發(fā)布時(shí)間：2018-04-13 22:13

  本文選題：胰島素抵抗 + EGCG��； 參考：《西南師范大學(xué)學(xué)報(bào)(自然科學(xué)版)》2017年11期

【摘要】：目的:研究EGCG(Epigallocatechin Gallate)是否抑制骨骼肌組織的TRB3(Tribbles Homologue 3)表達(dá),激活PI3K/AKT信號(hào)通路,促進(jìn)骨骼肌對(duì)葡萄糖的攝取和利用.方法:80只SD(Sprague Dawley)大鼠隨機(jī)分為正常對(duì)照組(20只)、模型對(duì)照組(20只)、EGCG低劑量治療組(20只)和EGCG高劑量治療組(20只).模型對(duì)照組、EGCG低劑量治療組和EGCG高劑量治療組給予高糖高脂飲食6個(gè)月后,EGCG低劑量治療組和EGCG高劑量治療組分別給予EGCG治療,治療4周和8周分別處死各組大鼠各半,檢測(cè)血清中葡萄糖、胰島素含量并計(jì)算胰島素抵抗指數(shù);檢測(cè)骨骼肌組織TRB3和AKT的表達(dá)及AKT的磷酸化程度.結(jié)果:模型組中葡萄糖、胰島素和胰島素抵抗指數(shù)(p0.05),EGCG治療4周和8周后,各指標(biāo)均降低(p0.05);模型組中AKT的mRNA和蛋白質(zhì)在各組中無(wú)差異,但P-AKT(473)在模型組表達(dá)下調(diào),治療后表達(dá)上調(diào),8周治療較4周明顯(p0.05).模型組中TRB3的mRNA和蛋白質(zhì)表達(dá)增加(p0.05),治療后TRB3表達(dá)的下調(diào),8周治療較4周明顯(p0.05);結(jié)論:EGCG可降低血糖,其機(jī)制可能與抑制TRB3的表達(dá),增加AKT的磷酸化程度,激活PI3K/AKT信號(hào)通路,促進(jìn)骨骼肌細(xì)胞對(duì)葡萄糖的攝取和利用,抑制胰島素抵抗.
[Abstract]:Aim: to investigate whether EGCG(Epigallocatechin Gallate inhibits the expression of TRB3(Tribbles Homologue 3 in skeletal muscle, activates PI3K/AKT signaling pathway, and promotes glucose uptake and utilization in skeletal muscle.Methods 80 SD(Sprague Dawley rats were randomly divided into normal control group (n = 20), model control group (n = 20) and EGCG high dose group (n = 20).After 6 months of high glucose and high fat diet, the low dose group and the high dose group of EGCG were treated with EGCG respectively. The rats of each group were killed for 4 weeks and 8 weeks, respectively.The serum glucose, insulin content and insulin resistance index were measured. The expression of TRB3 and AKT and the phosphorylation of AKT in skeletal muscle were detected.Results: after 4 and 8 weeks of treatment, the levels of glucose, insulin and insulin resistance index were all decreased in model group, and the mRNA and protein of AKT in model group were not different in each group, but the expression of P-AKTn473) was down-regulated in model group.After treatment, the expression of upregulation was significantly increased in 8 weeks than in 4 weeks of treatment (P 0.05).In the model group, the expression of mRNA and protein in TRB3 increased p0.05, and the down-regulation of TRB3 expression in the model group was significantly higher than that in the 4th week after treatment. Conclusion the expression of mRNA and protein in the model group can be reduced by inhibiting the expression of TRB3, increasing the phosphorylation of AKT and activating the PI3K/AKT signaling pathway.Promote the uptake and utilization of glucose in skeletal muscle cells and inhibit insulin resistance.
【作者單位】： 云南省第三人民醫(yī)院內(nèi)分泌科;昆明醫(yī)科大學(xué)生物化學(xué)與分子生物學(xué)系;昆明醫(yī)科大學(xué)第一附屬醫(yī)院糖尿病科;昆明醫(yī)科大學(xué)第一附屬醫(yī)院移植科;昆明學(xué)院醫(yī)學(xué)院生物化學(xué)教研室;
【基金】：國(guó)家自然科學(xué)基金項(xiàng)目(81360128) 云南省應(yīng)用基礎(chǔ)研究基金項(xiàng)目(2013FD052,2015FB046) 云南省教育廳研究基金項(xiàng)目(2012C006,2013C081)
【分類(lèi)號(hào)】：R587.1
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本文編號(hào)：1746423