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Am J Physiol Endocrinol Metab 269: E834-E839, 1995;
0193-1849/95 $5.00
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AJP - Endocrinology and Metabolism, Vol 269, Issue 5 E834-E839, Copyright © 1995 by American Physiological Society


ARTICLES

Contribution of fructose and lactate produced in placenta to calculation of fetal glucose oxidation rate

J. E. McGowan, P. W. Aldoretta and W. W. Hay Jr
Division of Perinatal Medicine, University of Colorado School of Medicine, Denver 80262, USA.

We examined the rate of production of [14C]fructose and [14C]lactate from [U-14C]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 16 +/- 3% of total fetal CO2 production; oxidation of lactate accounted for 3.3 +/- 0.1%. Thus 80% of total fetal CO2 production resulted from direct oxidation of carbon atoms in glucose; the "direct" glucose oxidation fraction was 0.46 +/- 0.04. During maternal tracer infusion (n = 15), CO2 production from fructose was 21 +/- 3, 20 +/- 3, and 30 +/- 4% and from lactate was 16 +/- 3, 13 +/- 3, and 11 +/- 4% in hypo-, normo-, and hyperglycemic animals, respectively; the direct glucose oxidation fraction was 0.40 +/- 0.04, 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 products of a metabolic substrate tracer should be considered in studies of fetal oxidative metabolism.


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Am. J. Physiol. Regul. Integr. Comp. Physiol.Home page
P. W. Aldoretta and W. W. Hay Jr.
Effect of glucose supply on ovine uteroplacental glucose metabolism
Am J Physiol Regulatory Integrative Comp Physiol, October 1, 1999; 277(4): R947 - R958.
[Abstract] [Full Text] [PDF]




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