Experimental IUGR and later diabetes

被引:81
作者
Martin-Gronert, M. S. [1 ]
Ozanne, S. E. [1 ]
机构
[1] Univ Cambridge, Dept Clin Biochem, Addenbrookes Hosp, Cambridge CB2 2QR, England
关键词
animal models; epigenetic modifications; insulin signalling; intrauterine growth restriction; low birth weight; type; 2; diabetes;
D O I
10.1111/j.1365-2796.2007.01800.x
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
It is widely accepted that an association exists between the intrauterine environment in which a fetus grows and develops and the subsequent development of type 2 diabetes. Any disturbance in maternal ability to provide nutrients and oxygen to the fetus can lead to fetal intrauterine growth restriction (IUGR). Here we will review IUGR in rodent models, in which maternal metabolism has been experimentally manipulated to investigate the molecular basis of the relationship between IUGR and development of type 2 diabetes in later life, and the identification of the molecular derangements in specific metabolically - sensitive organs/tissues.
引用
收藏
页码:437 / 452
页数:16
相关论文
共 121 条
[1]   Intra-uterine transmission of disease [J].
Aerts, L ;
Van Assche, FA .
PLACENTA, 2003, 24 (10) :905-911
[2]   The endocrine pancreas in virgin and pregnant offspring of diabetic pregnant rats [J].
Aerts, L ;
Vercruysse, L ;
VanAssche, FA .
DIABETES RESEARCH AND CLINICAL PRACTICE, 1997, 38 (01) :9-19
[3]  
AERTS L, 1990, FRONTIERS DIABETES R, V3, P561
[4]   Expression of PDX-1 is reduced in pancreatic islets from pups of rat dams fed a low protein diet during gestation and lactation [J].
Arantes, VC ;
Teixeira, VPA ;
Reis, MAB ;
Latorraca, MQ ;
Leite, AR ;
Carneiro, EM ;
Yamada, AT ;
Boschero, AC .
JOURNAL OF NUTRITION, 2002, 132 (10) :3030-3035
[5]  
Barker D.J. P., 1994, MOTHERS BABIES DIS L
[6]   METABOLIC CLEARANCE RATE, BLOOD PRODUCTION, INTERCONVERSION AND TRANSPLACENTAL PASSAGE OF CORTISOL AND CORTISONE IN PREGNANCY NEAR TERM [J].
BEITINS, IZ ;
BAYARD, F ;
ANCES, IG ;
KOWARSKI, A ;
MIGEON, CJ .
PEDIATRIC RESEARCH, 1973, 7 (05) :509-519
[7]   Placental 11 beta-hydroxysteroid dehydrogenase: A key regulator of fetal glucocorticoid exposure [J].
Benediktsson, R ;
Calder, AA ;
Edwards, CRW ;
Seckl, JR .
CLINICAL ENDOCRINOLOGY, 1997, 46 (02) :161-166
[8]   Development of β-cell mass in fetuses of rats deprived of protein and/or energy in last trimester of pregnancy [J].
Bertin, E ;
Gangnerau, MN ;
Bellon, G ;
Bailbé, D ;
De Vacqueur, AA ;
Portha, B .
AMERICAN JOURNAL OF PHYSIOLOGY-REGULATORY INTEGRATIVE AND COMPARATIVE PHYSIOLOGY, 2002, 283 (03) :R623-R630
[9]   GESTATIONAL HYPERGLYCEMIA AND INSULIN RELEASE BY THE FETAL-RAT PANCREAS INVITRO - EFFECT OF AMINO-ACIDS AND GLYCERALDEHYDE [J].
BIHOREAU, MT ;
KTORZA, A ;
PICON, L .
DIABETOLOGIA, 1986, 29 (07) :434-439
[10]   Oxidant status in maternal and cord plasma and placental tissue in gestational diabetes [J].
Biri, A ;
Onan, A ;
Devrim, E ;
Babacan, F ;
Kavutcu, M ;
Durak, I .
PLACENTA, 2006, 27 (2-3) :327-332