Evidence map›Paper›PMID 42050206›Full record

ArticleArchives of gynecology and obstetrics2026

Role of placental glucose metabolism in steroidogenesis in healthy pregnancies at term.

Muhammad Umar Sajjad, Tore Henriksen, Guttorm Haugen, Trond M Michelsen

Abstract read
In one paragraph

Article in Archives of gynecology and obstetrics, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

4 authors.

Muhammad Umar SajjadDepartment of Obstetrics, Division of Obstetrics and Gynecology, Oslo University Hospital, Rikshospitalet, Sognsvannsveien 20, 0372, Oslo, Norway.
Tore HenriksenDepartment of Obstetrics, Division of Obstetrics and Gynecology, Oslo University Hospital, Rikshospitalet, Sognsvannsveien 20, 0372, Oslo, Norway.
Guttorm HaugenInstitute of Clinical Medicine, University of Oslo, Oslo, Norway.
Trond M MichelsenDepartment of Obstetrics, Division of Obstetrics and Gynecology, Oslo University Hospital, Rikshospitalet, Sognsvannsveien 20, 0372, Oslo, Norway. trmi1@ous-hf.no.ORCID 0000-0001-9534-6255

Funding

Helse Sør-Øst RHF 2018087
6 · The paper itself

Abstract

backgroundThe human placenta consumes, on average, one third of the glucose from maternal blood. However, the role of placental glucose consumption in the production of estradiol and progesterone remains unclear. We hypothesized that placental glucose consumption in humans is associated with steroid production via a non-glycolytic pathway.

methodsWe included 41 healthy pregnancies at term. Blood samples were obtained from the maternal radial artery, uterine vein, and from the umbilical artery and vein during scheduled cesarean delivery. Blood flow in the uterine artery and umbilical vein was measured using Doppler ultrasound. Plasma concentrations of estradiol, progesterone, glucose, insulin, lactate, and ketones were analyzed. We calculated uteroplacental uptake and consumption of maternal glucose and ketones, and the loss of uteroplacental lactate in 6-carbon units as well as the release of steroid hormones into maternal circulation.

resultsOur data revealed a net placental release of estradiol and progesterone into maternal circulation [24.1 (5.34, 49.8) and 560.3 (61.2, 798.2) nmol/min, respectively]. The release of estradiol was positively associated with uteroplacental glucose uptake (ρ = 0.59, p < 0.001) and consumption (ρ = 0.43, p = 0.005), while progesterone exhibited similar associations (ρ = 0.61, p < 0.001; ρ = 0.43, p = 0.005). Notably, both hormones correlated positively with lactate-adjusted uteroplacental glucose consumption but not with acetate-equivalent uteroplacental ketone consumption.

conclusionPlacental release of estradiol and progesterone correlates with uteroplacental consumption of glucose that primarily occurs via non-glycolytic pathways in the third trimester placenta.

Indexed as

EstradiolGlucosePlacentaProgesteroneAdultBlood GlucoseFemaleHumansInsulinKetonesLactic AcidPlacental CirculationPregnancyTerm BirthUmbilical VeinsUterine ArteryBlood GlucoseEstradiolGlucoseInsulinKetonesLactic AcidProgesteroneGlucoseMetabolitesPlacentaSteroidogenesisSteroids

Identifiers

PMID42050206
PMCPMC13124754

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.