Uteroplacental Glucose Uptake and Fetal Glucose Consumption: A Quantitative Study in Human Pregnancies

Context: Maternal glucose levels and body mass index (BMI) are determinants of fetal overgrowth, but their relation to fetal glucose consumption is not well characterized in human pregnancy. Objectives: To quantify uteroplacental glucose uptake and the allocation of glucose between the placenta and fetus and to identify factors that affect fetal glucose consumption. Design: Human in vivo study in term pregnancies. Setting: Oslo University Hospital, Norway. Participants: One hundred seventy-nine healthy women with elective cesarean section. Interventions: Uterine and umbilical blood flow was determined using Doppler ultrasonography. Glucose and insulin were measured in the maternal radial artery and uterine vein and the umbilical artery and vein. In a subcohort (n = 33), GLUT1 expression was determined in isolated syncytiotrophoblast basal and microvillous plasma membranes. Main Outcome Measures: Uteroplacental glucose uptake and placental and fetal glucose consumption quantified by the Fick principle. Results: Median (Q1, Q3) uteroplacental glucose uptake was 117.1 (59.1, 224.9) μmol⋅min-1, and fetal and placental glucose consumptions were 28.9 (15.4, 41.8) µmol⋅min-1⋅kg fetus-1 and 51.4 (-65.8, 185.4) µmol⋅min-1⋅kg placenta-1, respectively. Fetal glucose consumption correlated with birth weight (ρ: 0.34; P < 0.001) and maternal-fetal glucose gradient (ρ: 0.60; P < 0.001), but not with maternal BMI or uteroplacental glucose uptake. Uteroplacental glucose uptake was correlated to placental glucose consumption (ρ: 0.77; P < 0.001). Fetal and placental glucose consumptions were inversely correlated (ρ: -0.47; P < 0.001), but neither was correlated with placental GLUT1 expression. Conclusion: These findings suggest that fetal glucose consumption is balanced against the placental needs for glucose and that placental glucose consumption is a key modulator of maternal-fetal glucose transfer in women.