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作 者:陈思凡[1] 柯梁汝[2] 郑琳[1] 单智铭[2] 周妮曼[2] 冯翔[1]
机构地区:[1]中山大学公共卫生学院广东省营养膳食与健康重点实验室,广东广州510089 [2]中山大学中山医学院,广东广州510089
出 处:《食品科学》2010年第23期285-288,共4页Food Science
基 金:广东省医学科研基金资助项目(A2010143)
摘 要:目的:研究白藜芦醇(resveratrol,Res)对胰岛素抵抗状态下3T3-L1脂肪细胞葡萄糖代谢的影响,并探讨其分子机制。方法:用地塞米松诱导3T3-L1细胞建立胰岛素抵抗模型,用不同剂量Res进行干预,添加或不添加胰岛素刺激,测定各组细胞的葡萄糖消耗量,实时荧光定量PCR检测各组细胞的脂联素(adiponectin)、瘦素(leptin)和抵抗素(resistin)mRNA表达,Western blotting检测腺苷酸激活蛋白激酶(AMP-activated protein kinase,AMPK)的蛋白质表达及磷酸化水平。结果:各组细胞经胰岛素刺激,0.01、0.1、1μmol/L的Res组的葡萄糖消耗量分别是对照组的1.3、1.5、1.4倍(P<0.05),添加Res可促进脂联素、瘦素mRNA的表达,降低抵抗素mRNA表达,增加AMPKα的磷酸化水平。结论:Res可以明显改善胰岛素抵抗状态下3T3-L1细胞葡萄糖代谢。其机制可能是通过增加脂联素、瘦素表达,降低抵抗素表达从而介导AMPKα磷酸化实现的。Objective: To explore the effect and mechanism of resveratrol on glucose metabolism in insulin-resistant 3T3-L1 adipocytes. Methods: Insulin-resistant model was established by the induction of dexamethasone in 3T3-L1 adipocytes. The glucose consumption of insulin-resistant 3T3-L1 adipocytes with and without resveratrol stimulation was determined. The mRNA expression of leptin, adiponectin and resistin was determined by real time PCR, and the expression and phosphorylation of AMPKα were determined by Western blotting. Results: After insulin stimulation with the concentration of 0.01, 0.1μmol/L and 1μmol/L, resveratrol could increase the glucose consumption by 1.3, 1.5 folds and 1.4 folds compared with the control (P 0.05). Meanwhile, resveratrol could increase mRNA expression of adiponectin and leptin and decrease mRNA expression of resistin. Moreover, resveratrol increased the phosphorylation of AMPKα. Conclusion: Resveratrol can improve glucose metabolism in insulin-resistant 3T3-L1 adipocytes. The molecular mechanism may be the phosphorylation of AMPKα by increasing the expression of adiponectin and leptin and inhibiting the expression of resistin.
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