Development and application of rodent models for type 2 diabetes

被引:129
作者
Chen, D [1 ]
Wang, MW [1 ]
机构
[1] Chinese Acad Sci, Shanghai Inst Mat Med, Natl Ctr Drug Screening, Shanghai 201203, Peoples R China
关键词
pharmacology; rodents; type; 2; diabetes;
D O I
10.1111/j.1463-1326.2004.00392.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The increasing worldwide incidence of diabetes in adults constitutes a global public health burden. It is predicted that by 2025, India, China and the United States will have the largest number of people with diabetes [1]. According to the 2003 estimates of the International Diabetes Federation, the diabetes mellitus prevalence in the USA is 8.0% and approximately 90-95% of diabetic Americans have type 2 diabetes - about 16 million people. Type 2 diabetes is a complex, heterogeneous, polygenic disease characterized mainly by insulin resistance and pancreatic P-cell dysfunction. Appropriate experimental models are essential tools for understanding the molecular basis, pathogenesis of the vascular and neural lesions, actions of therapeutic agents and genetic or environmental influences that increase the risks of type 2 diabetes. Among the animal models available, those developed in rodents have been studied most thoroughly for reasons such as short generation time, inherited hyperglycaemia and/or obesity in certain strains and economic considerations. In this article, we review the current status of most commonly used rodent diabetic models developed spontaneously, through means of genetic engineering or artificial manipulation. In addition to these models, the Psammomys obesus, rhesus monkeys and many other species are studied intensively and reviewed by Shaffir [2], Bailey and Flatt [3,4] and Hansen [5].
引用
收藏
页码:307 / 317
页数:11
相关论文
共 79 条
[1]   Altered endothelial/pericyte ratio in Goto-Kakizaki rat retina [J].
Agardh, CD ;
Agardh, E ;
Zhang, H ;
Ostenson, CG .
JOURNAL OF DIABETES AND ITS COMPLICATIONS, 1997, 11 (03) :158-162
[2]  
Bailey D. H., 1993, IEEE Parallel & Distributed Technology: Systems & Applications, V1, P43, DOI 10.1109/88.219861
[3]  
Bailey SCC, 2002, J TURBUL, V3
[4]   Hepatic expression of microsomal triglyceride transfer protein and in vivo secretion of triglyceride-rich lipoproteins are increased in obese diabetic mice [J].
Bartels, ED ;
Lauritsen, M ;
Nielsen, LB .
DIABETES, 2002, 51 (04) :1233-1239
[5]   Genetic manipulation of insulin signaling, action and secretion in mice - Insights into glucose homeostasis and pathogenesis of type 2 diabetes [J].
Baudry, A ;
Leroux, L ;
Jackerott, M ;
Joshi, RL .
EMBO REPORTS, 2002, 3 (04) :323-328
[6]   Actions of CCK in the controls of food intake and body weight: Lessons from the CCK-A receptor deficient OLETF rat [J].
Bi, S ;
Moran, TH .
NEUROPEPTIDES, 2002, 36 (2-3) :171-181
[7]  
COLEMAN DL, 1982, DIABETES, V31, P1
[8]   LESSONS FROM STUDIES WITH GENETIC FORMS OF DIABETES IN THE MOUSE [J].
COLEMAN, DL .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1983, 32 (07) :162-164
[9]   IMPAIRED EXPRESSION AND FUNCTIONAL-ACTIVITY OF THE BETA(3)-ADRENERGIC AND BETA(1)-ADRENERGIC RECEPTORS IN ADIPOSE-TISSUE OF CONGENITALLY OBESE (C57BL/6J OB/OB) MICE [J].
COLLINS, S ;
DANIEL, KW ;
ROHLFS, EM ;
RAMKUMAR, V ;
TAYLOR, IL ;
GETTYS, TW .
MOLECULAR ENDOCRINOLOGY, 1994, 8 (04) :518-527
[10]  
Combs TP, 2002, ENDOCRINOLOGY, V143, P998, DOI 10.1210/endo.143.3.8662