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目的探讨mTOR及其下游效应因子S6K1在胰岛素抵抗(IR)发生中的作用。方法C57BL/6雄性小鼠20只随机平均分为正常饮食组(NC组)和高脂饮食组(HF组)。后者喂养14周后建立IR模型。检测两组血清胰岛素水平和葡萄糖耐量,显微镜下观察胰岛形态学变化;检测骨骼肌中mTOR和S6K1 mRNA的表达,以及mTOR、S6K1和其磷酸化水平蛋白的表达。结果与NC组相比,HF组小鼠表现出明显的IR症状,其体重和空腹胰岛素分别升高了21.99%(P<0.05)和181.82%(P<0.01);胰岛β细胞团面积也显著增加,糖耐量明显受损,骨骼肌细胞中mTOR mRNA和蛋白分别升高了25.61%(P<0.05)和37.41%(P<0.01),S6K1 mRNA和蛋白分别升高了54.98%(P<0.01)和37.36%(P<0.01),S6K1磷酸化水平蛋白表达在高脂饮食后升高了680.15%(P<0.01)。结论mTOR/S6K1信号通路与高脂饮食诱导IR的发生密切相关。
Objective To investigate the role of mTOR and its downstream effector S6K1 in insulin resistance (IR). Methods Twenty male C57BL / 6 mice were randomly divided into normal diet group (NC group) and high fat diet group (HF group). The latter fed 14 weeks after the establishment of IR model. Serum insulin and glucose tolerance were measured. Morphological changes of islets were observed under microscope. The expressions of mTOR and S6K1 mRNA and protein of mTOR, S6K1 and their phosphorylation were detected in skeletal muscle. Results Compared with the NC group, the HF group showed obvious IR symptoms. The body weight and fasting insulin increased by 21.99% (P <0.05) and 181.82% (P <0.01) respectively. The islet β-cell mass area also significantly increased (P <0.01). The mRNA and protein of S6K1 increased by 54.98% (P <0.01) in Skeletal muscle cells (P <0.01) ) And 37.36% (P <0.01) respectively. The phosphorylation level of S6K1 protein increased by 680.15% (P <0.01) after high-fat diet. Conclusion The mTOR / S6K1 signaling pathway is closely related to the induction of IR by high-fat diet.