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作 者:尚文斌[1] 郭超[1] 赵娟[1] 于希忠[1] 张颢[1]
机构地区:[1]南京中医药大学第一临床医学院临床医学实验中心,江苏南京210023
出 处:《中国中药杂志》2014年第22期4448-4452,共5页China Journal of Chinese Materia Medica
基 金:国家自然科学基金项目(81073110)
摘 要:人参的主要活性成分人参皂苷Rb1(gisenoside Rb1,Rb1)能够激活胰岛素信号通路,促进脂肪细胞葡萄糖转运体(glucose transporters,GLUTs)的转位,增加葡萄糖的转运,但是其对GLUTs表达的影响尚不清楚。该研究利用肥胖糖尿病小鼠和体外脂肪细胞实验,主要研究Rb1对脂肪细胞GLUTs表达以及葡萄糖代谢的影响。在雄性肥胖糖尿病db/db小鼠中,按20 mg·kg-1体重每天腹腔注射Rb1治疗14 d后,Rb1明显降低肥胖糖尿病小鼠的胰岛素抵抗指数(HOMA-IR)(P<0.05,n=5),胰岛素水平和空腹血糖有下降趋势;在糖尿病小鼠附睾脂肪中,Rb1促使GLUT1和GLUT4蛋白表达量以及AKT磷酸化水平上调恢复;体外培养分化成熟的3T3-L1脂肪细胞中,加入10μmol·L-1Rb1处理24 h后,葡萄糖消耗显著增加(P<0.05,n=4),同时GLUT1和GLUT4的mRNA和蛋白表达量均显著上调(P<0.05,n=3),此外,在3T3-L1脂肪细胞中,Rb1处理3 h后,脂肪细胞的AKT被磷酸化激活。该研究结果表明人参皂苷Rb1不仅能够激活胰岛素信号通路,还能上调葡萄糖转运体的表达,促进葡萄糖的消耗,进一步阐明其改善机体胰岛素抵抗和糖代谢异常的作用机制。Previous studies have shown that ginsenoside Rb1( Rb1),one of active components in ginseng,can activate insulin signaling pathway and promote translocation of glucose transporters( GLUTs) to increase glucose uptake in adipocytes. However,the effect of Rb1 on the expressions of GLUTs remains unknown. In this study,the effects of Rb1 on GLUT1 and GLUT4 were observed in3T3-L1 adipocytes and epididymal adipose tissue of db / db obese diabetic mice. Male db / db mice were treated with Rb1 by intraperitoneal injection at the dosage of 20 mg·kg^-1for 14 d. Rb1 reduced HOMA-IR significantly( P〈 0. 05,n = 5),and FBG and FINS sowed declining trend after treatment with Rb1. Rb1 recovered the expressions of GLUT1 and GLUT4 and phosphorylation of AKT in adipose tissue of db / db mice. In vitro,glucose consumption in 3T3-L1 adipocytes treated with 10 μmol·L^-1Rb1 for 24 h was elevated( P〈 0. 05,n = 3),and mRNA of GLUT1 and GLUT4 were up-regulated( P〈 0. 05,n = 3) and proteins of GLUT1 and GLUT4 were also increased. AKT was activated in adipocytes treated with Rb1 for 3 h. It can be concluded that ginsenoside Rb1 can up-regulate the expression of GLUTs in adipose tissue,in addition to activate insulin signalling pathway,which may partially account for its insulin sensitizing activity and regulating effect of glucose metabolism.
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