MOLECULAR APPROACH TO INTRAUTERINE GROWTH-RETARDATION - AN OVERVIEW OF RECENT DATA

Citation
E. Alsat et al., MOLECULAR APPROACH TO INTRAUTERINE GROWTH-RETARDATION - AN OVERVIEW OF RECENT DATA, Reproduction, fertility and development, 7(6), 1996, pp. 1457-1464
Citations number
73
Categorie Soggetti
Reproductive Biology","Developmental Biology
ISSN journal
10313613
Volume
7
Issue
6
Year of publication
1996
Pages
1457 - 1464
Database
ISI
SICI code
1031-3613(1996)7:6<1457:MATIG->2.0.ZU;2-L
Abstract
Consideration of the abnormal regulation of fetal growth leading to in trauterine growth retardation must take account of the fundamental dif ferences between the regulation of growth before and after birth. The significance of endocrine regulators of growth differs greatly in uter o. During the first trimester of pregnancy, embryonic growth might be controlled at the level of the individual organs by nutrient supply an d by locally active growth factors. Later, fetal growth depends essent ially upon materno-placental cooperation in delivering nutrients to th e fetus. Therefore the major role of hormones in fetal growth is to me diate utilization of available substrate. Fetal growth seems to be reg ulated by fetal insulin, IGF-1 and certainly IGF-2, while growth hormo ne has only a secondary role to play. In late gestation, placental siz e and fetal growth rate are well correlated, pointing to a key role of the placenta in the regulation of fetal growth. It is therefore of im portance to understand the molecular mechanisms involved in regulating placental development and endocrine functions. TGF alpha and EGF migh t play a major role as suggested by the modulation of their receptors with placental development, and by the specific alterations of epiderm al growth factor receptors in intrauterine growth retardation. In addi tion, human placenta secretes specifically placental growth hormone. T he concentration of placental growth hormone is significantly decrease d in sera of pregnant women bearing a fetus with intrauterine growth r etardation.