持续果糖饮水诱导小鼠胰岛素抵抗机制

Mechanism of insulin resistance in mice induced by continuous fructose solution drinking

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。

Abstract:

【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 glucagon-like 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.