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目的 通过研究偏钒酸钠对小鼠的血糖及葡萄糖磷酸化关键酶的影响 ,探讨偏钒酸钠降血糖作用的可能机制。方法 将糖尿病小鼠和正常对照小鼠 ,随机分为口服偏钒酸钠组和非口服偏钒酸钠组 ,分别饮用 2 0 0mg/L偏钒酸钠溶液和 80mmol/L的NaCl对照溶液 ,持续 5周。在实验第 0至 5周的每周末 ,对各组小鼠的血糖、肝脏葡萄糖激酶、肌肉己糖激酶以及胰岛素水平进行检测。结果 在给予偏钒酸钠前 ,糖尿病小鼠血糖水平明显高于正常对照组 ,服药 1周后 ,血糖值即由(18 77± 1 2 8)mmol/L下降至 (8 94± 0 94 )mmol/L ,接近正常水平 ;其肝脏葡萄糖激酶和肌肉己糖激酶的活性则显著升高 ,分别由 (1 2 9± 0 6 4 )mIU·min-1·mg-1蛋白质和 (1 93± 0 5 0 )mIU·min-1·mg-1蛋白质上升至 (15 36± 1 5 7)mIU·min-1·mg-1蛋白质和 (18 6 2± 1 71)mIU·min-1·mg-1蛋白质 (P <0 0 1) ;而在服药前后糖尿病小鼠的胰岛素水平差异均无显著性。上述作用在小鼠服药期间始终存在。相关分析显示 ,糖尿病小鼠的血糖水平与葡萄糖激酶和己糖激酶的活性呈显著的负相关性。结论 偏钒酸钠的降血糖作用并不依赖于体内胰岛素水平的增加 ;改善糖尿病小鼠体内不良的葡萄糖磷酸化过程 ,可能是偏钒酸钠降血糖作用的机制之一。
Objective To investigate the possible mechanism of hypoglycemic effect of sodium metavanadate by studying the effect of sodium metavanadate on the blood glucose and key enzymes of glucose phosphorylation in mice. Methods Diabetic mice and normal control mice were randomly divided into oral sodium metavanadate group and non-oral sodium metavanadate group, drinking 200 mg / L sodium metavanadate solution and 80 mmol / L NaCl control solution respectively, For 5 weeks. At the end of each week from week 0 to week 5 of the experiment, the blood glucose, liver glucokinase, muscle hexokinase and insulin levels in each group of mice were examined. Results Before administration of sodium metavanadate, the blood glucose level of diabetic mice was significantly higher than that of the normal control group. After one week of treatment, the blood glucose level decreased from 18 77 ± 1 28 mmol / L to 8 94 ± 0 94, mmol / L, which was close to the normal level. The activities of hepatic glucokinase and muscle hexokinase were significantly increased by (1 29 ± 0 64) mIU · min-1 · mg-1 protein and (1 93 ± The protein of mU · min-1 · mg-1 increased to (15 36 ± 157) mIU · min-1 · mg-1 protein and (18 6 2 ± 1 71) mIU · min-1 · mg -1 protein (P <0.01). However, there was no significant difference in insulin levels between diabetic mice before and after taking the drug. The above effect always exists during the administration of the mice. Correlation analysis showed that there was a significant negative correlation between the blood glucose level and the activities of glucokinase and hexokinase in diabetic mice. CONCLUSION: The hypoglycemic effect of sodium metavanadate does not depend on the increase of insulin level in vivo. Improper glucose phosphorylation in diabetic mice may be one of the mechanisms of hypoglycemic effect of sodium metavanadate.