ijms-logo

Journal Browser

Journal Browser

Molecular Advances in Gestational Diabetes Mellitus

Special Issue Editor


E-Mail Website
Guest Editor
Department of Metabolism, Digestion and Reproduction, Imperial College London, Chelsea and Westminster Hospital, London SW10 9NH, UK
Interests: diabetes in pregnancy; gestational diabetes; preterm birth

Special Issue Information

Dear Colleagues,

Gestational diabetes mellitus (GDM) is increasing in prevalence globally, and it is substantially related to an increased risk of type 2 diabetes (T2DM) after pregnancy in both pregnant women and their offspring. Little is known about how modifiable risk factors act on a mechanistic level to lower the longer-term risk of T2DM in women and their offspring.

In this Special Issue, entitled “Molecular Advances in Gestational Diabetes Mellitus”, we aim to present papers which deal with the newest research in the field of the molecular mechanisms that underpin the transgenerational impact of GDM. We welcome reviews and original research papers from fundamental and clinical research addressing how the maternal metabolome, placental signaling pathways, umbilical cord DNA methylation, and stem cell differentiation in GDM pregnancies compare to non-GDM pregnancies, as well as the impact of lifestyle, metformin, and insulin on treatment pathways.

Dr. Natasha Singh
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • metabolome
  • placental insulin signaling
  • DNA methylation
  • mitochondrial oxidation
  • MTOR
  • amino acids lipidomics
  • proteomics
  • gluconeogenesis
  • GDM

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue polices can be found here.

Published Papers (2 papers)

Order results
Result details
Select all
Export citation of selected articles as:

Research

Jump to: Review

13 pages, 861 KiB  
Article
Dietary Regulation of Lipid Metabolism in Gestational Diabetes Mellitus: Implications for Fetal Macrosomia
by Natalia Frankevich, Vitaliy Chagovets, Alisa Tokareva, Natalia Starodubtseva, Elizaveta Limonova, Gennady Sukhikh and Vladimir Frankevich
Int. J. Mol. Sci. 2024, 25(20), 11248; https://doi.org/10.3390/ijms252011248 - 19 Oct 2024
Viewed by 446
Abstract
The primary therapeutic approach for managing hyperglycemia today is diet therapy. Lipids are not only a source of nutrients but also play a role in initiating adipocyte differentiation in the fetus, which may explain the development of fetal macrosomia and future metabolic disorders [...] Read more.
The primary therapeutic approach for managing hyperglycemia today is diet therapy. Lipids are not only a source of nutrients but also play a role in initiating adipocyte differentiation in the fetus, which may explain the development of fetal macrosomia and future metabolic disorders in children born to mothers with gestational diabetes mellitus (GDM). Alterations in the maternal blood lipid profile, influenced by adherence to a healthy diet in mothers with GDM and the occurrence of fetal macrosomia, represent a complex and not fully understood process. The aim of this study was to examine the characteristics of the blood plasma lipid profile in pregnant women with GDM across all trimesters based on adherence to diet therapy. The clinical part of the study followed a case-control design, including 110 women: 80 in the control group, 20 in a GDM group adhering to the diet, and 10 in a GDM group not adhering to the diet. The laboratory part was conducted as a longitudinal dynamic study, with venous blood samples collected at three time points: 11–13, 24–26, and 30–32 weeks of pregnancy. A significant impact of diet therapy on the composition of blood lipids throughout pregnancy was demonstrated, starting as early as the first trimester. ROC analysis indicated high effectiveness of the models developed, with an AUC of 0.98 for the 30- to 32-week model and sensitivity and specificity values of 1 and 0.9, respectively. An association was found between dietary habits, maternal blood lipid composition at 32 weeks, and newborn weight. The changes in lipid profiles during macrosomia development and under diet therapy were found to be diametrically opposed, confirming at the molecular level that diet therapy can normalize not only carbohydrate metabolism but also lipid metabolism in both the mother and fetus. Based on the data obtained, it is suggested that after further validation, the developed models could be used to improve the prognosis of macrosomia by analyzing blood plasma lipid profiles at various stages of pregnancy. Full article
(This article belongs to the Special Issue Molecular Advances in Gestational Diabetes Mellitus)
Show Figures

Figure 1

Review

Jump to: Research

25 pages, 4545 KiB  
Review
Cellular and Molecular Pathophysiology of Gestational Diabetes
by Johnatan Torres-Torres, Irma Eloisa Monroy-Muñoz, Javier Perez-Duran, Juan Mario Solis-Paredes, Zaira Alexi Camacho-Martinez, Deyanira Baca, Salvador Espino-y-Sosa, Raigam Martinez-Portilla, Lourdes Rojas-Zepeda, Hector Borboa-Olivares and Enrique Reyes-Muñoz
Int. J. Mol. Sci. 2024, 25(21), 11641; https://doi.org/10.3390/ijms252111641 - 30 Oct 2024
Viewed by 1179
Abstract
Gestational diabetes (GD) is a metabolic disorder characterized by glucose intolerance during pregnancy, significantly impacting maternal and fetal health. Its global prevalence is approximately 14%, with risk factors including obesity, family history of diabetes, advanced maternal age, and ethnicity, which are linked to [...] Read more.
Gestational diabetes (GD) is a metabolic disorder characterized by glucose intolerance during pregnancy, significantly impacting maternal and fetal health. Its global prevalence is approximately 14%, with risk factors including obesity, family history of diabetes, advanced maternal age, and ethnicity, which are linked to cellular and molecular disruptions in glucose regulation and insulin resistance. GD is associated with short- and long-term complications for both the mother and the newborn. For mothers, GD increases the risk of developing type 2 diabetes, cardiovascular diseases, and metabolic syndrome. In the offspring, exposure to GD in utero predisposes them to obesity, glucose intolerance, and metabolic disorders later in life. This review aims to elucidate the complex cellular and molecular mechanisms underlying GD to inform the development of effective therapeutic strategies. A systematic review was conducted using medical subject headings (MeSH) terms related to GD’s cellular and molecular pathophysiology. Inclusion criteria encompassed original studies, systematic reviews, and meta-analyses focusing on GD’s impact on maternal and fetal health, adhering to PRISMA guidelines. Data extraction captured study characteristics, maternal and fetal outcomes, key findings, and conclusions. GD disrupts insulin signaling pathways, leading to impaired glucose uptake and insulin resistance. Mitochondrial dysfunction reduces ATP production and increases reactive oxygen species, exacerbating oxidative stress. Hormonal influences, chronic inflammation, and dysregulation of the mammalian target of rapamycin (mTOR) pathway further impair insulin signaling. Gut microbiota alterations, gene expression, and epigenetic modifications play significant roles in GD. Ferroptosis and placental dysfunction primarily contribute to intrauterine growth restriction. Conversely, fetal macrosomia arises from maternal hyperglycemia and subsequent fetal hyperinsulinemia, resulting in excessive fetal growth. The chronic inflammatory state and oxidative stress associated with GD exacerbate these complications, creating a hostile intrauterine environment. GD’s complex pathophysiology involves multiple disruptions in insulin signaling, mitochondrial function, inflammation, and oxidative stress. Effective management requires early detection, preventive strategies, and international collaboration to standardize care and improve outcomes for mothers and babies. Full article
(This article belongs to the Special Issue Molecular Advances in Gestational Diabetes Mellitus)
Show Figures

Figure 1

Back to TopTop