Contribution of fructose and lactate produced in the placenta to
the calculation of fetal glucose oxidation rate.
McGowan, Jane E., Peter W. Aldoretta, and William W. Hay, Jr.
Division of Perinatal Medicine, University of Colorado School of
Medicine
APStracts 2:0123E, 1995.
We examined the rate of production of 14C-fructose and 14C-lactate
from 14C1-6-glucose by the placenta and the contribution of 14CO2
from fetal oxidation of these metabolic products to the calculation
of glucose oxidation rate in fetal sheep. During fetal tracer
infusions (n=16), oxidation of fructose contributed 163% of total
fetal CO2 production; oxidation of lactate accounted for 3.30.1%.
Thus, 80% of total fetal CO2 production resulted from direct
oxidation of carbon atoms in glucose; the "direct" glucose
oxidation fraction was 0.460.04. During maternal tracer infusion
(n=15), CO2 production from fructose was 213%, 203%, and 304% and
from lactate was 163%, 133%, and 114% in hypo-, normo-, and
hyperglycemic animals, respectively; the "direct" glucose
oxidation fraction was 0.400.04, not different from the fraction
obtained with the fetal tracer infusion. Fetal oxidation of
substrates derived from glucose metabolism in the placenta
contributes significantly to fetal CO2 production. Fetal oxidation of
placental product(s) of a metabolic substrate tracer should be
considered in studies of fetal oxidative metabolism
Received 29 June 1994; accepted in final form 22 May 1995.
APS Manuscript Number E236-4.
Article publication pending Am. J. Physiol. (Endocrinol. Metab.).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 8 June 1995.