摘要
目的:构建高脂饮食诱导肥胖小鼠模型,观察BVT.2733在改善胰岛素抵抗中的作用及对Visfatin表达的影响。方法:构建高脂饮食诱导的肥胖小鼠模型,分为肥胖对照组和BVT.2733治疗组,肥胖对照组给予安慰剂、治疗组给予BVT.2733灌胃2周,同时设正常饮食的小鼠为正常对照组。放射免疫法测小鼠空腹胰岛素水平,生化法检测血糖,实时定量RT-PCR检测内脏脂肪组织Visfatin的mRNA表达。观察各组小鼠脂肪组织的形态学变化。结果:与正常对照组相比,肥胖对照组小鼠脂肪细胞明显增大,体重增加,空腹血糖、血清胰岛素水平升高(P<0.05)。与肥胖对照组相比,BVT.2733治疗组小鼠脂肪细胞体积减小,空腹血清胰岛素水平明显下降(P<0.01),脂肪组织Visfatin mRNA表达显著降低(P<0.05)。结论:BVT.2733能够降低体重,减少脂肪组织,并且降低Visfatin的表达水平。
Objective:To investigate the effects of BVT.2733 on the expression of Visfatin and insulin resistance in the dietinduced obese (DIO) mice model. Methods:The C57BL/6J mice were randomly divided into the normal diet group and high-fat diet (HFD) group. After 20 weeks,the obese mice were randomly divided into obese control group and BVT.2733 treatment group. And they were orally administered placebo and BVT.2733,respectively,for two weeks. The levels of plasma glucose and serum insulin were measured by biochemistry technology and radioimmunity. The visfatin mRNA expression in adipose tissue were analyzed by realtime quantitative PCR. And the morphology changes of adipocyte were also observed. Results: Comparing to normal controls,the weight, plasma glucose and serum insulin levels increased in HFD group (P 〈 0.05), and the size of adipoeyte in HFD group was big. Comparing to obese controls,in BVT.2733 treatment group,the serum insulin significantly decreased (P 〈 0.01) and the adipocyte sizes reduced,while the mRNA expression of visfatin down-regulated (P 〈 0.05). Conelusion:BVT.2733 could reduce body weight significantly, ameliorate insulin resistance, and down-regulate the expression of Visfatin.
出处
《南京医科大学学报(自然科学版)》
CAS
CSCD
北大核心
2012年第7期933-936,共4页
Journal of Nanjing Medical University(Natural Sciences)
基金
南京市医学科技发展项目(YKK11102)