Author:

Keywords:

Animals, Diabetes Mellitus, Experimental, Disease Models, Animal, Embryonic and Fetal Development, Female, Fetal Blood, Fetal Growth Retardation, Insulin, MEDLINE, Malnutrition, Pregnancy, Pregnancy in Diabetics, Rats, Science & Technology, Life Sciences & Biomedicine, Obstetrics & Gynecology, STREPTOZOTOCIN-DIABETIC RATS, LOW-PROTEIN-DIET, ENDOTHELIUM-DEPENDENT VASODILATION, IMPAIRED GLUCOSE-TOLERANCE, BETA-CELL MASS, BLOOD-PRESSURE, ENDOCRINE PANCREAS, PREGNANT RATS, 11-BETA-HYDROXYSTEROID DEHYDROGENASE, AMINO-ACIDS, 1114 Paediatrics and Reproductive Medicine, Obstetrics & Reproductive Medicine, 3215 Reproductive medicine, 4204 Midwifery

Abstract:

OBJECTIVE: In the present review we discuss rat models in which intra-uterine growth restriction is obtained through pharmacological (streptozotocin), dietary (global food restriction, low protein diet), or surgical (uterine artery ligation) manipulation of the maternal animal. METHODS: A MEDLINE search was performed on rat models of intrauterine growth restriction (IUGR), ie, streptozotocin, food restriction, low protein diet, or uterine artery ligation and pregnancy and fetal programming, long-term effects or adult offspring. RESULTS: We address the impact of the different maternal conditions for the fetal and neonatal development. The rat models we concentrate on were all associated with fetal hypoinsulinemia and intrauterine growth restriction. Both fetus and neonate adapt to the altered perinatal environment. Some of these adaptations may predispose the offspring to the development of insulin resistance, cardiovascular disease, obesity, and even overt diabetes in later life. CONCLUSION: The adaptations of the fetal metabolism to the altered intrauterine environment have consequences for the offspring, persisting into adulthood and into the next generation.