Effect of glucose supply on ovine uteroplacental glucose metabolism.
To test the hypothesis that glucose supply to the uteroplacenta (UP) regulates UP glucose metabolism into oxidative and nonoxidative pathways, we studied eight late-gestation pregnant sheep at low (LG) and high (HG) maternal glucose concentrations (G(M)), using Fick principle and tracer glucose methodology. UP glucose consumption (UPGC) correlated directly with G(M) (r = 0.75, P = 0.0006), and UP glucose decarboxylation (r = 0.80, P = 0.0001), and lactate production (r = 0.90, P = 0.0001) rates were directly correlated with UPGC. The combined fractional production rate for lactate, fructose, and CO(2) from UPGC was the same in LG and HG periods. The fraction of UP oxygen consumption used for glucose oxidation increased by about 50% from LG to HG conditions; however, there was no change in UP oxygen consumption. Nearly half of UPGC was not accounted for by lactate, fructose, and CO(2) production, and about two-thirds of UP oxygen consumption was not accounted for by immediate oxidation of glucose carbon just taken up by the UP. These results indicate that glucose supply directly regulates UP glucose oxidative metabolism and that there is a reciprocal relationship between UP glucose oxidation and the oxidation of other substrates.
Aldoretta
P W
PW
Division of Perinatal Medicine, University of Colorado School of Medicine, Denver, Colorado 80262, USA.
Hay
W W
WW
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D005260:Female; D005632:Fructose / Q000097:blood / Q000378:metabolism; D005947:Glucose / Q000378:metabolism*; D019344:Lactic Acid / Q000097:blood / Q000378:metabolism; D010084:Oxidation-Reduction; D010100:Oxygen / Q000097:blood; D010920:Placenta / Q000378:metabolism*; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000097:blood*; D014599:Uterus / Q000378:metabolism*
D001786:Blood Glucose; D005632:Fructose; D019344:Lactic Acid; D005947:Glucose; D010100:Oxygen