Animal Models in Diabetes and Pregnancy

被引:142
作者
Jawerbaum, Alicia [1 ]
White, Veronica [1 ]
机构
[1] Univ Buenos Aires, Consejo Nacl Invest Cient & Tecn, Ctr Estudios Farmacol & Botan, Sch Med,Lab Reprod & Metab, Buenos Aires, DF, Argentina
关键词
NEURAL-TUBE DEFECTS; BETA-CELL MASS; GLUCOSE-INDUCED DYSMORPHOGENESIS; STREPTOZOTOCIN-TREATED RAT; ZINC SUPEROXIDE-DISMUTASE; ENDOTHELIAL GROWTH-FACTOR; ACTIVATED-RECEPTOR-GAMMA; FETAL ENDOCRINE PANCREAS; CONGENITAL HEART-DEFECTS; DELAYED LUNG MATURATION;
D O I
10.1210/er.2009-0038
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
The worldwide increase in the incidence of diabetes, the increase in type 2 diabetes in women at reproductive ages, and the cross-generation of the intrauterine programming of type 2 diabetes are the bases for the growing interest in the use of experimental diabetic models in order to gain insight into the mechanisms of induction of developmental alterations in maternal diabetes. In this scenario, experimental models that present the most common features of diabetes in pregnancy are highly required. Several important aspects of human diabetic pregnancies such as the increased rates of spontaneous abortions, malformations, fetoplacental impairments, and offspring diseases in later life can be approached by using the appropriate animal models. The purpose of this review is to give a practical and critical guide into the most frequently used experimental models in diabetes and pregnancy, discuss their advantages and limitations, and describe the aspects of diabetes and pregnancy for which these models are thought to be adequate. This review provides a comprehensive view and an extensive analysis of the different models and phenotypes addressed in diabetic animals throughout pregnancy. The review includes an analysis of the surgical, chemical-induced, and genetic experimental models of diabetes and an evaluation of their use to analyze early pregnancy defects, induction of congenital malformations, placental and fetal alterations, and the intrauterine programming of metabolic diseases in the offspring's later life. ( Endocrine Reviews 31: 680-701, 2010)
引用
收藏
页码:680 / 701
页数:22
相关论文
共 277 条
[1]   Is there a relationship between PCNA expression and diabetic placental development during pregnancy? [J].
Acar, Nuray ;
Korgun, Emin Turkay ;
Cayli, Sevil ;
Sahin, Zeliha ;
Demir, Ramazan ;
Ustunel, Ismail .
ACTA HISTOCHEMICA, 2008, 110 (05) :408-417
[2]  
Aerts L, 1979, J Dev Physiol, V1, P219
[3]   RAT FETAL ENDOCRINE PANCREAS IN EXPERIMENTAL DIABETES [J].
AERTS, L ;
VANASSCHE, FA .
JOURNAL OF ENDOCRINOLOGY, 1977, 73 (02) :339-&
[4]   Intra-uterine transmission of disease [J].
Aerts, L ;
Van Assche, FA .
PLACENTA, 2003, 24 (10) :905-911
[5]   THE DIABETIC INTRAUTERINE MILIEU HAS A LONG-LASTING EFFECT ON INSULIN-SECRETION BY B-CELLS AND ON INSULIN UPTAKE BY TARGET TISSUES [J].
AERTS, L ;
SODOYEZGOFFAUX, F ;
SODOYEZ, JC ;
MALAISSE, WJ ;
VANASSCHE, FA .
AMERICAN JOURNAL OF OBSTETRICS AND GYNECOLOGY, 1988, 159 (05) :1287-1292
[6]   MATERNAL DIABETES DURING PREGNANCY - CONSEQUENCES FOR THE OFFSPRING [J].
AERTS, L ;
HOLEMANS, K ;
VANASSCHE, FA .
DIABETES-METABOLISM REVIEWS, 1990, 6 (03) :147-167
[7]   Responses of mitochondrial biogenesis and function to maternal diabetes in rat embryo during the placentation period [J].
Alcolea, M. P. ;
Llado, I. ;
Garcia-Palmer, F. J. ;
Gianotti, M. .
AMERICAN JOURNAL OF PHYSIOLOGY-ENDOCRINOLOGY AND METABOLISM, 2007, 293 (03) :E636-E644
[8]   Adverse effects of hyperglycemia on kidney development in rats -: In vivo and in vitro studies [J].
Amri, R ;
Freund, N ;
Vilar, J ;
Merlet-Bénichou, C ;
Lelièvre-Pégorier, M .
DIABETES, 1999, 48 (11) :2240-2245
[9]   Taurine supplement in early life altered islet morphology, decreased insulitis and delayed the onset of diabetes in non-obese diabetic mice [J].
Arany, E ;
Strutt, B ;
Romanus, P ;
Remacle, C ;
Reusens, B ;
Hill, DJ .
DIABETOLOGIA, 2004, 47 (10) :1831-1837
[10]   Developmental programming of the metabolic syndrome by maternal nutritional imbalance: how strong is the evidence from experimental models in mammals? [J].
Armitage, JA ;
Khan, IY ;
Taylor, PD ;
Nathanielsz, PW ;
Poston, L .
JOURNAL OF PHYSIOLOGY-LONDON, 2004, 561 (02) :355-377