ArticlePlacenta2013
Placental glucose transporter 3 (GLUT3) is up-regulated in human pregnancies complicated by late-onset intrauterine growth restriction.
Article in Placenta, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT03024918 (Unequal Placental Sharing in Monochorionic Diamniotic Twins), which is not on this map. Cited by 48 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Unequal Placental Sharing in Monochorionic Diamniotic Twins: an Observational Study to Investigate Prediction and Outcome: the TWINSHARE Study
Who cites it
48 citing papers in PubMed, 89 citations in OpenAlex.
- Tumor necrosis factor alpha inhibition improves fetal growth in a rat model of preeclampsia.Placenta · 2026Article
- In vivo physiological ramifications of placental SLC2A3-RNA interference throughout gestation in sheep.Journal of animal science · 2026Article
- Dual inhibitory potential of ganoderic acid A on GLUT1/3: computational andRSC advances · 2024Article
- Disrupted Prenatal Metabolism May Explain the Etiology of Suboptimal Neurodevelopment: A Focus on Phthalates and Micronutrients and their Relationship to Autism Spectrum Disorder.Advances in nutrition (Bethesda, Md.) · 2024Review
- Neurodevelopment Is Dependent on Maternal Diet: Placenta and Brain Glucose Transporters GLUT1 and GLUT3.Nutrients · 2024Review
- Placental Expression of Glucose and Zinc Transporters in Women with Gestational Diabetes.Journal of clinical medicine · 2024Article
- Cannabidiol Exposure During Rat Pregnancy Leads to Labyrinth-Specific Vascular Defects in the Placenta and Reduced Fetal Growth.Cannabis and cannabinoid research · 2024Article
- The Impact of SLC2A8 RNA Interference on Glucose Uptake and the Transcriptome of Human Trophoblast Cells.Cells · 2024Article
- The impact of early pregnancy metabolic disorders on pregnancy outcome and the specific mechanism.European journal of medical research · 2023Review
- Article
- Impact of Placental SLC2A3 Deficiency during the First-Half of Gestation.International journal of molecular sciences · 2022Article
- Role of Placental Glucose Transporters in Determining Fetal Growth.Reproductive sciences (Thousand Oaks, Calif.) · 2022Review
- In vivo investigation of ruminant placenta function and physiology-a review.Journal of animal science · 2022Review
- Fetomaternal Expression of Glucose Transporters (GLUTs)-Biochemical, Cellular and Clinical Aspects.Nutrients · 2022Review
- Article
- Placental expression of glucose transporters GLUT-1, GLUT-3, GLUT-8 and GLUT-12 in pregnancies complicated by gestational and type 1 diabetes mellitus.Journal of diabetes investigation · 2022Article
- Placental Nutrient Transporters and Maternal Fatty Acids in SGA, AGA, and LGA Newborns From Mothers With and Without Obesity.Frontiers in cell and developmental biology · 2022Article
- Circulating extracellular vesicles exhibit a differential miRNA profile in gestational diabetes mellitus pregnancies.PloS one · 2022Article
- Differential Expression of Glucose Transporter Proteins GLUT-1, GLUT-3, GLUT-8 and GLUT-12 in the Placenta of Macrosomic, Small-for-Gestational-Age and Growth-Restricted Foetuses.Journal of clinical medicine · 2021Article
- Placental glucose transporter 1 and 3 gene expression in Monochorionic twin pregnancies with selective fetal growth restriction.BMC pregnancy and childbirth · 2021Observational
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
introductionTransport of glucose from maternal blood across the placental trophoblastic tissue barrier is critical to sustain fetal growth. The mechanism by which GLUTs are regulated in trophoblasts in response to ischemic hypoxia encountered with intrauterine growth restriction (IUGR) has not been suitably investigated.
objectiveTo investigate placental expression of GLUT1, GLUT3 and GLUT4 and possible mechanisms of GLUT regulation in idiopathic IUGR.
methodsWe analyzed clinical, biochemical and histological data from placentas collected from women affected by idiopathic full-term IUGR (n = 10) and gestational age-matched healthy controls (n = 10).
resultsWe found increased GLUT3 protein expression in the trophoblast (cytotrophoblast greater than syncytiotrophoblast) on the maternal aspect of the placenta in IUGR compared to normal placenta, but no differences in GLUT1 or GLUT4 were found. No differential methylation of the GLUT3 promoter between normal and IUGR placentas was observed. Increased GLUT3 expression was associated with an increased nuclear concentration of HIF-1α, suggesting hypoxia may play a role in the up-regulation of GLUT3. DISCUSSION: Further studies are needed to elucidate whether increased GLUT3 expression in IUGR is a marker for defective villous maturation or an adaptive response of the trophoblast in response to chronic hypoxia.
conclusionsPatients with IUGR have increased trophoblast expression of GLUT3, as found under the low-oxygen conditions of the first trimester.
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Registered trials
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.