黄芪多糖的胰岛素增敏作用及其对蛋白酪氨酸磷酸酯酶1B的影响

目的:探讨黄芪多糖(APS)对遗传性胰岛素抵抗小鼠的胰岛素增敏作用及其机制。方法:8周龄C57BL/6J小鼠分别饲以高脂饮食或正常饮食4周,高脂饮食小鼠以胰岛素耐量实验(ITT)证实成功复制胰岛素抵抗模型后,将动物随机分为2组:胰岛素抵抗+APS组APS 700 mg/(kg.d),灌胃],胰岛素抵抗组(等体积生理盐水灌胃)继续饲以高脂饮食;正常饮食小鼠随机分为对照组和APS组,APS剂量和方法同前。每组动物8只,继续喂养8周后取血检测血糖及胰岛素耐量,免疫印迹法检测骨骼肌胰岛素受体β亚单位(IR-β)和胰岛素受体底物1(IRS-1)的表达,以及蛋白酪氨酸磷酸酯酶1B(PTP1B)的活性。结果:胰岛素抵抗组小鼠体重增加,血糖、血胰岛素水平显著高于对照组,胰岛素敏感性明显低于对照组。经APS治疗8周后,胰岛素抵抗小鼠的体重、餐后血糖和血胰岛素水平显著降低;骨骼肌IR-β和IRS-1酪氨酸磷酸化水平显著增强,PTP1B活性显著降低。APS治疗对对照组小鼠无明显影响。结论:APS对胰岛素抵抗小鼠具有胰岛素增敏作用;其机制与增加骨骼肌IR-β和IRS-1酪氨酸磷酸化水平,抑制PTP1B活性,增强胰岛素信号转导有关。

Insulin-Sensitization of Astragalus Polysaccharide and Its Effect on Protein Tyrosine Phosphatase 1B

Objective: To investigate the effect of Astragalus polysaccharide(APS) on insulin-sensitization and its effect on protein tyrosine phosphatase 1B(PTP1B).Methods: Eight-week old C57BL/6J mice were fed with the high-fat diet for four weeks to establish insulin resistance(IR).The control and the high-fat fed mouse were then treated with APS(700 mg/kg per day) or the same amount of saline for eight weeks.Insulin sensitivity was identified by the insulin-tolerance test.Further analyses on the possible changes in insulin receptor subunit β(IR-β),insulin receptor substrate-1(IRS-1),and PTP1B expressions in skeletal muscle were performed by Western blotting.Results: The IR mice responded to APS with a significant decrease in body weight and plasma glucose,and improved insulin sensitivity.APS treatment reduced PTP1B activity,increased the insulin-induced tyrosine phosphorylation of IR-β and IRS-1 in the skeletal muscle of IR mice.There was no change in the activity of PTP1B in APS-treated normal control mice.Conclusion: APS enabled insulin-sensitizing and hypoglycemic activity at least in part by decreasing the activity of PTP1B,and increasing the activity of IR-β and IRS-1 in the skeletal muscles of IR C57BL/6J mice.