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目的:制备一种发病过程类似人类的糖调节受损大鼠模型。建立评价大鼠糖调节受损的诊断标准。方法:SPF级Wistar雄性大鼠高脂高糖饲料喂养12周,诱发大鼠胰岛素抵抗及胰岛β细胞损伤,建立大鼠糖调节受损模型。通过本实验制定的诊断标准筛选IGR大鼠模型,对筛选出的大鼠进行各项指标的测定以明确诊断标准的合理性。结果:筛选出的大鼠体重较对照组明显升高(P<0.05);空腹及OGTT 2h血糖较对照组有明显升高且存在显著差异(P<0.05);高糖钳夹实验胰岛素输注速率较对照组降低且存在显著差异(P<0.05);正糖钳夹实验第1时相、第2时相胰岛素分泌均较对照组低且存在显著差异(P<0.05)。结论:本实验糖调节受损大鼠模型造模成功,诊断标准具有科学性。本模型的建立简单易行,成模率高,是人类糖调节受损发病机制及干预手段研究的理想动物模型。
OBJECTIVE: To prepare a rat model of impaired glucose regulation similar to humans in the pathogenesis. Establish a diagnostic criteria for assessing impaired glucose regulation in rats. Methods: Rats with SPF grade Wistar were fed with high-fat and high-sugar diet for 12 weeks to induce insulin resistance and pancreatic β-cell injury in rats and to establish a model of impaired glucose regulation in rats. IGR rat model was screened through the diagnostic criteria developed in this experiment, and the indexes of the selected rats were determined to confirm the rationality of diagnostic criteria. Results: The body weight of the selected rats was significantly higher than that of the control group (P <0.05). The fasting blood glucose and blood glucose of OGTT 2h group were significantly higher than those of the control group (P <0.05) (P <0.05). Compared with the control group, the rate of insulin secretion in the first phase and the second phase of the positive glucose clamp experiment was significantly lower than that of the control group (P <0.05). Conclusion: The rat model of impaired glucose regulation succeeded in modeling and the diagnostic criteria were scientific. The establishment of this model is simple and easy, with high rate of formation, which is an ideal animal model for studying the pathogenesis and intervention of human impaired glucose regulation.