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茶多酚对代谢综合征大鼠过氧化物酶体增殖物激活受体及胰岛素信号传导通路的作用研究

来自:中国糖尿病杂志  编辑:夏燕萍 俞茂华 陈蔚等|点击数:|2016-03-03

 

【摘要】  目的  研究茶多酚对MS大鼠糖脂代谢的改善作用及其分子作用机制。 方法  高糖高脂饮食诱导方案建立大鼠MS模型,30只雄性SD大鼠随机分成茶多酚(TPn=10)组、MS对照(MSn=10)组和常规喂养的正常对照(NCn=10)组。给予茶多酚干预16周后测定各组血糖、血脂、胰岛素、FFA水平。RT-PCRWestern blot分别检测各组脂肪组织过氧化物酶体增殖物激活受体(PPAR-γ)、下游基因胰岛素受体底物(IRS-1IRS-2)、磷脂酰肌醇3-激酶(PI3K)、蛋白激酶B、葡萄糖转运蛋白(GLUT-1GKUT-4)的mRNA及蛋白表达水平。  结果  茶多酚(TP)组FPGTGTCLDL-CFFA水平均较MS组下降(P0.05)。TP组脂肪组织PPAR-γ、IRS-1IRS-2PI3K、蛋白激酶BGKUT-4mRNA及蛋白表达水平较MS组上调(P0.05),GLUT-1mRNA表达及蛋白表达水平比较,差异无统计学意义(P0.05)。 结论  茶多酚可改善MS大鼠的糖脂代谢,减轻IR,其作用机制可能是通过上调MS大鼠PPAR-γ的表达,进而影响其下游基因IRS-1IRS-2PI3K、蛋白激酶BGKUT-4的表达来发挥改善胰岛素抵抗的作用。

      【关键词】  茶多酚;代谢综合征;过氧化物酶体增殖物激活受体;胰岛素抵抗

The effect of tea polyphenols on the expression of PPAR-γand regulating insulin signaling pathways in SD rats with metabolic syndrome

      Abstract  Objective  To observe the effects of tea polyphenols (TP) on SD rats with metabolic syndromeMSand its molecular mechanism.  Methods  In this study metabolic syndrome (MS) model was induced by high glucose and high fat diet in SD rat. A total of 30 male SD rats were randomly divided into three groups: MS+TP intervention group (TP group, n=10), MS control group (MS group, n=10), normal control group fed with routine diet (NC group, n=10).Before and after 16 weeks intervention, the levels of blood glucose, blood lipid, fasting insulin and FFA were measured. The mRNA and protein  expressions of PPAR-γ, IRS-1, IRS-2, PI3K, protein  kinase B, GLUT-1, and GLUT-4 in adipose tissue were detected by reverse transcriptase polymerase chain reaction (RT-PCR) and  western blot assay.  Results  The levels of FPG, TG, TC, LDL-C and FFA in TP group were significantly lower than that in MS groupP0.05. Compared with MS group, the expressions of the mRNA and protein level of PPAR-γ, IRS-1, IRS-2, PI3K, protein kinase B and GLUT-4 in adipose tissue of TP group were upregulated P0.05. Compared with MS group, the expression of GLUT-1 in TP group has no significant changeP0.05.  Conclusion  TP can significantly improved glucolipid metabolism and insulin resistance in SD rats with metabolic syndrome, which may be mediated by increasing the expression of PPAR-γ, and then affecting its downstream genes of IRS-1, IRS-2, PI3K, protein kinase Band GLUT-4.

Key words  Tea polyphenols(TP)Metabolic syndrome(MS)PPAR-γ;Peroxisome proliferators-activated receptor-γ(PPAR-γ);Insulin resistance(IR)

上一篇:糖尿病大鼠肾脏解耦联蛋白2表达及促红细胞生成素干预的研究 下一篇:脂肪酸合成酶和碳水化合物反应元件结合蛋白在1型糖尿病小鼠肾脏的表达及其胰岛素对其的调节作用

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