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Bridging Basic and Clinical Science: Shared Molecular and Metabolic Mechanisms in Preeclampsia, Gestational Diabetes and Gestational Weight Gain

Special Issue Editors


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Guest Editor
Coordinación de Nutrición y Bioprogramación, Instituto Nacional de Perinatología, Secretaría de Salud, Mexico City 11000, Mexico
Interests: gestational weight gain; adolescent pregnancy; nutritional status; nutrient metabolism; oxidative stress; genetic variants; cytokines; perinatal outcomes; breastfeeding

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Guest Editor
Community Interventions Research Branch, Instituto Nacional de Perinatología, Mexico City 11000, Mexico
Interests: maternal-fetal metabolic complications; DOHaD; pregnancy outcomes; clinical translation; maternal obesity; biomarkers

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Guest Editor
Dirección de Investigación, Instituto Nacional de Perinatología “Isidro Espinosa de los Reyes”, Mexico City, Mexico
Interests: human fetal membranes; inflammation; maternal-placental-fetal interface; miRNAs; infectious diseases; reproductive immunology; preterm labor

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Guest Editor
Coordinación de Nutrición y Bioprogramacíon, Instituto Nacional de Perinatología, Mexico City, Mexico
Interests: nutrition during pregnancy; gestational weight gain; body composition; adipokines; inflammation; biomarkers

Special Issue Information

Dear Colleagues,

This Special Issue, "Bridging Basic and Clinical Science: Shared Molecular and Metabolic Mechanisms in Preeclampsia, Gestational Diabetes and Gestational Weight Gain," aims to foster a deeper, integrated understanding of the common molecular and metabolic pathways underpinning these significant pregnancy-specific complications. Our goal is to highlight the shared pathophysiological roots—including systemic inflammation, insulin resistance, oxidative stress, altered lipid metabolism, and placental dysfunction—to catalyze the identification of novel diagnostic biomarkers, therapeutic targets, and preventive strategies that can address these conditions more effectively, individually and synergistically, ultimately striving to improve maternal and offspring health outcomes globally.

We invite original research articles, comprehensive reviews, and insightful commentaries that explore the genetic, epigenetic, proteomic, metabolomic, and cellular factors contributing to these interconnected pathologies. The scope encompasses studies from basic molecular investigations to clinical and translational research, seeking relevant findings across these fields. While the primary focus is on the shared mechanisms and interrelationships among preeclampsia (PE), gestational diabetes mellitus (GDM), and excessive gestational weight gain (GWG), high-quality original research papers and reviews addressing the molecular and metabolic aspects of each condition independently will also be considered. Submissions focusing on basic science discoveries with clinical relevance, translational studies, omics-based approaches, novel interventions, and insights into the maternal-fetal interface are particularly encouraged. This collection will bridge the gap between fundamental molecular insights and clinical applications.

We welcome contributions focusing on, but not limited to, the following themes:

  • Shared molecular and metabolic pathways: Investigations into common mechanisms such as insulin resistance, systemic inflammation, oxidative stress, altered lipid metabolism, and mitochondrial dysfunction in PE, GDM, and GWG.
  • Placental biology and maternal–fetal interface: Studies exploring the role of placental development, function, and signaling in the pathogenesis of these conditions, including molecular insights into immune cell interactions, angiogenesis, and nutrient transport.
  • Omics approaches: Research utilizing genomics, epigenomics, transcriptomics, proteomics, and metabolomics to identify novel biomarkers, genetic predispositions, or therapeutic targets.
  • Fetal programming and DOHaD: Studies on the perinatal origins of adult diseases, including the long-term impact of maternal metabolic health during pregnancy on offspring health.
  • Molecular biomarkers: Identification and validation of molecular and metabolic biomarkers for the early prediction, diagnosis, or prognosis of PE, GDM, and GWG.
  • Therapeutic and preventive strategies: Molecular and cellular mechanisms underlying current or novel interventions aimed at preventing or managing these pregnancy complications.
  • Cellular and animal models: Findings from in vitro and in vivo models that provide mechanistic insights into these conditions.
  • Environmental and lifestyle factors: Molecular responses to environmental stressors, nutrition, and lifestyle interventions in the context of these pathologies.

We look forward to your valuable contributions to this Special Issue, which will undoubtedly foster collaborative advancements in understanding and addressing these critical pregnancy-related health issues.

Dr. Reyna Sámano
Dr. Hector Borboa-Olivares
Dr. Verónica Zaga-Clavellina
Dr. Gabriela Chico-Barba
Guest Editors

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Keywords

  • preeclampsia
  • gestational diabetes
  • gestational weight gain
  • metabolic mechanisms
  • molecular pathways
  • placental biology
  • maternal–fetal interface
  • biomarkers
  • insulin resistance
  • inflammation
  • translational research

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Published Papers (1 paper)

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Research

21 pages, 596 KB  
Article
Role of FTO rs9939609 and LEPR rs1137101 Genetic Variants in Gestational Weight Gain and Neonatal Weight Among Pregnant Adolescents
by Reyna Sámano, Hugo Martínez-Rojano, Ashley Díaz-Medina, Irma Eloísa Monroy-Muñoz, Gabriela Chico-Barba, María Eugenia Mendoza-Flores, Héctor Borboa-Olivares, Verónica Zaga-Clavellina, Ricardo Gamboa, Melissa Daniela Gonzalez-Fernandez, Ángela Felipe-Hernández, Rosalba Sevilla-Montoya and Alejandro Martínez-Juárez
Int. J. Mol. Sci. 2026, 27(8), 3413; https://doi.org/10.3390/ijms27083413 - 10 Apr 2026
Viewed by 499
Abstract
Gestational weight gain (GWG) and birth weight (BW) have a multifactorial etiology, which makes identifying the most influential determinants difficult. The association between variants of the FTO and LEPR genes has been explored as contributing factors to obesity in various age groups; however, [...] Read more.
Gestational weight gain (GWG) and birth weight (BW) have a multifactorial etiology, which makes identifying the most influential determinants difficult. The association between variants of the FTO and LEPR genes has been explored as contributing factors to obesity in various age groups; however, their role in GWG and BW in adolescent mothers and their offspring is uncertain. To determine whether the presence of polymorphisms rs9939609 (FTO) and rs1137101 (LEPR) is associated with gestational weight gain and newborn weight in a cohort of adolescent mothers. Methods: A prospective cohort study of 305 mother-child dyads was conducted between 2020 and 2024. Genotyping of the single nucleotide variants (SNVs) rs9939609 of the FTO gene and rs1137101 of the LEPR gene was performed using real-time PCR and high-resolution melting analysis (qPCR-HRM), using maternal peripheral blood and umbilical cord blood samples. GWG, BW, energy intake, and other perinatal data were recorded and classified. Genetic data from 305 mother–offspring dyads were analyzed. The median maternal age was 16 years, and 71.4% had a normal pre-pregnancy body mass index (BMI). The most frequent genotypes were TT for FTO rs9939609 and AG for LEPR rs1137101. In both groups, the genotypic distribution significantly deviated from Hardy–Weinberg equilibrium (p < 0.0001). The AA genotype of FTO was associated with a higher probability of excessive gestational weight gain (GWG) after adjustment for pre-pregnancy BMI and dietary and sociodemographic factors. High protein and lipid intake increased the risk of excessive GWG, whereas adequate intake of carbohydrates and legumes showed a protective effect. An initial significant association was identified between the LEPR rs1137101 variant (AA allele) and low birth weight (LBW); however, this association was lost after adjustment for confounding factors. The FTO rs9939609 variant was significantly associated with GWG. On the other hand, the LEPR rs1137101 variant in the offspring showed an association with BW categorized by percentiles (in crude analysis), while the FTO variant showed no relationship with birth weight. Full article
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