Evidence map›Paper›PMID 37497352›Full record

ReviewFrontiers in endocrinology2023

Expression of nutrient transporters in placentas affected by gestational diabetes: role of leptin.

Pilar Guadix, Isabel Corrales, Teresa Vilariño-García, Carmen Rodríguez-Chacón, Flora Sánchez-Jiménez, Carlos Jiménez-Cortegana, José L Dueñas, Víctor Sánchez-Margalet, Antonio Pérez-Pérez

Open access · goldAbstract readReview
In one paragraph

Review in Frontiers in endocrinology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
9.2field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

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.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed, 31 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors at 3 institutions in 1 country.

Pilar GuadixObstetrics and Gynecology Service, Virgen Macarena University Hospital, School of Medicine, University of Seville, Seville, Spain.
Isabel CorralesObstetrics and Gynecology Service, Virgen Macarena University Hospital, School of Medicine, University of Seville, Seville, Spain.
Teresa Vilariño-GarcíaClinical Biochemistry Service, Virgen del Rocio University Hospital, School of Medicine, University of Seville, Seville, Spain.
Carmen Rodríguez-ChacónClinical Biochemistry Service, Virgen Macarena University Hospital and Department of Medical Biochemistry and Molecular Biology and Immunology, School of Medicine, University of Seville, Seville, Spain.
Flora Sánchez-JiménezClinical Biochemistry Service, Virgen Macarena University Hospital and Department of Medical Biochemistry and Molecular Biology and Immunology, School of Medicine, University of Seville, Seville, Spain.
Carlos Jiménez-CorteganaClinical Biochemistry Service, Virgen Macarena University Hospital and Department of Medical Biochemistry and Molecular Biology and Immunology, School of Medicine, University of Seville, Seville, Spain.
José L DueñasObstetrics and Gynecology Service, Virgen Macarena University Hospital, School of Medicine, University of Seville, Seville, Spain.
Víctor Sánchez-MargaletClinical Biochemistry Service, Virgen Macarena University Hospital and Department of Medical Biochemistry and Molecular Biology and Immunology, School of Medicine, University of Seville, Seville, Spain.
Antonio Pérez-PérezClinical Biochemistry Service, Virgen Macarena University Hospital and Department of Medical Biochemistry and Molecular Biology and Immunology, School of Medicine, University of Seville, Seville, Spain.
Universidad de Sevilla · ESHospital Universitario Virgen Macarena · ESHospital Universitario Virgen del Rocío · ES

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Gestational diabetes mellitus (GDM) is the most frequent pathophysiological state of pregnancy, which in many cases produces fetuses with macrosomia, requiring increased nutrient transport in the placenta. Recent studies by our group have demonstrated that leptin is a key hormone in placental physiology, and its expression is increased in placentas affected by GDM. However, the effect of leptin on placental nutrient transport, such as transport of glucose, amino acids, and lipids, is not fully understood. Thus, we aimed to review literature on the leptin effect involved in placental nutrient transport as well as activated leptin signaling pathways involved in the expression of placental transporters, which may contribute to an increase in placental nutrient transport in human pregnancies complicated by GDM. Leptin appears to be a relevant key hormone that regulates placental transport, and this regulation is altered in pathophysiological conditions such as gestational diabetes. Adaptations in the placental capacity to transport glucose, amino acids, and lipids may underlie both under- or overgrowth of the fetus when maternal nutrient and hormone levels are altered due to changes in maternal nutrition or metabolic disease. Implementing new strategies to modulate placental transport may improve maternal health and prove effective in normalizing fetal growth in cases of intrauterine growth restriction and fetal overgrowth. However, further studies are needed to confirm this hypothesis.

Indexed as

Diabetes, GestationalPlacentaAmino AcidsFemaleFetal MacrosomiaGlucoseHumansLeptinLipidsMembrane Transport ProteinsNutrientsPregnancyAmino AcidsGlucoseLEP protein, humanLeptinLipidsMembrane Transport ProteinsNutrientsamino acidsfetal macrosomiagestational diabetes mellitusglucoseleptinlipidsnutrient transportersplacental transport

Identifiers

PMID37497352
PMCPMC10366688
OpenAlexW4383876442

What OpenQuestion holds

Textmetadata
LicenceCC BY
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Registered trials

None linked

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.