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作 者:王敏[1] 王磊[1] 任续功[1] 单祥鸣[1] 吴丽娜 吕春梅[1] 袁广梅[1] M.Ram Sairam Natalia Danilovich
机构地区:[1]德州市人民医院内二科,山东德州253014 [2]德州市立医院保健科,山东德州253000 [3]加拿大蒙特利尔临床研究所分子生殖实验室
出 处:《山东大学学报(医学版)》2006年第5期492-495,500,共5页Journal of Shandong University:Health Sciences
摘 要:目的:探讨雌激素减少与代谢综合征的相关性。方法:在基因库中搜索已知的对脂肪组织有影响的10个基因,筛选其启动子中可能存在的雌激素调控因子的基因。以不同月龄、不同基因型的卵泡刺激素受体敲除(FORKO)雌鼠为动物模型,测量其腹内白色脂肪组织(WAT)重量、体重,计算腹内WAT与体重的比率;口服葡萄糖(2g/kg),测快速血糖(0,30,60,120min)行葡萄糖耐量实验;用组织学方法观察脂肪细胞、肝脏细胞的形态;用放射免疫法测定血清瘦素。结杲:①在7个肥胖相关基因中找到了可能的雌激素调控位点;②FORKO雌鼠于3月龄时出现肥胖,腹内WAT的重量明显高于野生型(P〈0.05);③FORKO雌鼠随月龄的增长葡萄糖耐量逐渐减低(P〈0.05);④FORKO雌鼠腹内WAT细胞在3月龄时体积较小,表现为增生(P〈0.05),而在8个月时表现为肥大(P〈0.05);⑤FORKO雌鼠于8月龄时WAT细胞、棕色脂肪(BAT)细胞及肝细胞内均有大量脂酯颗粒堆积;⑥月龄3~5个月的FORKO雌鼠空腹的血清瘦素水平均明显高于野生雌鼠(P〈0.05)。结论:FORKO雌鼠因雌激素减少而表现出腹型肥胖、高血糖、高瘦素和胰岛素抵抗等代谢紊乱,提示雌激素减少可导致代谢综合征。Objective: To investigate the relationship between estrogen deficiency and metabolic syndromes. Methods: This study focused on the follicle stimulating hormone receptor knockout ( FORKO ) female mice. The data of 10 genes of adipocyte related factors that might have impact on the metabolic activity of the adipose tissue were screened in the gene bank. The bodyweights and gonadal fat pads weights of different genotype at different ages were weighed, and the ratio of gonadal fat pad weight to bodyweight was calculated respectively. Glucose tolerance test(glucose was given 2mg/kg bodyweight orally) was performed among the three genotypes' female mice at different ages respectively. Histology was used to observe the shape and size of white adipocytes, brown adipocytes and hepatic cells. Serum leptin was measured at the age of 3-5 months. Results: Aadipocyte related factors containing putive hormone responsive elements in their promoter regions were found in 7 genes. Null mutants of 3-month showed signs of obesity with increased deposition of abdominal fat and mutant females exhibited age dependent glucose intorlerance. There were more lipid drops in mutants' adipocytes and hepatic cells than those in wild type females. Serum leptin levels were much higher in null mutants both at fast and fed status than those in wild type female mice. Conclusion: Estrogen deficiency may contribute to metabolic syndromes, such as visceral obesity and glucose intorlerance in FORKO female mouse
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