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Maternal and Early Life Programming of Childhood Health: A Nutritional and Epigenetic Investigation

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

Deadline for manuscript submissions: closed (30 April 2019) | Viewed by 16161

Special Issue Editors


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Guest Editor
School of Public Health, Physiotherapy and Sports Science, University College Dublin, Dublin, Ireland
Interests: developmental origins of health and disease; diet; lifestyle; biomarkers; inflammation; obesity; metabolic health
Special Issues, Collections and Topics in MDPI journals

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Guest Editor
Institute of Epidemiology and Preventive Medicine, College of Public Health, National Taiwan University, Taipei, Taiwan
Interests: nutritional epidemiology; lifecourse epidemiology; DOHaD; body composition; maternal and child nutrition
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Accumulating evidence suggests that early life exposure to a range of environmental factors, including nutrition, plays a key role in defining offspring health, both in childhood and in later life. According to the Developmental Origins of Health and Disease (DOHaD) hypothesis, transient environmental exposures during critical periods of growth and development (such as the periconceptional, fetal, and early infant phases of life) can alter normal physiology and have a persistent impact on metabolism and gene expression thereby influencing disease risk in later life. Such long-term consequences may not only be limited to one generation but may lead to poor health in future generations, even in the absence of direct exposure. Epigenetic phenomena (particularly DNA methylation) have been proposed as mechanisms by which fetal or early life environment may affect offspring phenotype and health years after exposure.

This Special Issue, “Maternal and Early Life Programming of Childhood Health: A Nutritional and Epigenetic Investigation”, will include original research and scientific perspectives on the influence of maternal, paternal and early life exposures (with a focus on nutrition, either as individual components or patterns) on a range of offspring health outcomes (including obesity, cardiometabolic health, type 2 diabetes, cancer, respiratory conditions, osteoporosis and neurodevelopmental disorders). In addition, the influence of these exposures on the epigenome will be discussed and the role of epigenetics in mediating diet-health relationships will be explored.  

Dr. Catherine Phillips
Dr. Ling-Wei Chen
Guest Editors

Manuscript Submission Information

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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

  • Pregnancy
  • Maternal
  • Paternal
  • Nutrition
  • Dietary patterns
  • Fetal programming
  • Epigenetics
  • Obesity
  • Cardiometabolic health
  • Type 2 diabetes
  • Cancer
  • Asthma
  • Osteoporosis
  • Neurodevelopment

Published Papers (4 papers)

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Research

16 pages, 1573 KiB  
Article
Adherence to the Healthy Eating Index-2015 across Generations Is Associated with Birth Outcomes and Weight Status at Age 5 in the Lifeways Cross-Generation Cohort Study
by Pilar Navarro, John Mehegan, Celine M. Murrin, Cecily C. Kelleher and Catherine M. Phillips
Nutrients 2019, 11(4), 928; https://doi.org/10.3390/nu11040928 - 25 Apr 2019
Cited by 25 | Viewed by 5592
Abstract
Maternal dietary quality during pregnancy is associated with offspring outcomes. These associations have not been examined in three-generation families. We investigated associations between parental and grandparental dietary quality, determined by healthy eating index (HEI)-2015, and offspring birth outcomes and weight status at age [...] Read more.
Maternal dietary quality during pregnancy is associated with offspring outcomes. These associations have not been examined in three-generation families. We investigated associations between parental and grandparental dietary quality, determined by healthy eating index (HEI)-2015, and offspring birth outcomes and weight status at age 5. The Lifeways cohort study in the Republic of Ireland comprises 1082 index-child’s mothers, 333 index-child’s fathers, and 707 grandparents. HEI-2015 scores were generated for all adults from prenatal dietary information collected using a validated food frequency questionnaire. In an adjusted model, greater adherence to the maternal HEI was associated with lower likelihood of low birth weight (LBW) (OR: 0.72, 95% CI: 0.50–0.99, p = 0.04). Similarly, maternal grandmothers (MGM) with higher HEI scores were less likely to have grandchildren with LBW (OR: 0.87, 95% CI: 0.61–0.96, p = 0.04) and more likely to have macrosomia (OR: 1.10, 95% CI: 1.01–1.22, p = 0.03). Higher paternal and paternal grandmothers (PGM) HEI scores were associated with lower likelihood of childhood obesity (OR: 0.89, 95% CI: 0.30–0.94, p = 0.03) and overweight (OR: 0.83, 95% CI: 0.22–0.99, p = 0.04), respectively. Mediation analysis showed significant direct relationship of MGM and PGM HEI scores on grandchildren’s birthweight and obesity, respectively. In conclusion, maternal line dietary quality appears to influence fetal growth whereas paternal line dietary quality appears to influence postnatal growth. Full article
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17 pages, 2133 KiB  
Article
Effect of Sucrose Ingestion at the End of a Critical Window that Increases Hypertension Susceptibility on Peripheral Mechanisms Regulating Blood Pressure in Rats. Role of Sirtuins 1 and 3
by Vicente Castrejón-Téllez, Mariana Villegas-Romero, Israel Pérez-Torres, Gabriela Zarco, María Esther Rubio-Ruiz, Elizabeth Carreón-Torres, Eulises Díaz-Díaz, Oscar Emanuel Grimaldo and Verónica Guarner-Lans
Nutrients 2019, 11(2), 309; https://doi.org/10.3390/nu11020309 - 01 Feb 2019
Cited by 9 | Viewed by 3127
Abstract
Susceptibility to develop hypertension may be established during early stages of life that include the intrauterine period, infancy and childhood. We recently showed that blood pressure increased when rats reached adulthood when sucrose was ingested for a short-term critical window from postnatal day [...] Read more.
Susceptibility to develop hypertension may be established during early stages of life that include the intrauterine period, infancy and childhood. We recently showed that blood pressure increased when rats reached adulthood when sucrose was ingested for a short-term critical window from postnatal day 12 to 28 in the rat, which corresponds to days around weaning. Here, we studied several factors that might participate in the increased susceptibility to hypertension when adulthood is reached by analyzing the changes produced at the end of the sucrose ingestion during this critical period. Body weight of the rats at the end of the sucrose period was decreased even if there was an increased ingestion in Kcal. We found an increase in blood pressure accompanied by a decrease in endothelial nitric oxide synthase (eNOS) expression in the aorta. When insulin was administered to rats receiving sucrose, glucose in plasma diminished later than in controls and this slight insulin resistance may reduce nitric oxide synthase action. Oleic acid that modulates eNOS expression was increased, lipoperoxidation was elevated and total non-enzymatic anti-oxidant capacity was decreased. There was also a decrease in SOD2 expression. We also studied the expression of Sirt1, which regulates eNOS expression and Sirt3, which regulates SOD2 expression as possible epigenetic targets of enzyme expression involved in the long- term programming of hypertension. Sirt3 was decreased but we did not find an alteration in Sirt1 expression. We conclude that these changes may underpin the epigenetic programming of increased susceptibility to develop hypertension in the adults when there was exposure to high sucrose levels near weaning in rats. Full article
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19 pages, 1972 KiB  
Article
Direct and Long-Term Metabolic Consequences of Lowly vs. Highly-Digestible Starch in the Early Post-Weaning Diet of Mice
by José M. S. Fernández-Calleja, Lianne M. S. Bouwman, Hans J. M. Swarts, Annemarie Oosting, Jaap Keijer and Evert M. Van Schothorst
Nutrients 2018, 10(11), 1788; https://doi.org/10.3390/nu10111788 - 17 Nov 2018
Cited by 7 | Viewed by 3725
Abstract
Starches of low and high digestibility have different metabolic effects. Here, we examined whether this gives differential metabolic programming when fed in the immediate post-weaning period. Chow-fed mice were time-mated, and their nests were standardized and cross-fostered at postnatal days 1–2. After postnatal [...] Read more.
Starches of low and high digestibility have different metabolic effects. Here, we examined whether this gives differential metabolic programming when fed in the immediate post-weaning period. Chow-fed mice were time-mated, and their nests were standardized and cross-fostered at postnatal days 1–2. After postnatal week (PW) 3, individually housed female and male offspring were switched to a lowly-digestible (LDD) or highly-digestible starch diet (HDD) for three weeks. All of the mice received the same high-fat diet (HFD) for nine weeks thereafter. Energy and substrate metabolism and carbohydrate fermentation were studied at the end of the HDD/LDD and HFD periods by extended indirect calorimetry. Glucose tolerance (PW 11) and metabolic flexibility (PW14) were analyzed. Directly in response to the LDD versus the HDD, females showed smaller adipocytes with less crown-like structures in gonadal white adipose tissue, while males had a lower fat mass and higher whole body fat oxidation levels. Both LDD-fed females and males showed an enlarged intestinal tract. Although most of the phenotypical differences disappeared in adulthood in both sexes, females exposed to LDD versus HDD in the early post-weaning period showed improved metabolic flexibility in adulthood. Cumulatively, these results suggest that the type of starch introduced after weaning could, at least in females, program later-life health. Full article
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13 pages, 1726 KiB  
Article
Maternal Melatonin Therapy Attenuates Methyl-Donor Diet-Induced Programmed Hypertension in Male Adult Rat Offspring
by You-Lin Tain, Julie Y. H. Chan, Chien-Te Lee and Chien-Ning Hsu
Nutrients 2018, 10(10), 1407; https://doi.org/10.3390/nu10101407 - 02 Oct 2018
Cited by 32 | Viewed by 3072
Abstract
Although pregnant women are advised to consume methyl-donor food, some reports suggest an adverse outcome. We investigated whether maternal melatonin therapy can prevent hypertension induced by a high methyl-donor diet. Female Sprague-Dawley rats received either a normal diet, a methyl-deficient diet (L-MD), or [...] Read more.
Although pregnant women are advised to consume methyl-donor food, some reports suggest an adverse outcome. We investigated whether maternal melatonin therapy can prevent hypertension induced by a high methyl-donor diet. Female Sprague-Dawley rats received either a normal diet, a methyl-deficient diet (L-MD), or a high methyl-donor diet (H-MD) during gestation and lactation. Male offspring were assigned to four groups (n = 7–8/group): control, L-MD, H-MD, and H-MD rats were given melatonin (100 mg/L) with their drinking water throughout the period of pregnancy and lactation (H-MD+M). At 12 weeks of age, male offspring exposed to a L-MD or a H-MD diet developed programmed hypertension. Maternal melatonin therapy attenuated high methyl-donor diet-induced programmed hypertension. A maternal L-MD diet and H-MD diet caused respectively 938 and 806 renal transcripts to be modified in adult offspring. The protective effects of melatonin against programmed hypertension relate to reduced oxidative stress, increased urinary NO2 level, and reduced renal expression of sodium transporters. A H-MD or L-MD diet may upset the balance of methylation status, leading to alterations of renal transcriptome and programmed hypertension. A better understanding of reprogramming effects of melatonin might aid in developing a therapeutic strategy for the prevention of hypertension in adult offspring exposed to an excessive maternal methyl-supplemented diet. Full article
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