文章摘要
黄琼.S100A16在饮食诱导肥胖大鼠中的作用研究[J].南京医科大学学报,2014,(1):
S100A16在饮食诱导肥胖大鼠中的作用研究
The role of S100A16 in rats with diet-induced obesity
投稿时间:2013-07-04  修订日期:2013-12-03
DOI:10.7655/NYDXBNS201401023
中文关键词: 胰岛素敏感性,肥胖,大鼠模型,S100A16,转录因子
英文关键词: Insulin sensitivity  obese  rat model  S100A16  transcription factor
基金项目:基金项目:;江苏省科技支撑项目(BE2011802), 国家自然科学基金( 81270952, 81070684);南京医科大学第一附属医院创新团队工程
作者单位E-mail
黄琼 南京医科大学第一临床学院 13914490100@163.com 
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中文摘要:
      目的:探讨S100A16蛋白对体重增加过程的影响,进一步研究S100A16蛋白在肥胖及肥胖相关疾病的发生发展过程中的作用。方法:去正常8周龄大鼠随机分为正常饮食组(NF, n=10)和高脂饮食组(HF, n=10),建立饮食诱导的肥胖(DIO)大鼠模型,喂食14周时进行腹腔葡萄糖耐量试验(IPGTT)及胰岛素释放试验(IRT),喂食16周处死后称量皮下及内脏脂肪重量,采用HE染色方法 (hematoxylin and eosin staining, HE) 观察肝脏脂肪变性程度,放射免疫分析法检血糖,血清胰岛素,尿酸等血清生化指标,同时应用Western blotting 方法检测脂肪组织中 S100A16及糖脂代谢相关转录因子的蛋白表达。结果:DIO组大鼠的体重,内脏脂肪明显高于正常组,血清总胆固醇和尿酸DIO组高于正常组但糖耐量和胰岛素释放低于正常组,western blotting 显示DIO组大鼠脂肪组织中S100A16,PPAR-γ, C/EPB-?的蛋白表达明显高于正常组。结论:高脂饮食可上调S100A16及相关转录因子的表达;S100A16的高表达可促进脂质生成及肥胖发生,并对机体胰岛素释放及胰岛素敏感性产生负性影响。
英文摘要:
      Objective: To investigate the effect of S100A16 on weight gain process, the development of obesity and obesity related diseases occur. Methods: Rats aged 8 weeks were randomly divided into normal diet group (NF, n = 10) and a high-fat diet group (HF, n = 10), providing diet for 16 weeks to establish a diet induced obesity (DIO) rat model. When feeding at 14 weeks, rats were processed intraperitoneal glucose tolerance test (IPGTT) and insulin release test (IRT). When rats were executed after 16 weeks, weighted subcutaneous and visceral fat weight. Then we used HE staining method (hematoxylin and eosin staining, HE) to observe the liver steatosis degree, radiation immunity analysis to check blood sugar, insulin, serum uric acid, serum biochemical indicator, and Western blotting to study the expression of S100A16 and glucolipid metabolism related protein expression of transcription factors in liver and adipose tissue. Results: DIO group rats weight, visceral fat is significantly higher than normal group. The serum total cholesterol and uric acid in DIO group was higher than normal glucose tolerance and insulin release is lower than the normal group. Western blotting showed that in liver and fat tissue of DIO group, S100A16, PPAR-γ, C/EPB-? expression were significantly higher than those of normal group. Conclusion: High fat diet can increase the expression of S100A16 and related expression of transcription factors; S100A16 over expression can promote lipid generated and result in a negative impact on insulin release and insulin sensitivity.
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