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Metabolites
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Advances in Gestational Diabetes and Metabolomics
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Advances in Gestational Diabetes and Metabolomics

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: closed (15 March 2022) | Viewed by 7107

Special Issue Editor

Dr. Anamaria Savu

E-Mail Website
Guest Editor
Canadian VIGOUR Centre and Faculty of Medicine and Dentistry, University of Alberta, Edmonton, AB, Canada
Interests: statistical methods; gestational diabetes; diabetes mellitus; cardiovascular diseases; maternal outcomes; neonatal outcomes; excess weight

Special Issue Information

Dear Colleagues,

Women experience a series of physical and metabolic adaptations during pregnancy, such as alterations in blood glucose and lipid balance. Several processes are believed to occur. The hormones produced by the placenta and weight gain during pregnancy lead to the body's cells being unable to use insulin properly, giving rise to insulin resistance and elevated blood glucose levels. When the pancreas is unable to produce the extra insulin needed during pregnancy, gestational diabetes occurs. Although glucose intolerance manifests continuously, measured blood glucose levels surpassing certain thresholds indicates a diagnosis of gestational diabetes. In recent years a steady increase in gestational rates has been observed in many populations across the globe. Also, it has become apparent that different glycaemic groups exist among those diagnosed with gestational diabetes, depending on whether elevated blood glucose occurs after fasting or ingesting a glucose load.

This special issue is devoted to understanding associations between glucose intolerance developed in pregnancy and the metabolism's biochemical intermediate or end products, and the profile of metabolites. Therefore, we invite manuscripts devoted to identifying metabolic biomarkers as predictors of future development of gestational diabetes or adverse maternal and child outcomes following the manifestation of gestational diabetes. Finally, we invite manuscripts that can help understand the pathophysiology and various glycaemic subtypes of gestational diabetes and the recent surge in the rates of this condition.

Dr. Anamaria Savu
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. Metabolites is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • gestational diabetes
  • pathophysiology of glucose intolerance in pregnancy
  • biomarkers of glucose intolerance in pregnancy
  • metabolomics in glucose intolerance in pregnancy
  • insulin resistance
  • fasting plasma glucose
  • post-load blood glucose
  • glycaemic types
  • maternal outcomes
  • child outcomes
  • excess weight

Published Papers (3 papers)

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Research

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17 pages, 1094 KiB  
Article
Metabolomic Profiles in Childhood and Adolescence Are Associated with Fetal Overnutrition
by Ellen C. Francis, Katerina Kechris, Catherine C. Cohen, Gregory Michelotti, Dana Dabelea and Wei Perng
Metabolites 2022, 12(3), 265; https://doi.org/10.3390/metabo12030265 - 19 Mar 2022
Cited by 4 | Viewed by 2289
Abstract
Fetal overnutrition predisposes offspring to increased metabolic risk. The current study used metabolomics to assess sustained differences in serum metabolites across childhood and adolescence among youth exposed to three typologies of fetal overnutrition: maternal obesity only, gestational diabetes mellitus (GDM) only, and obesity [...] Read more.
Fetal overnutrition predisposes offspring to increased metabolic risk. The current study used metabolomics to assess sustained differences in serum metabolites across childhood and adolescence among youth exposed to three typologies of fetal overnutrition: maternal obesity only, gestational diabetes mellitus (GDM) only, and obesity + GDM. We included youth exposed in utero to obesity only (BMI ≥ 30; n = 66), GDM only (n = 56), obesity + GDM (n = 25), or unexposed (n = 297), with untargeted metabolomics measured at ages 10 and 16 years. We used linear mixed models to identify metabolites across both time-points associated with exposure to any overnutrition, using a false-discovery-rate correction (FDR) <0.20. These metabolites were included in a principal component analysis (PCA) to generate profiles and assess metabolite profile differences with respect to overnutrition typology (adjusted for prenatal smoking, offspring age, sex, and race/ethnicity). Fetal overnutrition was associated with 52 metabolites. PCA yielded four factors accounting for 17–27% of the variance, depending on age of measurement. We observed differences in three factor patterns with respect to overnutrition typology: sphingomyelin-mannose (8–13% variance), skeletal muscle metabolism (6–10% variance), and 3-carboxy-4-methyl-5-propyl-2-furanpropanoic acid (CMPF; 3–4% variance). The sphingomyelin-mannose factor score was higher among offspring exposed to obesity vs. GDM. Exposure to obesity + GDM (vs. GDM or obesity only) was associated with higher skeletal muscle metabolism and CMPF scores. Fetal overnutrition is associated with metabolic changes in the offspring, but differences between typologies of overnutrition account for a small amount of variation in the metabolome, suggesting there is likely greater pathophysiological overlap than difference. Full article
(This article belongs to the Special Issue Advances in Gestational Diabetes and Metabolomics)
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Review

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16 pages, 315 KiB  
Review
Maternal and Fetal Metabolites in Gestational Diabetes Mellitus: A Narrative Review
by Ionela Mihaela Vladu, Diana Clenciu, Adina Mitrea, Anca Amzolini, Simona Elena Micu, Anda Elena Crisan, Ion Cristian Efrem, Maria Fortofoiu, Mircea Catalin Fortofoiu, Adrian Mita, Anca Barau Alhija, Adina Dorina Glodeanu and Maria Mota
Metabolites 2022, 12(5), 383; https://doi.org/10.3390/metabo12050383 - 22 Apr 2022
Cited by 6 | Viewed by 2546
Abstract
Gestational diabetes mellitus (GDM) is a major public health issue of our century due to its increasing prevalence, affecting 5% to 20% of all pregnancies. The pathogenesis of GDM has not been completely elucidated to date. Increasing evidence suggests the association of environmental [...] Read more.
Gestational diabetes mellitus (GDM) is a major public health issue of our century due to its increasing prevalence, affecting 5% to 20% of all pregnancies. The pathogenesis of GDM has not been completely elucidated to date. Increasing evidence suggests the association of environmental factors with genetic and epigenetic factors in the development of GDM. So far, several metabolomics studies have investigated metabolic disruptions associated with GDM. The aim of this review is to highlight the usefulness of maternal metabolites as diagnosis markers of GDM as well as the importance of both maternal and fetal metabolites as prognosis biomarkers for GDM and GDM’s transition to type 2 diabetes mellitus T2DM. Full article
(This article belongs to the Special Issue Advances in Gestational Diabetes and Metabolomics)

Other

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6 pages, 522 KiB  
Case Report
Glucocorticoid-Induced Hyperinsulinism in a Preterm Neonate with Inherited ABCC8 Variant
by Emmanuelle Motte-Signoret, Cécile Saint-Martin, Christine Bellané-Chantelot, Bernard Portha and Pascal Boileau
Metabolites 2022, 12(9), 847; https://doi.org/10.3390/metabo12090847 - 8 Sep 2022
Cited by 1 | Viewed by 1548
Abstract
Glucose homeostasis is a real challenge for extremely preterm infants (EPIs) who have both limited substrate availability and immature glucose metabolism regulation. In the first days of life, EPIs frequently develop transient glucose intolerance, which has a complex pathophysiology that associates unregulated gluconeogenesis, [...] Read more.
Glucose homeostasis is a real challenge for extremely preterm infants (EPIs) who have both limited substrate availability and immature glucose metabolism regulation. In the first days of life, EPIs frequently develop transient glucose intolerance, which has a complex pathophysiology that associates unregulated gluconeogenesis, immature insulin secretion, and peripheral insulin resistance. In this population, glucocorticoid therapy is frequently administrated to prevent severe bronchopulmonary dysplasia. During this treatment, glucose intolerance classically increases and may lead to hyperglycemia. We report a case of neonatal hypoglycemia that was concomitant to a glucocorticoids administration, and that led to a congenital hyperinsulinism diagnosis in an EPI with a heterozygous ABCC8 variant. The variant was inherited from his mother, who had developed monogenic onset diabetes of the youth (MODY) at the age of 23. ABCC8 encodes a beta-cell potassium channel unit and causes congenital hyperinsulinism or MODY depending on the mutation location. Moreover, some mutations have been observed in the same patient to cause both hyperinsulinism in infancy and MODY in adulthood. In our case, the baby showed repeated and severe hypoglycemias, which were undoubtedly time-associated with the betamethasone intravenous administration. This hyperinsulinism was transient, and the infant has not yet developed diabetes at three years of age. We take the opportunity presented by this unusual clinical presentation to provide a review of the literature, suggesting new insights regarding the pathophysiology of the beta-pancreatic cells’ insulin secretion: glucocorticoids may potentiate basal insulin secretion in patients with ABCC8 mutation. Full article
(This article belongs to the Special Issue Advances in Gestational Diabetes and Metabolomics)
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