Placental transport of threonine and its utilization in the normal
and growth restricted fetus.
Anderson, Anne H., Paul V. Fennessey, Giacomo Meschia, Randall B.
Wilkening, and Frederick C. Battaglia.
Departments of Pediatrics and Physiology, University of Colorado
School of Medicine, Denver, Colorado, 80262
APStracts 4:0020E, 1997.
Placental transport and feto-placental utilization of threonine (THR)
were compared at 130+/-1 days gestational age between 7 control ewes
(C) and 6 ewes in which intrauterine growth restriction (IUGR) had
been induced by exposure to high ambient temperature from 33+/-1 to
112+/-2 days gestation. THR fluxes were measured using simultaneous
intravenous infusions of L-[1-13C] THR into the mother and L-[U-14C]
THR into the fetus. The IUGR group had less fetal weight (1.27+/-.14
vs. 3.10+/-.10 Kg, P<.01) and placental weight (120+/-17 vs.
295+/-14 g, P<.01) than the C group. The direct flux of
maternal THR into the fetal systemic circulation was less in the IUGR
fetuses, both relative to fetal weight (1.40+/-.19 vs. 2.19+/-.18
[mu]mol min-1(Kg fetus)-1,P=.0107) and placental weight (1.5+/-.0.2
vs. 2.3+/-0.2 [mu]mol min-1(100 g placenta)-1, P=.0187). In both
groups, there was excretion of CO2 produced from fetal THR. The rate
of CO2 production from fetal plasma THR carbon by fetus plus placenta
was reduced in the IUGR group (1.50+/-.23 vs. 2.86+/-.32 [mu]mol min
-1(Kg fetus)-1, P=0.0065). We conclude that the flux of maternal THR
into the IUGR fetus is markedly reduced because of a reduction in
placental mass and because of a weight specific reduction in THR
placental transport. The reduced flux is routed into fetal THR
accretion via a decrease in fetal THR oxidation.
Received 25 October 1996; accepted in final form 21 January 1997.
APS Manuscript Number E531-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1997 The American Physiological Society.
Published in APStracts on 19 February 1997