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Early Overnutrition and Long-Term Health Effects

A special issue of Nutrients (ISSN 2072-6643).

Deadline for manuscript submissions: closed (28 October 2019) | Viewed by 7663

Special Issue Editor


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Guest Editor
Swiss Federal Institute of Technology, ETH Zürich, Department of Health Sciences and Technology, Institute for Neuroscience, Schorenstrasse 16, 8603 Schwerzenbach, Switzerland
Interests: eating disorders; maternal overnutrition; psychiatric disorders; addiction; stress; nutrition; cognitive function; aging
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Special Issue Information

Dear Colleagues,

Research in the past two decades has shown that the origin of obesity and other non-communicable diseases starts already before birth and is influenced by nutrition. Nutrition of an individual during early development: during gestation, lactation, and postnatally is known to induce lifelong health adversities. Therefore, the quality and quantity of nutrition during these sensitive time periods of development can increase the risk to develop different diseases, such as obesity, metabolic syndrome, cardiovascular disorder, cognitive function, as well as psychopathological disorders. This special issue will cover how early nutrition can affect the long-term health of an individual:

  • How early overnutrition affects the risk of developing different health advertise;
  • How specific non-communicable diseases are associated with early-life overnutrition;
  • The long-term effects of overnutrition during different stages of development, from fetal life to juvenilty;
  • Can prevention of early-life overnutrition help in overcoming these different non-communicble diseases later in life?

Dr. Daria Peleg-Raibstein
Guest Editor

Manuscript Submission Information

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Keywords

  • Maternal nutrition
  • Postnatal nutrition
  • Behavior
  • Development
  • Cognitive abilities
  • Obesity
  • Overnutrition
  • Metabolic disorders
  • Mental disorders
  • Breastfeeding
  • Children
  • Juvenile

Published Papers (2 papers)

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Research

14 pages, 5073 KiB  
Article
Maternal Exposure to High-Fat Diet Induces Long-Term Derepressive Chromatin Marks in the Heart
by Guillaume Blin, Marjorie Liand, Claire Mauduit, Hassib Chehade, Mohamed Benahmed, Umberto Simeoni and Benazir Siddeek
Nutrients 2020, 12(1), 181; https://doi.org/10.3390/nu12010181 - 9 Jan 2020
Cited by 17 | Viewed by 3810
Abstract
Heart diseases are a leading cause of death. While the link between early exposure to nutritional excess and heart disease risk is clear, the molecular mechanisms involved are poorly understood. In the developmental programming field, increasing evidence is pointing out the critical role [...] Read more.
Heart diseases are a leading cause of death. While the link between early exposure to nutritional excess and heart disease risk is clear, the molecular mechanisms involved are poorly understood. In the developmental programming field, increasing evidence is pointing out the critical role of epigenetic mechanisms. Among them, polycomb repressive complex 2 (PRC2) and DNA methylation play a critical role in heart development and pathogenesis. In this context, we aimed at evaluating the role of these epigenetic marks in the long-term cardiac alterations induced by early dietary challenge. Using a model of rats exposed to maternal high-fat diet during gestation and lactation, we evaluated cardiac alterations at adulthood. Expression levels of PRC2 components, its histone marks di- and trimethylated histone H3 (H3K27me2/3), associated histone mark (ubiquitinated histone H2A, H2AK119ub1) and target genes were measured by Western blot. Global DNA methylation level and DNA methyl transferase 3B (DNMT3B) protein levels were measured. Maternal high-fat diet decreased H3K27me3, H2Ak119ub1 and DNA methylation levels, down-regulated the enhancer of zeste homolog 2 (EZH2), and DNMT3B expression. The levels of the target genes, isl lim homeobox 1 (Isl1), six homeobox 1 (Six1) and mads box transcription enhancer factor 2, polypeptide C (Mef2c), involved in cardiac pathogenesis were up regulated. Overall, our data suggest that the programming of cardiac alterations by maternal exposure to high-fat diet involves the derepression of pro-fibrotic and pro-hypertrophic genes through the induction of EZH2 and DNMT3B deficiency. Full article
(This article belongs to the Special Issue Early Overnutrition and Long-Term Health Effects)
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13 pages, 5725 KiB  
Article
Calorie Restriction in Adulthood Reduces Hepatic Disorders Induced by Transient Postnatal Overfeeding in Mice
by Catherine Yzydorczyk, Na Li, Eve Rigal, Hassib Chehade, Dolores Mosig, Jean Baptiste Armengaud, Thibaud. Rolle, Anithan Krishnasamy, Eulalia Orozco, Benazir Siddeek, Christian Juvet, Catherine Vergely and Umberto Simeoni
Nutrients 2019, 11(11), 2796; https://doi.org/10.3390/nu11112796 - 16 Nov 2019
Cited by 18 | Viewed by 3124
Abstract
Impaired early nutrition influences the risk of developing metabolic disorders in later life. We observed that transient postnatal overfeeding (OF) in mice induces long-term hepatic alterations, characterized by microsteatosis, fibrosis associated with oxidative stress (OS), and stress-induced premature senescence (SIPS). In this study, [...] Read more.
Impaired early nutrition influences the risk of developing metabolic disorders in later life. We observed that transient postnatal overfeeding (OF) in mice induces long-term hepatic alterations, characterized by microsteatosis, fibrosis associated with oxidative stress (OS), and stress-induced premature senescence (SIPS). In this study, we investigated whether such changes can be reversed by moderate calorie restriction (CR). C57BL/6 male mice pups were maintained during lactation in litters adjusted to nine pups in the normal feeding (NF) group and three pups in the transient postnatal OF group. At six months of age, adult mice from the NF and OF groups were randomly assigned to an ad libitum diet or CR (daily energy supply reduced by 20%) for one month. In each group, at the age of seven months, analysis of liver structure, liver markers of OS (superoxide anion, antioxidant defenses), and SIPS (lipofuscin, p53, p21, p16, pRb/Rb, Acp53, sirtuin-1) were performed. CR in the OF group reduced microsteatosis, decreased levels of superoxide anion, and increased protein expression of catalase and superoxide dismutase. Moreover, CR decreased lipofuscin staining, p21, p53, Acp53, and p16 but increased pRb/Rb and sirtuin-1 protein expression. CR did not affect the NF group. These results suggest that CR reduces hepatic disorders induced by OF. Full article
(This article belongs to the Special Issue Early Overnutrition and Long-Term Health Effects)
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