The study aimed at improving experimental diabetic animal models and looking for excellent models of human - like pathogenic process of diabetes became much more significant in the pathogenesis of diabetes and its complications.Group A was administrated once with 120 mg·kg-1 STZ by intraperitoneal injection;Group B was administrated once every one days for total of three times with 20,15 and 10 mg·kg-1 respectively by intraperitoneal injection; control group was administrated with citrate buffer only in the same way. The blood glucose and glycosylated hemoglobin levels,body weight change,daily food and water intake were observed. The success rate and model features of the modeling methods were compared. The blood glucose and glycosylated hemoglobin levels of all experimental groups were significantly higher than those of control group,and all the groups suffered from weight loss,polydipsia and other typical clinical symptoms of diabetes. The success rate of Group B was higher than those of Group A. The mouse of Group A reached the clinical symptoms of diabetes mellitus in 3 days after STZ administrated,with higher level of blood glucose (26.5±1.46 mmol·L-1)than the Group B that the blood glucose reach 19.2±1.07 mmol·L-1 after STZ administrated 4 weeks. The results showed that the mouse had a higher insulin level,but a less damage to β-cells of Group B produced a IGT (Impaired Glucose Tolerance)slowly after STZ injection.Multiple low-dose administration of STZ through tail vein making a less damage to β-cells,it induced IGT of the experimental rats slowly,which could be a better simulation of fasting blood glucose of clinical diabetic patients than traditional method; the method was even closer to the pathogenesis of diabetes,as well as the disease mechanism research.% 研究旨在通过改良传统链脲佐菌素（STZ）诱导 I 型糖尿病动物模型的注射剂量和诱导方式，探究一种能够诱导小鼠产生迟发性糖耐量异常的动物模型。小鼠随机分三组，A 组通过腹腔注射方式按体重比120 mg·kg-1注射 STZ；B 组每间隔一日分别按体重比20、15和10 mg·kg-1腹腔注射 STZ；对照组只注射柠檬酸-柠檬酸钠（pH4.4）缓冲液。观察两种方法造模成功率、造模组血糖、糖基化血红蛋白（GHbA1c）、体重变化，糖耐量变化。两种不同方法造模组，血糖、糖基化血红蛋白均明显高于对照组，并出现“三多一少”的糖尿病典型病征。A 组 STZ 注射一周后空腹血糖（26.5±1.46 mmol·L-1）一直维持较高水平，B 组在 SZT注射后小鼠血糖升高缓慢，至第4周后升至（19.2±1.07 mmol·L-1）。成模后的血清胰岛素水平和 GHbA1c 水平结果表明，B 组方法获得的动物模型胰腺β细胞破坏程度较低，血糖上升更为缓慢。通过小剂量腹腔多次注射，可减少胰腺β细胞的破坏程度，诱导小鼠模型缓慢产生糖耐量异常，较传统方法能更好模拟糖尿病患者的真实空腹血糖，较准确地反映糖尿病的发病过程。
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