Ovine fetal leucine kinetics and protein metabolism during acute
metabolic acidosis.
Ross, J., Milley.
Division of Neonatology, Department of Pediatrics, University of
Utah School of Medicine, Salt Lake City, UT 84132
APStracts 3:0219E, 1996.
Fetal acidosis is associated with poor fetal growth. Because protein
accretion is an important component of fetal growth, we used seven
chronically prepared fetal lambs (10 - 16 d post operation) to find
if fetal metabolic acidosis affected fetal protein accretion, and, if
so, whether such effects were due to decreased synthesis or increased
breakdown of proteins. Fetal leucine kinetics were measured during
infusion of 1-[14C] leucine by the reciprocal pool method. After
control measurements, metabolic acidosis was induced by fetal
infusion of 0.5 N HCl and the measurements repeated. Although fetal
leucine concentration rose (164 +/- 11 vs. 216 +/- 15 [mu]M;
P<0.001), fetal leucine uptake fell during acidosis (3.33 +/-
0.30 vs. 1.43 +/- 0.35 [mu]mol x kg-1 x min-1; P<0.05).
However, the influx of leucine from protein breakdown increased (12.6
+/- 2.6 vs. 14.7 +/- 2.6 [mu]mol x kg-1 x min-1; P<0.02). The
incorporation of leucine into fetal protein was unaffected by
acidosis, so that fetal protein accretion, fell (0.48 +/- 1.04 vs.
-2.32 +/- 1.53 [mu]mol x kg-1 x min-1; P<0.001). Fetal leucine
decarboxylation increased during acidosis (2.85 +/- 0.33 vs. 3.75 +/-
0.61 [mu]mol x kg-1 x min-1; P<0.05). We conclude that fetal
metabolic acidosis stimulates pathways to degrade both protein and at
least one of the subsequently derived amino acids, leucine. The
consequence of such changes induced by acidosis is decreased protein
accretion, a finding incompatible with normal fetal growth.
Received 17 May 1996; accepted in final form 31 October 1996.
APS Manuscript Number E248-6.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996