[1]李传伟,牛佳鹏,阎胜利,等.高尿酸血症致糖尿病大鼠模型构建方法研究[J].青岛大学学报(医学版),2018,54(04):379-383.[doi:10.11712/jms201804001]
 LI Chuanwei,NIU Jiapeng,YAN Shengli,et al.A STUDY ON THE METHOD FOR ESTABLISHING A RAT MODEL OF DIABETES INDUCED BY HYPERURICEMIA[J].JOURNAL OF QINGDAO UNIVERSITY (MEDICAL SCIENCES),2018,54(04):379-383.[doi:10.11712/jms201804001]
点击复制

高尿酸血症致糖尿病大鼠模型构建方法研究()
分享到:

《青岛大学学报(医学版)》[ISSN:2096-5532/CN:37-1217/R]

卷:
第54卷
期数:
2018年04期
页码:
379-383
栏目:
出版日期:
2018-07-05

文章信息/Info

Title:
A STUDY ON THE METHOD FOR ESTABLISHING A RAT MODEL OF DIABETES INDUCED BY HYPERURICEMIA
文章编号:
2096-5532(2018)04-0379-05
作者:
李传伟1牛佳鹏2阎胜利2孟冬梅2陈西广1邢士超2
(1 中国海洋大学海洋生命学院生化与海洋生物材料实验室,山东 青岛 266003; 2 青岛大学附属医院痛风实验室)
Author(s):
LI Chuanwei NIU Jiapeng YAN Shengli MENG Dongmei CHEN Xiguang XING Shichao
(Biochemical and Marine Biological Materials Laboratory, College of Marine Life Sciences, Ocean University of China, Qingdao 266003, China)
关键词:
高尿酸血症糖尿病2型模型动物
Keywords:
hyperuricemia type 2 diabetes models animal
分类号:
R589.7;R587.1
DOI:
10.11712/jms201804001
文献标志码:
A
摘要:

目的 拟建立一种高尿酸血症致糖尿病的典型动物模型。
方法 选取70只12周龄Wistar大鼠,随机分为对照组(A组,30只)和模型组(B组,40只)。A组大鼠给予普通饮食,蒸馏水灌胃。B组大鼠饮食分两个阶段:第一阶段,饲喂高酵母饲料,腺嘌呤溶液(100 mg?kg-1?d-1)灌胃;在大鼠血尿酸(SUA)水平显著下降时进入第二阶段,此阶段继续喂食高酵母饲料,但灌胃的腺嘌呤溶液剂量改为50 mg?kg-1?d-1,同时给予氧嗪酸钾皮下注射。实验期间监测大鼠SUA、血糖、胰岛素等相关生化指标,观察并记录大鼠的进食和排泄情况、体质量变化及精神状态。
结果 与A组相比,B组大鼠自建模第2周起SUA水平明显升高(t=4.92~16.24,P<0.05);B组大鼠空腹胰岛素及葡萄糖耐量试验(OGTT) 2 h胰岛素水平随SUA的升高而降低,与A组相比,均自第3周起显现出持续的统计学差异(t=2.679~12.904,P<0.05);与A组相比,B组大鼠空腹血糖及OGTT 2 h血糖水平升高,自第10周起表现出统计学差异(t=2.910~13.539,P<0.05)。自第9周起,B组大鼠表现出典型的糖尿病临床症状:多尿、多饮、消瘦、精神萎靡、活动减少。
结论 造模大鼠的各项指标与临床症状相符,表明高尿酸血症致糖尿病大鼠模型构建成功。



 

Abstract:
Objective To establish a typical animal model of diabetes induced by hyperuricemia.
Methods A total of 70 12-week-old Wistar rats were randomly divided into control group (group A, n=30) and model group (group B, n=40). The rats in group A were given a normal diet and intragastric administration of distilled water. The rats in group B were fed in two stages. In the first stage, high-yeast feed was provided, and adenine solution (100 mg?kg-1?d-1) was given by gavage. The second stage of feeding began when the level of rat serum uric acid (SUA) decreased significantly. At this stage, the supply of high-yeast feed continued, but the amount of adenine solution was decreased to 50 mg?kg-1?d-1; meanwhile, subcutaneous injection of potassium oxonate was given to these rats. During the experiment, the rats were monitored for biochemical parameters such as SUA, blood glucose, and insulin, and their food intake, excretion, body weight, and mental status were observed and recorded.
Results Compared with group A, group B had a significantly increased level of SUA since the second week of modeling (t=4.92-16.24, P<0.05). In group B, the levels of fasting insulin and oral glucose tolerance test (OGTT) 2 h insulin decreased with the increase in SUA, and both were significantly different from those in group A since the 3rd week (t=2.679-12.904, P<0.05); the levels of fasting blood glucose and OGTT 2 h blood glucose increased and were significantly different from those in group A since the 10th week (t=2.910-13.539, P<0.05). Since the 9th week, the rats in group B showed typical clinical symptoms of diabetes: polyuria, polydipsia, weight loss, low spirit, and decreased activity.
Conclusion The indices of the model rats were consistent with the clinical symptoms, which indicates the successful establishment of a rat model of diabetes induced by hyperuricemia.
更新日期/Last Update: 2018-07-08