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J Clin Endocrinol Metab. 2019 Mar 1;104(3):873-882. doi: 10.1210/jc.2018-01154.

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

Author information

1
Department of Obstetrics Rikshospitalet, Division of Obstetrics and Gynecology, Oslo University Hospital, Oslo, Norway.
2
Division of Reproductive Sciences, Department of Obstetrics and Gynecology, University of Colorado Anschutz Medical Campus, Aurora, Colorado.
3
Research Unit, Sørlandet Hospital, Arendal, Norway.
4
University of Oslo, Oslo, Norway.
5
Norwegian Advisory Unit on Women's Health, Oslo University Hospital, Oslo, Norway.
6
Department of Fetal Medicine, Division of Obstetrics and Gynecology, Oslo University Hospital, Oslo, Norway.
7
Division of Neonatology, Department of Pediatrics, University of Colorado Anschutz Medical Campus, Aurora, Colorado.

Abstract

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.

PMID:
30339207
DOI:
10.1210/jc.2018-01154

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