Abstract
Summary: This report explored the possibility that maternal hyperglycemia during pregnancy might produce a competition between glucose (G) and ascorbic acid (AA) and reduce the transfer of AA to the fetus using an in vivo single-pass placental perfusion technique in the guinea pig. Levels of G in maternal plasma increased from 104 ± 4 mg/dl (x ± S.E.) before AA + G infusion to 370 ± 19 mg/dl at the end of each study (P < 0.001). Preinfusion levels of AA in maternal and fetal plasma were 0.29 ± 0.02 mg/dl and 0.46 ± 0.03 mg/dl, respectively. Maternal infusion of AA or AA + G produced significant increases in maternal plasma AA (P < 0.025) and fetal plasma AA (P < 0.001); however, fetal plasma AA from dams infused with AA + G were significantly below fetal plasma values obtained when only AA was infused (P < 0.005) suggesting that when maternal plasma G is increased, the placental transport of AA to the fetus is reduced. Preinfusion levels of AA in placental tissue were 10.8 ± 0.5 mg/dl and infusion of AA or AA + G produced significant increases in AA in this organ (P < 0.001). Comparison of the AA in placental tissue from fetuses of dams infused with either solution demonstrates that significantly less AA was present after AA + G infusion (P < 0.005). Additionally, when AA + G was infused a significant decrease in AA transferred across the placenta was found (P < 0.001) as maternal plasma G increased beyond 200 mg/dl. The data suggest that in the guinea pig glucose may compete with ascorbic acid transfer across the placenta and that maternal hyperglycemia may reduce the bioavailability of AA to the fetus.
Speculation: An acute episode of maternal hyperglycemia interferes with the placental transfer of ascorbic acid. Therefore, maternal hyperglycemia during gestational diabetes may result in a decreased supply of ascorbic acid to the fetus.
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Norkus, E., Bassi, J. & Rosso, P. Maternal Hyperglycemia and its Effect on the Placental Transport of Ascorbic acid. Pediatr Res 16, 746–750 (1982). https://doi.org/10.1203/00006450-198209000-00008
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DOI: https://doi.org/10.1203/00006450-198209000-00008