Dietary Ingestion of Calories and Micronutrients Modulates the DNA Methylation Profile of Leukocytes from Older Individuals

Passador, J.; Toffoli, Leandro Vaz; Fernandes, Karen Barros Parron; Neves-Souza, R. D.; Pelosi, Gislaine Garcia; Gomes, M.V.

doi:10.1007/s12603-018-1085-6

Cited by 7 publications

(6 citation statements)

References 35 publications

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“…Our study participants had a wide scope of Cu concentrations, ranging from 200 to 1600 μg/L. The observed preference for Cuassociated hypomethylation was consistent with the findings of previous study that higher Cu was associated with a lower global DNA methylation profile of leukocytes [22]. Kennedy et al [23] also observed that hypomethylation is more common than hypermethylation among top CpGs associated with copper concentration.…”

Section: Discussionsupporting

confidence: 90%

“…Investigating DNA methylation alterations related to Cu is important to understand the metabolism and pathogenesis of copper. A study comprising 126 elder individuals indicated that the daily intake of Cu had a negative correlation with the global DNA methylation profile of leukocytes [22]. To date, only one genomewide DNA methylation study has been conducted to investigate associations between placental Cu and DNA methylation alterations in humans, and they observed nine Cu-associated differentially methylated regions (DMRs) and 15 suggestive cytosine-phosphoguanine sites (CpGs) (p Values < 1 × 10 −5 ) [23].…”

Section: Introductionmentioning

confidence: 99%

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Profile of copper-associated DNA methylation and its association with incident acute coronary syndrome

et al. 2021

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Background Acute coronary syndrome (ACS) is a cardiac emergency with high mortality. Exposure to high copper (Cu) concentration has been linked to ACS. However, whether DNA methylation contributes to the association between Cu and ACS is unclear. Methods We measured methylation level at > 485,000 cytosine-phosphoguanine sites (CpGs) of blood leukocytes using Human Methylation 450 Bead Chip and conducted a genome-wide meta-analysis of plasma Cu in a total of 1243 Chinese individuals. For plasma Cu-related CpGs, we evaluated their associations with the expression of nearby genes as well as major cardiovascular risk factors. Furthermore, we examined their longitudinal associations with incident ACS in the nested case-control study. Results We identified four novel Cu-associated CpGs (cg20995564, cg18608055, cg26470501 and cg05825244) within a 5% false discovery rate (FDR). DNA methylation level of cg18608055, cg26470501, and cg05825244 also showed significant correlations with expressions of SBNO2, BCL3, and EBF4 gene, respectively. Higher DNA methylation level at cg05825244 locus was associated with lower high-density lipoprotein cholesterol level and higher C-reactive protein level. Furthermore, we demonstrated that higher cg05825244 methylation level was associated with increased risk of ACS (odds ratio [OR], 1.23; 95% CI 1.02–1.48; P = 0.03). Conclusions We identified novel DNA methylation alterations associated with plasma Cu in Chinese populations and linked these loci to risk of ACS, providing new insights into the regulation of gene expression by Cu-related DNA methylation and suggesting a role for DNA methylation in the association between copper and ACS.

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Section: Discussionsupporting

confidence: 90%

Section: Introductionmentioning

confidence: 99%

Profile of copper-associated DNA methylation and its association with incident acute coronary syndrome

et al. 2021

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“…However, they do not solve the problem of hypermethylation of specific loci of genes associated with DNA repair, apoptosis, and cancer suppression [ 886 , 887 , 888 ]. Intake of vitamin A and retinoic acid, vitamin C, vitamin E, vitamin D can potentially modulate the global DNA methylation profile, histone modifications, and microRNA activity [ 763 , 774 , 889 , 890 ]. Polyamines spermine and spermidine stimulate the activity of DNMT and inhibit aberrant DNA methylation [ 891 ].…”

Section: Pharmacological Interventions Protecting Genomementioning

confidence: 99%

“…Vitamin A Influence on global and site-specific DNA methylation profiles. [763,764] Retinoic acid Regulation of epigenetic processes, including DNA methylation, histone modifications, the formation of polycomb repressive complex 2, and induction of transcription factors.…”

Section: Vitamins and Their Derivativesmentioning

confidence: 99%

Genome-Protecting Compounds as Potential Geroprotectors

Proshkina

Shaposhnikov

Moskalev

2020

IJMS

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Throughout life, organisms are exposed to various exogenous and endogenous factors that cause DNA damages and somatic mutations provoking genomic instability. At a young age, compensatory mechanisms of genome protection are activated to prevent phenotypic and functional changes. However, the increasing stress and age-related deterioration in the functioning of these mechanisms result in damage accumulation, overcoming the functional threshold. This leads to aging and the development of age-related diseases. There are several ways to counteract these changes: (1) prevention of DNA damage through stimulation of antioxidant and detoxification systems, as well as transition metal chelation; (2) regulation of DNA methylation, chromatin structure, non-coding RNA activity and prevention of nuclear architecture alterations; (3) improving DNA damage response and repair; (4) selective removal of damaged non-functional and senescent cells. In the article, we have reviewed data about the effects of various trace elements, vitamins, polyphenols, terpenes, and other phytochemicals, as well as a number of synthetic pharmacological substances in these ways. Most of the compounds demonstrate the geroprotective potential and increase the lifespan in model organisms. However, their genome-protecting effects are non-selective and often are conditioned by hormesis. Consequently, the development of selective drugs targeting genome protection is an advanced direction.

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“…Studies performed on primates have observed that a high-calorie maternal diet may alter the chromatin structure of the fetus through epigenetic covalent histone modifications [31]. The dietary ingestion of calories was found to be significantly correlated with DNA methylation on leukocytes from 126 older individuals [32]. The study by Strakovsky, Zhang [33] showed that a high-fat maternal diet altered hepatic metabolism in the newborn in a sex-specific way.…”

Section: Nutrition Conditionsmentioning

confidence: 99%

Epigenetics, Maternal Diet and Metabolic Programming

Ramírez‐Alarcón¹,

Sánchez-Agurto²,

Lamperti³

et al. 2019

TOBIOJ

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Background: The maternal environment influences embryonic and fetal life. Nutritional deficits or excesses alter the trajectory of fetus/offspring’s development. The concept of “developmental programming” and “developmental origins of health and disease” consists of the idea that maternal diet may remodel the genome and lead to epigenetic changes. These changes are induced during early life, permanently altering the phenotype in the posterior adult stage, favoring the development of metabolic diseases such as obesity, dyslipidemia, hypertension, hyperinsulinemia, and metabolic syndrome. In this review, it is aimed to overview epigenetics, maternal diet and metabolic programming factors and determine which of these might affect future generations. Scope and Approach: Nutrients interfere with the epigenome by influencing the supply and use of methyl groups through DNA transmethylation and demethylation mechanisms. They also influence the remodeling of chromatin and arginine or lysine residues at the N-terminal tails of histone, thus altering miRNA expression. Fats, proteins, B vitamins and folates act as important cofactors in methylation processes. The metabolism of carbon in the methyl groups of choline, folic acid and methionine to S-Adenosyl Methionine (SAM), acts as methyl donors to methyl DNA, RNA, and proteins. B-complex vitamins are important since they act as coenzymes during this process. Key Findings and Conclusion: Nutrients, during pregnancy, potentially influence susceptibility to diseases in adulthood. Additionally, the deficit or excess of nutrients alter the epigenetic machinery, affecting genes and influencing the genome of the offspring and therefore, predisposing the development of chronic diseases in adults.

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Dietary Ingestion of Calories and Micronutrients Modulates the DNA Methylation Profile of Leukocytes from Older Individuals

Cited by 7 publications

References 35 publications

Profile of copper-associated DNA methylation and its association with incident acute coronary syndrome

Profile of copper-associated DNA methylation and its association with incident acute coronary syndrome

Genome-Protecting Compounds as Potential Geroprotectors

Epigenetics, Maternal Diet and Metabolic Programming

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