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Maternal Diet, Epigenetic Mechanisms and Metabolic Programming

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Nutrigenetics and Nutrigenomics".

Deadline for manuscript submissions: 25 December 2024 | Viewed by 5998

Special Issue Editors


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Guest Editor
1. Biomedical Sciences, School of Medicine, Southern Illinois University, Carbondale, IL 62901, USA
2. Department of Child Health, University of Arizona, Phoenix, AZ 85721, USA
3. Department of Neuroscience, Carleton University, Ottawa, ON K1S 5B6, Canada
Interests: maternal nutrition; offspring; neurodevelopment; neurological diseases; stroke; vascular dementia; aging

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Co-Guest Editor
Department of Health Sciences, Brock University, St. Catharines, ON, Canada
Interests: prenatal programming; prenatal diet and offspring neurodevelopment; prenatal diet and exercise interventions for offspring brain development

Special Issue Information

Dear Colleagues,

The maternal environment influences embryonic and fetal development. Among environmental factors, nutrition is the most vital one that modulates the expression of genes involved in metabolic pathways and a variety of phenotypes associated with growth, development, and health. Maternal diet and nutritional factors affect various aspects of metabolic programming. These changes are induced in early life, and may alter the phenotype later in life, influencing the development of metabolic diseases and neurodevelopment. In particular, dietary imbalances during pregnancy may affect neurodevelopment during the sensitive period, thereby increasing the susceptibility of offspring to neurological diseases (e.g., stroke and vascular dementia).

Identification of dietary factors’ role in development, including methyl group donors (e.g., folate, choline) and bioactive compounds (e.g., polyphenols), is of great importance; however, insufficient knowledge exists in addressing how maternal diet influences epigenetic mechanisms during offspring development and how to prevent potential negative effects on later life.

In this Special Issue, original articles and reviews addressing the effects of maternal diet and nutrition on metabolic programming and potential mechanisms of maternal epigenetic regulation of gene expression that have persistent effects on offspring health and development are welcome.

I look forward to receiving your contributions.

Dr. Nafisa M. Jadavji
Dr. John Krzeczkowski
Guest Editors

Manuscript Submission Information

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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. Nutrients is an international peer-reviewed open access semimonthly 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 2900 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

  • maternal diet
  • epigenetic mechanisms
  • metabolic programming
  • offspring’s health
  • folate
  • neurological diseases
  • neurodevelopmental disorders

Published Papers (3 papers)

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Research

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10 pages, 1271 KiB  
Article
Changes in Serum Oxytocin Levels under Physiological and Supraphysiological Gonadal Steroid Hormone Conditions in Women of Reproductive Age: A Preliminary Study
by Ayaka Tachibana, Yuri Yamamoto, Hiroki Noguchi, Asuka Takeda, Kou Tamura, Hidenori Aoki, Saki Minato, Maimi Uchishiba, Shota Yamamoto, Shuhei Kamada, Atsuko Yoshida, Riyo Kinouchi, Kanako Yoshida and Takeshi Iwasa
Nutrients 2022, 14(24), 5350; https://doi.org/10.3390/nu14245350 - 16 Dec 2022
Cited by 5 | Viewed by 2374
Abstract
Oxytocin (OT) affects many behavioral, psychological, and physiological functions, including appetite and body weight regulation. Central and peripheral OT levels are markedly affected by gonadal steroids, especially estrogen, and the anorectic effects of estrogen are partially mediated by OT in rodents. In this [...] Read more.
Oxytocin (OT) affects many behavioral, psychological, and physiological functions, including appetite and body weight regulation. Central and peripheral OT levels are markedly affected by gonadal steroids, especially estrogen, and the anorectic effects of estrogen are partially mediated by OT in rodents. In this study, the relationship between the estrogen milieu and serum OT levels was evaluated in women of reproductive age under physiological (n = 9) and supraphysiological estrogenic conditions (n = 7). Consequently, it was found that serum OT levels were increased in physiological (the ovulatory phase) and supraphysiological (on the day of the human chorionic gonadotropin trigger in an ovarian stimulation cycle) estrogenic conditions, and that serum OT levels were positively correlated with serum estradiol levels. On the other hand, serum OT levels were negatively correlated with serum progesterone levels, and there was no correlation between serum and follicular OT levels. These results suggest that OT levels may be positively and negatively regulated by estrogen and progesterone, respectively, in humans. However, the physiological roles of these actions of gonadal steroids on OT remain unclear. Full article
(This article belongs to the Special Issue Maternal Diet, Epigenetic Mechanisms and Metabolic Programming)
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Review

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35 pages, 1533 KiB  
Review
Preterm Birth and Its Association with Maternal Diet, and Placental and Neonatal Telomere Length
by Nikoletta Lis, Demetris Lamnisos, Aikaterini Bograkou-Tzanetakou, Elena Hadjimbei and Irene P. Tzanetakou
Nutrients 2023, 15(23), 4975; https://doi.org/10.3390/nu15234975 - 30 Nov 2023
Cited by 1 | Viewed by 1753
Abstract
Preterm birth (PTB), a multi-causal syndrome, is one of the global epidemics. Maternal nutrition, but also neonatal and placental telomere length (TL), are among the factors affecting PTB risk. However, the exact relationship between these factors and the PTB outcome, remains obscure. The [...] Read more.
Preterm birth (PTB), a multi-causal syndrome, is one of the global epidemics. Maternal nutrition, but also neonatal and placental telomere length (TL), are among the factors affecting PTB risk. However, the exact relationship between these factors and the PTB outcome, remains obscure. The aim of this review was to investigate the association between PTB, maternal nutrition, and placental-infant TL. Observational studies were sought with the keywords: maternal nutrition, placental TL, newborn, TL, and PTB. No studies were found that included all of the keywords simultaneously, and thus, the keywords were searched in dyads, to reach assumptive conclusions. The findings show that maternal nutrition affects PTB risk, through its influence on maternal TL. On the other hand, maternal TL independently affects PTB risk, and at the same time PTB is a major determinant of offspring TL regulation. The strength of the associations, and the extent of the influence from covariates, remains to be elucidated in future research. Furthermore, the question of whether maternal TL is simply a biomarker of maternal nutritional status and PTB risk, or a causative factor of PTB, to date, remains to be answered. Full article
(This article belongs to the Special Issue Maternal Diet, Epigenetic Mechanisms and Metabolic Programming)
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Other

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12 pages, 2306 KiB  
Brief Report
In Vitro Circadian Clock Gene Expression Assessments in Mesenchymal Stem Cells from Human Infants: A Pilot Study
by Melissa L. Erickson, Devin Dobias, Madeline Rose Keleher, Dana Dabelea, Bryan C. Bergman, Josiane L. Broussard and Kristen E. Boyle
Nutrients 2024, 16(1), 52; https://doi.org/10.3390/nu16010052 - 23 Dec 2023
Viewed by 1252
Abstract
Background: Exposure to intrauterine obesity can disrupt clock gene rhythmicity in animal models. The aim of this pilot study was to determine if maternal obesity alters rhythmic expression of core clock in mesenchymal stem cells (MSCs) from umbilical cords of human infants born [...] Read more.
Background: Exposure to intrauterine obesity can disrupt clock gene rhythmicity in animal models. The aim of this pilot study was to determine if maternal obesity alters rhythmic expression of core clock in mesenchymal stem cells (MSCs) from umbilical cords of human infants born to mothers with obesity (Ob-MSC) vs. normal weight (NW-MSC). Methods: We compared in vitro rhythmic expression patterns of core clock (BMAL1, CLOCK, PER2) and clock-output (NR1D1), components in undifferentiated Ob-MSCs (n = 3) vs. NW-MSCs (n = 3). MSCs were harvested every 2 h, following a dexamethasone shock, for 30 h. Adipogenesis or myogenesis was induced in vitro and markers of adipogenesis and fat storage were assessed, respectively. Results: We detected significant rhythmicity in expression patterns of BMAL1, PER2, and NR1D1 at the group level in Ob- and NW-MSCs (p < 0.05). PER2 oscillatory amplitude was 3-fold higher in Ob-MSCs vs. NW-MSCs (p < 0.006). During adipogenesis, Ob-MSCs had higher PPARγ protein content (p = 0.04) vs. NW-MSC. During myogenesis, Ob-MSCs had higher saturated triacylglycerols (p = 0.04) vs. NW-MSC. Conclusion: Rhythmic expressions of BMAL1, PER2, and NR1D1 are detectable in undifferentiated MSCs. Higher PER2 oscillatory amplitude was paralleled by higher markers of fat storage during differentiation in Ob-MSCs vs. NW-MSCs, and supports that the core clock and cellular metabolism may be linked in infant MSCs. Full article
(This article belongs to the Special Issue Maternal Diet, Epigenetic Mechanisms and Metabolic Programming)
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