The physiology of obese-hyperglycemic mice [ob/ob mice]

被引:241
作者
Lindström, Per [1 ]
机构
[1] Umea Univ, Dept Integrat Med Biol, Sect Histol & Cell Biol, S-90187 Umea, Sweden
来源
THESCIENTIFICWORLDJOURNAL | 2007年 / 7卷
关键词
obese hyperglycemic; mice; leptin; pancreatic islets; insulin resistance; immunity; and reproduction;
D O I
10.1100/tsw.2007.117
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
This review summarizes key aspects of what has been learned about the physiology of leptin deficiency as it can be observed in obese-hyperglycemic ob/ob mice. These mice lack functional leptin. They are grossly overweight and hyperphagic, particularly at young ages, and develop severe insulin resistance. They have been used as a model for obesity and as a rich source of pancreatic islets with high insulin release capacity. The leptin deficiency manifests also with regard to immune function, the cardiovascular system including angiogenesis, supportive tissue function, malignancies, and reproductive function. ob/ob Mice are well suited for studies on the interaction between leptin and insulin, and for studies on initial aspects of metabolic disturbances leading to type-2diabetes.
引用
收藏
页码:666 / 685
页数:20
相关论文
共 307 条
[1]   Pancreatic β-cells from obese-hyperglycemic mice are characterized by excessive firing of cytoplasmic Ca2+ transients [J].
Ahmed, M ;
Grapengiesser, E .
ENDOCRINE, 2001, 15 (01) :73-78
[2]   Use of genetic mouse models in the study of diabetic nephropathy [J].
Allen T.J. ;
Cooper M.E. ;
Lan H.Y. .
Current Atherosclerosis Reports, 2004, 6 (3) :197-202
[3]   A HISTOCHEMICAL AND MORPHOLOGICAL-STUDY OF SKELETAL-MUSCLE FROM OBESE HYPERGLYCEMIC OB/OB MICE [J].
ALMOND, RE ;
ENSER, M .
DIABETOLOGIA, 1984, 27 (03) :407-413
[4]   Role of changes in cardiac metabolism in development of diabetic cardiomyopathy [J].
An, Ding ;
Rodrigues, Brian .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2006, 291 (04) :H1489-H1506
[5]   DNA-REPLICATION IN TRANSPLANTED AND ENDOGENOUS PANCREATIC-ISLETS OF OBESE-HYPERGLYCEMIC MICE AT DIFFERENT STAGES OF THE SYNDROME [J].
ANDERSSON, A ;
KORSGREN, O ;
NAESER, P .
METABOLISM-CLINICAL AND EXPERIMENTAL, 1989, 38 (10) :974-978
[6]  
[Anonymous], NATURE GENET
[7]   INCREASED EXPRESSION OF MITOCHONDRIAL-ENCODED GENES IN SKELETAL-MUSCLE OF HUMANS WITH DIABETES-MELLITUS [J].
ANTONETTI, DA ;
REYNET, C ;
KAHN, CR .
JOURNAL OF CLINICAL INVESTIGATION, 1995, 95 (03) :1383-1388
[8]  
BAETENS D, 1978, DIABETES, V27, P1, DOI 10.2337/diabetes.27.1.1
[9]  
BAILEY CJ, 1987, INT J OBESITY, V11, P175
[10]   ROLE OF ADRENAL-GLANDS IN THE DEVELOPMENT OF ABNORMAL GLUCOSE AND INSULIN HOMEOSTASIS IN GENETICALLY-OBESE (OB/OB) MICE [J].
BAILEY, CJ ;
DAY, C ;
BRAY, GA ;
LIPSON, LG ;
FLATT, PR .
HORMONE AND METABOLIC RESEARCH, 1986, 18 (06) :357-360