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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 construct an obese mouse model induced by high fat diet and observe the effect of BVT.2733 on improving insulin resistance and its effect on Visfatin expression. Methods: Obesity model induced by high-fat diet was established and divided into obesity control group and BVT.2733 treatment group, obese control group given placebo, and treatment group given BVT.2733 gavage for 2 weeks. At the same time, normal mice For the normal control group. Fasting insulin levels in mice were measured by radioimmunoassay, blood glucose was measured by biochemical method, and Visfatin mRNA expression in visceral adipose tissue was detected by real-time quantitative RT-PCR. The morphological changes of adipose tissue in each group were observed. Results: Compared with the normal control group, adipocytes in obese control group increased significantly, body weight increased, fasting blood glucose and serum insulin levels increased (P <0.05). Compared with the obese control group, the volume of adipocytes decreased, the fasting serum insulin level decreased significantly (P <0.01) and the visfatin mRNA expression decreased significantly in the BVT.2733 treatment group (P <0.05). Conclusion: BVT.2733 can reduce body weight, reduce adipose tissue, and reduce Visfatin expression.