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Biomolecules
Special Issues
Early-Life Programming of Metabolic Diseases
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Early-Life Programming of Metabolic Diseases

A special issue of Biomolecules (ISSN 2218-273X). This special issue belongs to the section "Molecular Medicine".

Deadline for manuscript submissions: closed (15 June 2021) | Viewed by 11221

Special Issue Editor

Prof. Dr. Jamileh Movassat

E-Mail Website
Guest Editor
Université de Paris, BFA, UMR 8251, CNRS, Team “Biology and Pathology of the Endocrine Pancreas”, F-75013 Paris, France
Interests: diabetes; pancreatic beta cell; beta cell regeneration; insulin secretion; early-life programming; developmental origin of health and diseases; nutrition-related diseases; obesity; metabolic disorders; diabetes-associated cognitive impairment

Special Issue Information

Dear Colleagues,

The environmental conditions that are experienced in early life can profoundly influence human biology and long-term health. The Developmental Origins of Health and Disease (DOHaD) concept has highlighted the crucial importance of fetal and early postnatal environment in shaping the risk of developing obesity, type 2 diabetes mellitus, cardiovascular diseases, and other complications later in adult life. Although most studies have concentrated on the maternal environment, it is also becoming evident that paternal exposure to deleterious environmental factors can result in the later development of metabolic disorders in offspring. Such programmed effects might not be limited to the first directly exposed generation—they could also be transmitted to the next generations. The mechanisms which underpin the transmission of the programmed effects across generations are still unclear, but epigenetic changes certainly participate in the early life programming of metabolic diseases.

 In the face of the growing pandemic of obesity and diabetes worldwide, elucidation of mechanisms of non-genetic transgenerational transmission of metabolic disorders is of major interest. The identification of nutritional or toxicological factors that affect health in men or women of reproductive age could help to interrupt the vicious cycles of disease risk transmission to their descendants, and bears the potential to halt the diabetes and obesity epidemic encountered at present.

For this Special Issue, we invite review papers or original research articles that address the topic of early-life environmental programming of metabolic disorders, including both paternal and maternal transmission.

Prof. Dr. Jamileh Movassat
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. Biomolecules 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

  • DOHaD
  • environmental programming
  • epigenomics
  • metabolic programming
  • diabetes
  • obesity
  • metabolic syndrome

Published Papers (4 papers)

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Research

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20 pages, 3876 KiB  
Article
Paternal High-Protein Diet Programs Offspring Insulin Sensitivity in a Sex-Specific Manner
by Pengfei Gong, Danielle Bailbé, Lola Bianchi, Gaëlle Pommier, Junjun Liu, Stefania Tolu, Maria G. Stathopoulou, Bernard Portha, Valérie Grandjean and Jamileh Movassat
Biomolecules 2021, 11(5), 751; https://0-doi-org.brum.beds.ac.uk/10.3390/biom11050751 - 18 May 2021
Cited by 7 | Viewed by 2654
Abstract
The impact of maternal nutrition on offspring is well documented. However, the implication of pre-conceptional paternal nutrition on the metabolic health of the progeny remains underexplored. Here, we investigated the impact of paternal high-protein diet (HPD, 43.2% protein) consumption on the endocrine pancreas [...] Read more.
The impact of maternal nutrition on offspring is well documented. However, the implication of pre-conceptional paternal nutrition on the metabolic health of the progeny remains underexplored. Here, we investigated the impact of paternal high-protein diet (HPD, 43.2% protein) consumption on the endocrine pancreas and the metabolic phenotype of offspring. Male Wistar rats were given HPD or standard diet (SD, 18.9% protein) for two months. The progenies (F1) were studied at fetal stage and in adulthood. Body weight, glycemia, glucose tolerance (GT), glucose-induced insulin secretion in vivo (GIIS) and whole-body insulin sensitivity were assessed in male and female F1 offspring. Insulin sensitivity, GT and GIIS were similar between F1 females from HPD (HPD/F1) and SD fathers (SD/F1). Conversely, male HPD/F1 exhibited increased insulin sensitivity (p < 0.05) and decreased GIIS (p < 0.05) compared to male SD/F1. The improvement of insulin sensitivity in HPD/F1 was sustained even after 2 months of high-fat feeding. In male HPD/F1, the β cell mass was preserved and the β cell plasticity, following metabolic challenge, was enhanced compared to SD/F1. In conclusion, we provide the first evidence of a sex-specific impact of paternal HPD on the insulin sensitivity and GIIS of their descendants, demonstrating that changes in paternal nutrition alter the metabolic status of their progeny in adulthood. Full article
(This article belongs to the Special Issue Early-Life Programming of Metabolic Diseases)
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12 pages, 1357 KiB  
Article
Effect of Postnatal Nutritional Environment Due to Maternal Diabetes on Beta Cell Mass Programming and Glucose Intolerance Risk in Male and Female Offspring
by Danièle Bailbe, Junjun Liu, Pengfei Gong and Bernard Portha
Biomolecules 2021, 11(2), 179; https://0-doi-org.brum.beds.ac.uk/10.3390/biom11020179 - 28 Jan 2021
Cited by 2 | Viewed by 1777
Abstract
Besides the fetal period, the suckling period is a critical time window in determining long-term metabolic health. We undertook the present study to elucidate the impact of a diabetic suckling environment alone or associated with an in utero diabetic environment on beta cell [...] Read more.
Besides the fetal period, the suckling period is a critical time window in determining long-term metabolic health. We undertook the present study to elucidate the impact of a diabetic suckling environment alone or associated with an in utero diabetic environment on beta cell mass development and the risk of diabetes in the offspring in the long term. To that end, we have compared two experimental settings. In setting 1, we used Wistar (W) rat newborns resulting from W ovocytes (oW) transferred into diabetic GK rat mothers (pGK). These oW/pGK neonates were then suckled by diabetic GK foster mothers (oW/pGK/sGK model) and compared to oW/pW neonates suckled by normal W foster mothers (oW/pW/sW model). In setting 2, normal W rat newborns were suckled by diabetic GK rat foster mothers (nW/sGK model) or normal W foster mothers (nW/sW model). Our data revealed that the extent of metabolic disorders in term of glucose intolerance and beta cell mass are similar between rats which have been exposed to maternal diabetes both pre- and postnatally (oW/pGK/sGK model) and those which have been exposed only during postnatal life (nW/sW model). In other words, being nurtured by diabetic GK mothers from birth to weaning was sufficient to significantly alter the beta cell mass, glucose-induced insulin secretion and glucose homeostasis of offspring. No synergistic deleterious effects of pre-and postnatal exposure was observed in our setting. Full article
(This article belongs to the Special Issue Early-Life Programming of Metabolic Diseases)
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Review

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21 pages, 407 KiB  
Review
Early Life Exposure to Food Contaminants and Social Stress as Risk Factor for Metabolic Disorders Occurrence?—An Overview
by Laurence Guzylack-Piriou and Sandrine Ménard
Biomolecules 2021, 11(5), 687; https://0-doi-org.brum.beds.ac.uk/10.3390/biom11050687 - 03 May 2021
Cited by 3 | Viewed by 3095
Abstract
The global prevalence of obesity has been increasing in recent years and is now the major public health challenge worldwide. While the risks of developing metabolic disorders (MD) including obesity and type 2 diabetes (T2D) have been historically thought to be essentially driven [...] Read more.
The global prevalence of obesity has been increasing in recent years and is now the major public health challenge worldwide. While the risks of developing metabolic disorders (MD) including obesity and type 2 diabetes (T2D) have been historically thought to be essentially driven by increased caloric intake and lack of exercise, this is insufficient to account for the observed changes in disease trends. Based on human epidemiological and pre-clinical experimental studies, this overview questioned the role of non-nutritional components as contributors to the epidemic of MD with a special emphasis on food contaminants and social stress. This overview examines the impact of early life adverse events (ELAE) focusing on exposures to food contaminants or social stress on weight gain and T2D occurrence in the offspring and explores potential mechanisms leading to MD in adulthood. Indeed, summing up data on both ELAE models in parallel allowed us to identify common patterns that appear worthwhile to study in MD etiology. This overview provides some evidence of a link between ELAE-induced intestinal barrier disruption, inflammation, epigenetic modifications, and the occurrence of MD. This overview sums up evidence that MD could have developmental origins and that ELAE are risk factors for MD at adulthood independently of nutritional status. Full article
(This article belongs to the Special Issue Early-Life Programming of Metabolic Diseases)
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17 pages, 1523 KiB  
Review
Prenatal Hyperglycemia Exposure and Cellular Stress, a Sugar-Coated View of Early Programming of Metabolic Diseases
by Jessica Tozour, Francine Hughes, Arnaud Carrier, Didier Vieau and Fabien Delahaye
Biomolecules 2020, 10(10), 1359; https://0-doi-org.brum.beds.ac.uk/10.3390/biom10101359 - 23 Sep 2020
Cited by 7 | Viewed by 2998
Abstract
Worldwide, the number of people with diabetes has quadrupled since 1980 reaching 422 million in 2014 (World Health Organization). This distressing rise in diabetes also affects pregnant women and thus, in regard to early programming of adult diseases, creates a vicious cycle of [...] Read more.
Worldwide, the number of people with diabetes has quadrupled since 1980 reaching 422 million in 2014 (World Health Organization). This distressing rise in diabetes also affects pregnant women and thus, in regard to early programming of adult diseases, creates a vicious cycle of metabolic dysfunction passed from one generation to another. Metabolic diseases are complex and caused by the interplay between genetic and environmental factors. High-glucose exposure during in utero development, as observed with gestational diabetes mellitus (GDM), is an established risk factor for metabolic diseases. Despite intense efforts to better understand this phenomenon of early memory little is known about the molecular mechanisms associating early exposure to long-term diseases risk. However, evidence promotes glucose associated oxidative stress as one of the molecular mechanisms able to influence susceptibility to metabolic diseases. Thus, we decided here to further explore the relationship between early glucose exposure and cellular stress in the context of early development, and focus on the concept of glycemic memory, its consequences, and sexual dimorphic and epigenetic aspects. Full article
(This article belongs to the Special Issue Early-Life Programming of Metabolic Diseases)
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