Effect of low-protein diet-induced intrauterine growth retardation
on rat placental amino acid transport.
Malandro, Marc S., Mark J. Beveridge, Michael S. Kilberg, and Donald
A. Novak.
Departments of Biochemistry and Molecular Biology and Pediatrics,
University of Florida College of Medicine
APStracts 3:0078C, 1996.
Given the central role of the placenta in nutrient transport to the
fetus, one might propose that maternal nutrition would have a
regulatory effect on this nutrient delivery. We have examined the
effect of a low-protein, adequate-calorie diet on specific amino acid
transport processes by the rat placenta. Maternal weight, fetal
weight, and placental weight were all significantly reduced in dams
fed a low-protein (5% casein), isocaloric diet when compared to dams
pair-fed a control (20% casein) diet. Even though maternal serum
amino acid levels were maintained in the low-protein animals,
fetomaternal serum amino acid ratios were significantly reduced
suggesting a reduction in nutrient transfer to the fetus. Apical and
basal membrane vesicles were isolated from the placental trophoblast
and were used to examine the amino acid transport capacity of both
maternal-facing and fetal-facing membranes, respectively. Na+
-dependent neutral amino acid transport mediated by System A was
decreased in both membrane preparations, while transport mediated by
System ASC was unaffected. The Na+-dependent anionic amino acid
uptake by System X-AG (EAAC1) was reduced on the basal membrane,
while the Na+-independent component was similar between the low
-protein and control diet-fed dams. Cationic amino acid uptake was
also reduced on both membrane surfaces. A decreased steady-state mRNA
content for EAAC1 and CAT1 suggests that reduced synthesis of the
transporter proteins is responsible for the decrease in transport
activity. Taken together, these data support the hypothesis that
maternal protein malnutrition affects nutrient delivery to the fetus
by down-regulation of specific amino acid transport proteins.
Received 10 November 1995; accepted in final form 25 January
1996.
APS Manuscript Number C683-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 20 March 96