摘要
目的探讨果糖诱导小鼠胰岛素抵抗机制。方法小鼠随机分为3组,分别为单纯饮水的正常对照组,10%果糖饮水组,10%果糖+精氨酸饮水组。实验时间为4周,期间,分析血清促胰岛素肽(GIP)和胰高血糖素样肽-1(GLP-1)水平;4周后,测定各组小鼠空腹血糖和胰岛素水平,计算胰岛素抵抗指数;分析各组小鼠肝脏活性氧簇(ROS)水平。结果 10%果糖饮水导致小鼠发生胰岛素抵抗,果糖干预不影响小鼠血清GIP和GLP-1水平,但肝脏组织ROS水平升高(P<0.05);10%果糖+精氨酸饮水组胰岛素抵抗指数没有显著变化,血清GLP-1水平升高,肝脏组织ROS水平没有显著变化。结论 10%果糖饮水使小鼠肝脏组织ROS水平升高,而血清GLP-1水平不升高,无法发挥GLP-1对肝脏的保护作用,最终升高的ROS引起小鼠胰岛素抵抗。
【Objective】 To explore the mechanism of insulin resistance in mice induced by fructose solution drinking. 【Methods】 Mice were randomly assigned into 3 groups including normal control group, 10%fructose group and 10% fructose ＋ arginine group. All the groups were treated for 4 weeks. Serum glucagonlike peptide-1（GLP-1） and glucose-dependent insulin-releasing polypeptide（GIP） levels were analyzed during the treatment. After 4 weeks, fasting blood glucose and serum insulin levels were determined, index of insulin resistance was calculated by HOMA-IR, and liver reactive oxygen species（ROS） level was measured. 【Results】Drink of 10% fructose induced insulin resistance, significantly elevated the index of insulin resistance and liver ROS level compared to the control group（P 0.05）; whereas the levels of serum GLP-1 and GIP were not significantly different from those of the control group. However, in 10% fructose ＋ arginine group, the index of insulin resistance was not significantly different from that of the control group although it was higher,serum GLP-1 elevated significantly compared with that of the control group（P 0.05）, the liver ROS level was not significantly different from that of the control group. 【Conclusions】 Drinking 10% fructose may result in increased ROS level in liver tissue without elevating serum GLP-1 level; so the toxic effect of ROS can not be prevented by GLP-1, leading to insulin resistance in mice.
出处
《中国现代医学杂志》
CAS
北大核心
2015年第36期7-11,共5页
China Journal of Modern Medicine
