糖尿病大鼠模型建立及其脂肪组织PPARγ和GLUT-4表达的改变

Rat model of diabetes mellitus and the changes of PPARγ and GLUT-4 expressions in adipose tissue

  • 摘要: 目的:探讨糖尿病大鼠模型建立方法及过氧化物酶体增殖物激活受体γ(PPARγ)及葡萄糖转运蛋白4(GLUT-4)在高脂饮食联合小剂量链脲佐菌素(STZ)腹腔注射诱导的糖尿病形成中的作用。方法:35只雄性Wistar大鼠随机分为正常对照组(NC,n=15)和糖尿病造模组(DM,n=20),NC组饲以基础饲料,DM组饲以高脂饲料。5周后给予DM组单次腹腔注射STZ(30 mg/kg),以1周后空腹血糖>11.1 mmol/L为成模标准(n=15)。17周末测定血生化指标并计算胰岛素敏感指数(ISI),采用免疫组化法及Western-blot法分别检测脂肪组织中PPARγ及GLUT-4蛋白表达水平。结果:实验结束时DM组FBG、糖化血红蛋白(HbA1c)、糖化血清蛋白(GSP)较NC组均显著升高(P<0.01),肿瘤坏死因子α(TNF-α)较NC组明显升高(P<0.05),而ISI较NC组明显下降(P<0.05);脂肪PPARγ及GLUT-4蛋白表达与正常组相比明显下降(P<0.01)。结论:脂肪组织PPARγ及GLUT-4表达减弱在胰岛素抵抗、糖脂类代谢紊乱及糖...

     

    Abstract: Objective:To develop rat model of diabetes mellitus and to explore the effects of peroxisome proliferator activated receptor γ(PPARγ) and glucose transporter 4(GLUT-4) in the diabetic rats induced by high fat diet and low dose streptozotocin(STZ) injection.Methods: Thirty-five Wistar male rats were divided randomly into normal control group(NC,n=15) and diabetic group(DM,n=20),DM group rats were fed with high fat diet and injected with a low dose of STZ(30 mg/kg) once after 5 weeks.The rats with fasting blood glucose higher than 11.1 mmol/L detected one week later were chosen as the diabetic models(n=15).The serum biochemical parameters were detected after 17weeks.The expression levels of PPARγ and GLUT-4 in adipose tissue were determined with immunohistochemistry and western-blot,respectively.Results: Compared with NC group,DM group got higher FBG,Hemoglobin A1c(HbA1c),Triglyceride(TG),glucosylated serum protein(GSP,P<0.01),elevated tumor necrosis factor alpha(TNF-α,P<0.05) and lower insulin sensitivity index(ISI,P<0.05).Immunohistochemistry showed lower protein expression of PPARγ in adipose tissue of DM group compared with NC group(P<0.01).Western-blot analysis showed the expression of GLUT-4 in adipose tissue decreased significantly compared NC group(P<0.01).Conclution: Decreased protein expressions of PPARγ and GLUT-4 in adipose tissue may play important roles in insulin resistance,hyperlipemia and glucose homeostasis disorder in diabetes mellitus.

     

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