scholarly journals What is the evidence in humans that DNA methylation changes link events in utero and later life disease?

2013 ◽  
Vol 78 (6) ◽  
pp. 814-822 ◽  
Author(s):  
Rebecca M. Reynolds ◽  
Greta H. Jacobsen ◽  
Amanda J. Drake
Keyword(s):  
Dna Methylation ◽  
Later Life ◽  
In Utero

scholarly journals Methionine metabolism in Yucatan miniature swine

2016 ◽  
Vol 41 (6) ◽  
pp. 691-691 ◽  
Author(s):  
Laura E. McBreairty
Keyword(s):  
Dna Methylation ◽  
Supply And Demand ◽  
Later Life ◽  
In Utero ◽  
Methionine Metabolism ◽  
Miniature Swine ◽  
Methyl Group ◽  
Epigenetic Patterns ◽  
Poor Nutrition ◽  
Lower Capacity

Methionine is an essential amino acid which when not incorporated into protein, can be converted to S-adenosylmethionine, the universal methyl donor in over 200 transmethylation reactions, which include creatine and phosphatidylcholine (PC) synthesis, as well as deoxyribonucleic acid (DNA) methylation. Following transmethylation, homocysteine is formed, which can be converted to cysteine via transsulfuration or remethylated to methionine by receiving a methyl group from folate or betaine. Changes to methyl group availability in utero can lead to permanent changes in epigenetic patterns of DNA methylation, which has been implicated in “fetal programming”, a phenomenon associated with poor nutrition during fetal development that results in low birth weight and disease in later life. It has been shown that programming can also occur in the neonate. Our global objective was to understand how the variability of nutrients involved in methionine metabolism can affect methionine and methyl group availability. We hypothesize that nutrients that converge on methionine metabolism can affect methionine availability for its various functions. In this thesis, we used intrauterine growth restricted (IUGR) piglets to investigate whether a global nutritional insult in utero can lead to a perturbed methionine metabolism. Our results demonstrate that IUGR piglets have a lower capacity to dispose of homocysteine via both transsulfuration and remethylation pathways, as well as a lower incorporation of methyl groups into PC. The second objective of this thesis was to determine whether variation in methionine supply and demand can affect methionine availability. We demonstrated that stimulating either acute or chronic creatine synthesis leads to lower methyl incorporation into protein and PC in pigs. Furthermore, when methionine is limiting, supplementation with either folate or betaine leads to higher methionine availability for protein synthesis. Finally, because creatine is increasingly being utilized as an ergogenic and neuroprotective supplement, we wanted to determine whether provision of the creatine precursor, guanidinoacetate (GAA), could effectively increase tissue creatine stores. We showed that 2.5 weeks of supplementation with GAA is more effective than creatine at increasing hepatic and muscle creatine stores. The results of this thesis demonstrate that the presence of IUGR, an increased demand for creatine synthesis, or the supplementation with remethylation nutrients can each affect methionine availability; all are important when considering neonatal nutrient requirements. Furthermore, although GAA is effective at increasing levels of tissue creatine, higher GAA methylation can limit methionine availability for growth and synthesis of PC.

scholarly journals Impact of in Utero Folate Exposure on Dna Methylation and Its Potential Relevance for Later‐Life Health – Evidence from Mouse Models Translated to Human Cohorts

2021 ◽  
pp. 2100789
Author(s):  
Dieuwertje E Kok ◽  
Richmond Rebecca C ◽  
Michiel Adriaens ◽  
Chris T Evelo ◽  
Dianne Ford ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Mouse Models ◽  
Later Life ◽  
In Utero

scholarly journals Genome-wide DNA methylation at birth in relation to in utero arsenic exposure and the associated health in later life

2017 ◽  
Vol 16 (1) ◽  
Author(s):  
Akhilesh Kaushal ◽  
Hongmei Zhang ◽  
Wilfried J. J. Karmaus ◽  
Todd M. Everson ◽  
Carmen J. Marsit ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Arsenic Exposure ◽  
Later Life ◽  
In Utero ◽  
Genome Wide

Folate and DNA methylation during in utero development and aging

2004 ◽  
Vol 32 (6) ◽  
pp. 1006-1007 ◽  
Author(s):  
J.A. McKay ◽  
E.A. Williams ◽  
J.C. Mathers
Keyword(s):  
Dna Methylation ◽  
Folic Acid ◽  
Disease Risk ◽  
Neurological Diseases ◽  
Later Life ◽  
In Utero ◽  
Dietary Factors ◽  
Development And Aging ◽  
In Utero Development ◽  
The Impact

DNA methylation is one of several epigenetic mechanisms that play a regulatory role in genome programming and imprinting during embryogenesis. Aberrant DNA methylation has been implicated in the pathogenesis of a number of diseases associated with aging, including cancer and cardiovascular and neurological diseases. Evidence is accumulating that dietary factors in utero modulate disease risk in later life. Although folic acid is a key component of DNA methylation, the impact of folic acid availability in utero on DNA methylation patterns and disease risk in adulthood is at present poorly characterized. This review describes the relationship between folic acid and DNA methylation, and the association between DNA methylation during in utero development and aging.

scholarly journals Prenatal Air Pollution Exposure and Placental DNA Methylation Changes: Implications on Fetal Development and Future Disease Susceptibility

Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 3025
Author(s):  
Terisha Ghazi ◽  
Pragalathan Naidoo ◽  
Rajen N. Naidoo ◽  
Anil A. Chuturgoon
Keyword(s):  
Heavy Metals ◽  
Dna Methylation ◽  
Air Pollution ◽  
Fetal Programming ◽  
Fetal Development ◽  
Disease Susceptibility ◽  
Current Knowledge ◽  
Later Life ◽  
In Utero ◽  
Methylation Patterns

The Developmental Origins of Health and Disease (DOHaD) concept postulates that in utero exposures influence fetal programming and health in later life. Throughout pregnancy, the placenta plays a central role in fetal programming; it regulates the in utero environment and acts as a gatekeeper for nutrient and waste exchange between the mother and the fetus. Maternal exposure to air pollution, including heavy metals, can reach the placenta, where they alter DNA methylation patterns, leading to changes in placental function and fetal reprogramming. This review explores the current knowledge on placental DNA methylation changes associated with prenatal air pollution (including heavy metals) exposure and highlights its effects on fetal development and disease susceptibility. Prenatal exposure to air pollution and heavy metals was associated with altered placental DNA methylation at the global and promoter regions of genes involved in biological processes such as energy metabolism, circadian rhythm, DNA repair, inflammation, cell differentiation, and organ development. The altered placental methylation of these genes was, in some studies, associated with adverse birth outcomes such as low birth weight, small for gestational age, and decreased head circumference. Moreover, few studies indicate that DNA methylation changes in the placenta were sex-specific, and infants born with altered placental DNA methylation patterns were predisposed to developing neurobehavioral abnormalities, cancer, and atopic dermatitis. These findings highlight the importance of more effective and stricter environmental and public health policies to reduce air pollution and protect human health.

scholarly journals DNA methylation of BDNF as a biomarker of early-life adversity

2014 ◽  
Vol 112 (22) ◽  
pp. 6807-6813 ◽  
Author(s):  
Marija Kundakovic ◽  
Kathryn Gudsnuk ◽  
Julie B. Herbstman ◽  
Deliang Tang ◽  
Frederica P. Perera ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Environmental Exposure ◽  
Early Life ◽  
Later Life ◽  
Underlying Mechanism ◽  
In Utero ◽  
Long Term Effects ◽  
Early Life Adversity ◽  
The Brain

Early-life adversity increases the risk for psychopathology in later life. The underlying mechanism(s) is unknown, but epigenetic variation represents a plausible candidate. Early-life exposures can disrupt epigenetic programming in the brain, with lasting consequences for gene expression and behavior. This evidence is primarily derived from animal studies, with limited study in humans due to inaccessibility of the target brain tissue. In humans, although there is evidence for DNA methylation changes in the peripheral blood of psychiatric patients, a fundamental question remains as to whether epigenetic markers in the blood can predict epigenetic changes occurring in the brain. We used in utero bisphenol A (BPA) exposure as a model environmental exposure shown to disrupt neurodevelopment and exert long-term effects on behavior in animals and humans. We show that prenatal BPA induces lasting DNA methylation changes in the transcriptionally relevant region of the Bdnf gene in the hippocampus and blood of BALB/c mice and that these changes are consistent with BDNF changes in the cord blood of humans exposed to high maternal BPA levels in utero. Our data suggest that BDNF DNA methylation in the blood may be used as a predictor of brain BDNF DNA methylation and gene expression as well as behavioral vulnerability induced by early-life environmental exposure. Because BDNF expression and DNA methylation are altered in several psychiatric disorders that are associated with early-life adversity, including depression, schizophrenia, bipolar disorder, and autism, BDNF DNA methylation in the blood may represent a novel biomarker for the early detection of psychopathology.

Epigenetic Mechanisms of Maternal Dietary Protein and Amino Acids Affecting Growth and Development of Offspring

2019 ◽  
Vol 20 (7) ◽  
pp. 727-735 ◽  
Author(s):  
Yi Wu ◽  
Zhibin Cheng ◽  
Yueyu Bai ◽  
Xi Ma
Keyword(s):  
Amino Acids ◽  
Dna Methylation ◽  
Dietary Protein ◽  
Growth And Development ◽  
Later Life ◽  
Biological Macromolecules ◽  
Epigenetic Mechanisms ◽  
Maternal Circulation ◽  
Energy Processing ◽  
Living Organisms

Nutrients can regulate metabolic activities of living organisms through epigenetic mechanisms, including DNA methylation, histone modification, and RNA regulation. Since the nutrients required for early embryos and postpartum lactation are derived in whole or in part from maternal and lactating nutrition, the maternal nutritional level affects the growth and development of fetus and creates a profound relationship between disease development and early environmental exposure in the offspring’s later life. Protein is one of the most important biological macromolecules, involved in almost every process of life, such as information transmission, energy processing and material metabolism. Maternal protein intake levels may affect the integrity of the fetal genome and alter DNA methylation and gene expression. Most amino acids are supplied to the fetus from the maternal circulation through active transport of placenta. Some amino acids, such as methionine, as dietary methyl donor, play an important role in DNA methylation and body’s one-carbon metabolism. The purpose of this review is to describe effects of maternal dietary protein and amino acid intake on fetal and neonatal growth and development through epigenetic mechanisms, with examples in humans and animals.

scholarly journals A Genome-Wide Integrative Association Study of DNA Methylation and Gene Expression Data and Later Life Cognitive Functioning in Monozygotic Twins

2020 ◽  
Vol 14 ◽  
Author(s):  
Mette Soerensen ◽  
Dominika Marzena Hozakowska-Roszkowska ◽  
Marianne Nygaard ◽  
Martin J. Larsen ◽  
Veit Schwämmle ◽  
...  
Keyword(s):  
Gene Expression ◽  
Dna Methylation ◽  
Cognitive Functioning ◽  
Association Study ◽  
Gene Expression Data ◽  
Monozygotic Twins ◽  
Later Life ◽  
Expression Data ◽  
Genome Wide ◽  
A Genome

scholarly journals Epigenetics and DOHaD: from basics to birth and beyond

2017 ◽  
Vol 8 (5) ◽  
pp. 513-519 ◽  
Author(s):  
T. Bianco-Miotto ◽  
J. M. Craig ◽  
Y. P. Gasser ◽  
S. J. van Dijk ◽  
S. E. Ozanne
Keyword(s):  
Dna Methylation ◽  
Chronic Disease ◽  
Chronic Diseases ◽  
Early Life ◽  
Later Life ◽  
Metabolic Health ◽  
Number Of Children ◽  
Early Life Environment ◽  
Increased Risk ◽  
Early Life Exposures

Developmental origins of health and disease (DOHaD) is the study of how the early life environment can impact the risk of chronic diseases from childhood to adulthood and the mechanisms involved. Epigenetic modifications such as DNA methylation, histone modifications and non-coding RNAs are involved in mediating how early life environment impacts later health. This review is a summary of the Epigenetics and DOHaD workshop held at the 2016 DOHaD Society of Australia and New Zealand Conference. Our extensive knowledge of how the early life environment impacts later risk for chronic disease would not have been possible without animal models. In this review we highlight some animal model examples that demonstrate how an adverse early life exposure results in epigenetic and gene expression changes that may contribute to increased risk of chronic disease later in life. Type 2 diabetes and cardiovascular disease are chronic diseases with an increasing incidence due to the increased number of children and adults that are obese. Epigenetic changes such as DNA methylation have been shown to be associated with metabolic health measures and potentially predict future metabolic health status. Although more difficult to elucidate in humans, recent studies suggest that DNA methylation may be one of the epigenetic mechanisms that mediates the effects of early life exposures on later life risk of obesity and obesity related diseases. Finally, we discuss the role of the microbiome and how it is a new player in developmental programming and mediating early life exposures on later risk of chronic disease.

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