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Maternal Nutrition and Fetal Programming

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A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Clinical Nutrition".

Deadline for manuscript submissions: closed (20 December 2023) | Viewed by 5253

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Dr. Filipa I. Baptista

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Guest Editor

1. Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University of Coimbra,3000-548 Coimbra, Portugal
2. Center for Innovative Biomedicine and Biotechnology (CIBB), University of Coimbra, 3000-548 Coimbra, Portugal
3. Clinical Academic Center of Coimbra, 3000-548 Coimbra, Portugal
Interests: diabetes during pregnancy; prenatal stress; neurodevelopmental disorders; sex differences; microglia

Dr. Joana Gonçalves

E-Mail Website1 Website2
Co-Guest Editor

1. Coimbra Institute for Biomedical Imaging and Translational Research (CIBIT), University of Coimbra, 3000-548 Coimbra, Portugal
2. Institute for Nuclear Sciences Applied to Health (ICNAS), University of Coimbra, 3000-548 Coimbra, Portugal
Interests: neurodevelopmental disorders; gestational nutrition; sex dimorphism; excitation/inhibition balance; animal behavior
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Dear Colleagues,

Maternal nutrition plays a vital role in fetal development and growth. Nutritional insults during the critical windows of development, namely in pregnancy, may have long-term consequences on development, predisposing the offspring to several pathological conditions in postnatal life. This fetal programming, which permanently changes offspring physiology, has been associated with mental health problems.

Dietary imbalances, nutrient deficiencies, and maternal supplements during gestation may influence brain development during this sensitive developmental period, reshape brain structure and function, and program progeny susceptibility to neurodevelopmental disorders.

With this in mind, we would like to invite the submission of original articles and reviews addressing the impact of maternal nutritional status and maternal diets during pregnancy on progeny development and its association with neurodevelopmental disorders. Further insights on potential underlying mechanisms as neuroinflammation, gut microbiome changes, and fetal genetic programming are appreciated.

Dr. Filipa I. Baptista
Dr. Joana Gonçalves
Guest Editors

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Keywords

maternal nutrition
maternal diet
fetal programming
nutrient imbalance
neurodevelopmental disorders
psychiatric disorders
pregnancy
animal models
clinical studies

Published Papers (4 papers)

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Research

14 pages, 1654 KiB

Open AccessArticle

Fructose Consumption Affects Placental Production of H₂S: Impact on Preeclampsia-Related Parameters

by Madelín Pérez-Armas, Elena Fauste, Cristina Donis, Silvia Rodrigo, Lourdes Rodríguez, Juan J. Álvarez-Millán, María I. Panadero, Paola Otero and Carlos Bocos

Nutrients 2024, 16(2), 309; https://doi.org/10.3390/nu16020309 - 20 Jan 2024

Viewed by 984

Abstract

H₂S, a gasotransmitter that can be produced both via the transsulfuration pathway and non-enzymatically, plays a key role in vasodilation and angiogenesis during pregnancy. In fact, the involvement of H₂S production on plasma levels of sFLT1, PGF, and other molecules related to preeclampsia has been demonstrated. Interestingly, we have found that maternal fructose intake (a common component of the Western diet) affects tissular H₂S production. However, its consumption is allowed during pregnancy. Thus, (1) to study whether maternal fructose intake affects placental production of H₂S in the offspring, when pregnant; and (2) to study if fructose consumption during pregnancy can increase the risk of preeclampsia, pregnant rats from fructose-fed mothers (10% w/v) subjected (FF) or not (FC) to a fructose supplementation were studied and compared to pregnant control rats (CC). Placental gene expression, H₂S production, plasma sFLT1, and PGF were determined. Descendants of fructose-fed mothers (FC) presented an increase in H₂S production. However, if they consumed fructose during their own gestation (FF), this effect was reversed so that the increase disappeared. Curiously, placental synthesis of H₂S was mainly non-enzymatic. Related to this, placental expression of Cys dioxygenase, an enzyme involved in Cys catabolism (a molecule required for non-enzymatic H₂S synthesis), was significantly decreased in FC rats. Related to preeclampsia, gene expression of sFLT1 (a molecule with antiangiogenic properties) was augmented in both FF and FC dams, although these differences were not reflected in their plasma levels. Furthermore, placental expression of PGF (a molecule with angiogenic properties) was decreased in both FC and FF dams, becoming significantly diminished in plasma of FC versus control dams. Both fructose consumption and maternal fructose intake induce changes in molecules that contribute to increasing the risk of preeclampsia, and these effects are not always mediated by changes in H₂S production. Full article

(This article belongs to the Special Issue Maternal Nutrition and Fetal Programming)

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25 pages, 6922 KiB

Open AccessArticle

The Effect of Maternal High-Fat Diet on Adipose Tissue Histology and Lipid Metabolism-Related Genes Expression in Offspring Rats

by Sabriye Arslan, Hilal Yıldıran and Cemile Merve Seymen

Nutrients 2024, 16(1), 150; https://doi.org/10.3390/nu16010150 - 02 Jan 2024

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Abstract

The developing fetus is dependent on the maternal nutritional environment. This study was conducted to determine the effects of a maternal high-fat diet (HFD) applied during pregnancy and/or lactation on the expression levels of some lipid-related genes in rat models. Half of the pregnant rats (n: 6) were fed an HFD (energy from fat: 45%), while the other half (n: 6) were fed a control diet (CD) (energy from fat, 7.7%) during the pregnancy period. During lactation, dams in both groups were divided into two subgroups, with half fed the CD and the other half fed the HFD. Thus, four groups were obtained: CD-CD, CD-HFD, HFD-CD, and HFD-HFD. At the end of lactation, all mothers and half of the offspring were sacrificed. The remaining offspring were fed a CD for five weeks. The average birth weight of the CD group offspring was found to be lower than that of the HFD group (p < 0.05). The amount of adipose tissue was highest in CD-HFD (p < 0.05), while gene expression levels were similar between groups (p > 0.05), and the most degenerative histological changes were observed in the eight-week HFD-HFD (p < 0.05). This study suggests that maternal HFD during pregnancy and lactation may increase adiposity in offspring rats, especially during the weaning period. Full article

(This article belongs to the Special Issue Maternal Nutrition and Fetal Programming)

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21 pages, 4303 KiB

Open AccessArticle

Postnatal Overfeeding in Rodents Induces a Neurodevelopment Delay and Anxious-like Behaviour Accompanied by Sex- and Brain-Region-Specific Synaptic and Metabolic Changes

by Andreia Amaro, Diana Sousa, Mariana Sá-Rocha, Marcos Divino Ferreira-Junior, Daniela Rosendo-Silva, Lucas Paulo Jacinto Saavedra, Cátia Barra, Tamaeh Monteiro-Alfredo, Rodrigo Mello Gomes, Paulo Cezar de Freitas Mathias, Filipa I. Baptista and Paulo Matafome

Nutrients 2023, 15(16), 3581; https://doi.org/10.3390/nu15163581 - 15 Aug 2023

Viewed by 1035

Abstract

Nutritional disturbances during the early postnatal period can have long-lasting effects on neurodevelopment and may be related to behavioural changes at adulthood. While such neuronal connection disruption can contribute to social and behaviour alterations, the dysregulation of the neuroendocrine pathways involved in nutrient-sensing balance may also cause such impairments, although the underlying mechanisms are still unclear. We aimed to evaluate sex-specific neurodevelopmental and behavioural changes upon postnatal overfeeding and determine the potential underpinning mechanisms at the central nervous system level, with a focus on the interconnection between synaptic and neuroendocrine molecular alterations. At postnatal day 3 (PND3) litters were culled to three animals (small litter procedure). Neurodevelopmental tests were conducted at infancy, whereas behavioural tests to assess locomotion, anxiety, and memory were performed at adolescence, together with molecular analysis of the hippocampus, hypothalamus, and prefrontal cortex. At infancy, females presented impaired acquisition of an auditory response, eye opening, olfactory discrimination, and vestibular system development, suggesting that female offspring neurodevelopment/maturation was deeply affected. Male offspring presented a transitory delay in locomotor performance., while both offspring had lower upper limb strength. At adolescence, both sexes presented anxious-like behaviour without alterations in short-term memory retention. Both males and females presented lower NPY1R levels in a region-specific manner. Furthermore, both sexes presented synaptic changes in the hippocampus (lower GABA_A in females and higher GABA_A levels in males), while, in the prefrontal cortex, similar higher GABA_A receptor levels were observed. At the hypothalamus, females presented synaptic changes, namely higher vGLUT1 and PSD95 levels. Thus, we demonstrate that postnatal overfeeding modulates offspring behaviour and dysregulates nutrient-sensing mechanisms such as NPY and GABA in a sex- and brain-region-specific manner. Full article

(This article belongs to the Special Issue Maternal Nutrition and Fetal Programming)

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19 pages, 2251 KiB

Open AccessArticle

Effects on Fetal Metabolic Programming and Endocannabinoid System of a Normocaloric Diet during Pregnancy and Lactation of Female Mice with Pregestational Obesity

by Cynthia Barrera, Valeska Castillo, Rodrigo Valenzuela, Carina A. Valenzuela, Diego F. Garcia-Diaz and Miguel Llanos

Nutrients 2023, 15(16), 3531; https://doi.org/10.3390/nu15163531 - 11 Aug 2023

Cited by 1 | Viewed by 1120

Abstract

Fetal programming provides explanatory mechanisms for the currently high prevalence of gestational obesity. The endocannabinoid system (ECS) participates in the regulation of energy balance, and with a high-fat diet (HFD), it is overactivated. The aim of this study was to determine the effects of a nutritional intervention during pregnancy and lactation on obese female progenitors, on metabolic alterations of the offspring and on the involvement of ECS. Female mice (C57/BL/6-F0), 45 days old, and their offspring (males) were separated according to type of diet before and during gestation and lactation: CON-F1: control diet; HFD-F1 group: HFD (fat: 60% Kcal); INT-F1 group: HFD until mating and control diet (fat: 10% Kcal) afterward. Glucose tolerance and insulin sensitivity (IS) were tested at 2 and 4 months. At 120 days, mice were sacrificed, plasma was extracted for the determination of hormones, and livers for gene expression and the protein level determination of ECS components. INT-F1 group presented a lower IS compared to CON-F1, and normal levels of adiponectin and corticosterone in relation to the HFD-F1 group. The intervention increased hepatic gene expression for fatty-acid amide hydrolase and monoacylglycerol lipase enzymes; however, these differences were not observed at the protein expression level. Our results suggest that this intervention model normalized some hormonal parameters and hepatic mRNA levels of ECS components that were altered in the offspring of progenitors with pre-pregnancy obesity. Full article

(This article belongs to the Special Issue Maternal Nutrition and Fetal Programming)

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