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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。
Objective: To investigate the effect of astragalus polysaccharide (APS) on insulin sensitivity in hereditary insulin resistance mice and its mechanism. Methods: The 8-week-old C57BL / 6J mice were fed a high-fat diet or normal diet for 4 weeks, respectively. The high fat diet mice were confirmed by the insulin tolerance test (ITT) to replicate the insulin resistance model successfully. The animals were randomly divided into two groups: Insulin resistance + APS group [APS 700 mg / (kg · d), gavage], insulin resistance group (equal volume of saline gavage) continue to feed high-fat diet; normal diet mice were randomly divided into control group and APS group , APS dose and method with the former. Eight rabbits in each group were sacrificed for 8 weeks and blood was taken to measure blood glucose and insulin resistance. Western blotting was used to detect the expression of insulin receptor beta subunit (IR-β) and insulin receptor substrate 1 (IRS-1) , And protein tyrosine phosphatase 1B (PTP1B) activity. Results: The body weight, blood glucose and insulin levels in insulin resistance group were significantly higher than those in control group, and insulin sensitivity was significantly lower than that in control group. After 8 weeks of APS treatment, the body weight, postprandial blood glucose and insulin levels in insulin-resistant mice decreased significantly. The levels of tyrosine phosphorylation of IR-β and IRS-1 in skeletal muscle were significantly increased and PTP1B activity was significantly decreased. APS treatment had no significant effect on the control mice. CONCLUSION: APS can enhance the insulin sensitivity of insulin resistance mice. The mechanism is related to increasing the tyrosine phosphorylation of IR-β and IRS-1, inhibiting the activity of PTP1B and enhancing insulin signal transduction.