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作 者:王彦[1] 陈思思[2] 廉如[2] 陈显久[3] 杨静[1]
机构地区:[1]山西医科大学第一医院内分泌科,太原030001 [2]山西医科大学2004级七年制临床医学 [3]山西医科大学生物化学与分子生物学教研室
出 处:《中华内分泌代谢杂志》2012年第12期1016-1019,共4页Chinese Journal of Endocrinology and Metabolism
基 金:山西省科技攻关项目(20090321104)
摘 要:将3T3-L1前脂肪细胞诱导分化为成熟的脂肪细胞,用软脂酸制备脂肪细胞胰岛素抵抗模型,不同浓度的脂联素球状结构域(globular domain of adiponectin,gAd)干预已经产生胰岛素抵抗的3T3-L1脂肪细胞,葡萄糖氧化酶法检测培养液中葡萄糖的消耗量,实时荧光定量PCR法检测胰岛素受体底物(1RS)-1、磷脂酰肌醇3激酶(P13K)、蛋白激酶B(PKB)基因水平的变化,Western印迹检测IRS-1酪氨酸磷酸化水平。结果显示,与对照组相比,各实验组葡萄糖消耗量均显著增加(P〈0.01),且随着gAd浓度的增加.葡萄糖消耗量也逐渐增加;500ng/mlgAd组及1000ng/mlgAd组IRS—1、P13K、PKB的mRNA表达均比对照组显著增加(P〈0.05);同时,gAd可增加3T3-L1脂肪细胞胰岛素抵抗模型IRS-1酪氨酸磷酸化水平,且呈浓度依赖性.提示gAd能够促进3T3-LI脂肪细胞胰岛素抵抗模型葡萄糖的摄取,其机制可能与促进脂肪细胞胰岛素信号转导、改善胰岛素抵抗有关。Insulin resistance model of3T3-L1 adipocytes were prepared with plamotic acid. Adipocytes with generated insulin resistance were cultured with different concentrations of globular domain of adiponectin( gAd : 250, 500, 1 000 ng/ml). The cell culture medium glucose content was detected with the glucose oxidase method, the mRNA expressions of insulin receptor substrate-I ( IRS-1 ) , phosphatidylinositol-3 kinase ( PI3 K) , and protein kinase B(PKB) were detected with real-time quantitative PCR method. The phosphorylation of IRS-I was detected by Western blot. Compared with the control group, the experimental group showed significantly increased glucose consumption (P 〈 0. 01 ), and with the increasing gAd concentration, glucose consumption was gradually increasing. IRS-1 phosphorylation was increased gradually with the increasing concentration of gAd. These results suggest that gAd can promote glucose uptake by 3T3-L1 adipocyte model with generated insulin resistance. This may be correlated with promoting insulin signal transduction and improving insulin resistance in adipocytes.
关 键 词:脂联素球状结构域 3T3-L1脂肪细胞 胰岛素信号转导 胰岛素抵抗
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