州省优秀青年人才基金(2017) 贵州省教育厅青年基金(黔教合KY字[2013]198) 贵州省科技厅遵义医学院联合基金重点项目(黔科合LH字[2014]7543;[2015]7521) 遵义医学院重点学科建设经费;遵义医学院招标课题(2013F-68)
【分类号】:R114

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