Rat placental amino acid transport after protein-deprivation-induced intrauterine growth retardation.

Introduction The placenta is responsible for nutrient delivery to the fetus by the combined action of transport activities in the apical (maternal-facing) and basal (fetal-facing) membranes. We have described the developmental regulation of cationic amino acid transport in the rat placenta [I]. During the period of greatest fetal nutritional need, the final third of gestation, the placenta up-regulates the production of cationic transport proteins. In humans, intrauterine growth retardation (IUGR) affects a significant number of pregnancies. The deleterious effects of IUGR are not limited to gestational development, but rather are seen throughout the life of the child [2]. Factors contributing to IUGR in humans range from pathological conditions to alcohol, cocaine and tobacco abuse and poor maternal nutrition [3]. Although it has been documented that protein and protein-calorie malnutrition result in smaller fetuses with poor developmental outcomes, the mechanisms responsible have not been well described [4,5]. The multifactorial origins of IUGR in the human makes the examination of individual causes difficult. For this reason, we have chosen to investigate the effects of maternal protein deprivation in an animal model of IUGR. Previous work showed that rat dams deprived of both protein and calories throughout gestation exhibit decreased delivery of 2-aminoisobutyric acid (AIB), a System A substrate [6], to the fetus [7,8]. In contrast, Ahokas et al. [9] saw no significant difference in the fetal delivery of AIB after maternal calorie deprivation. Given that these previous studies examined amino acid transport in models deficient in both total calories and protein, one cannot distinguish the contribution of each separately. The present study uses apicaland basalenriched plasma-membrane vesicle preparations to show that maternal isocaloric protein deprivation causes a down-regulation of selected placen-