scholarly journals Link between methyl nutrients and the DNA methylation process in the course of selected diseases in adults

2021 ◽  
pp. 123-136
Author(s):  
Paulina Łoboś ◽  
Bożena Regulska-Ilow
Keyword(s):  
Dna Methylation ◽  
Vitamin B12 ◽  
Epigenetic Modification ◽  
The Body ◽  
Transcriptional Gene Silencing ◽  
Vitamin B9 ◽  
Primary Donor ◽  
One Carbon Metabolism ◽  
Folate And Vitamin B12 ◽  
Risk Of Cancer

DNA methylation is a reversible epigenetic modification that plays a crucial role in transcriptional gene silencing. Both excessive (hypermethylation) and reduced DNA methylation (hypomethylation) can contribute to the disturbance of the proper course of many important processes in the human body. The aim of the study was to discuss the relationship between methyl nutrients and the DNA methylation process in the course of selected diseases in adults. Methyl nutrients include folates (vitamin B9), riboflavin (vitamin B2), cobalamin (vitamin B12), pyridoxine (vitamin B6) and choline (vitamin B4), as well as methionine and betaine. These substances play the role of both substrates and cofactors in transformations related to one-carbon metabolism. The deficiency of methyl nutrients in the body can lead to disturbances in SAM synthesis, which is the primary donor of methyl groups in the DNA methylation process. However, the mechanism explaining the discussed relationship has not been fully explained so far. Both the concentration in the body and the intake of folate and vitamin B12 in the diet can, to some extent, have an effect on the level of DNA methylation in healthy people. In comparison, data on the effect of excessive intake of vitamin B12 in the diet on the risk of cancer development are inconsistent. An adequate betaine and choline intake in the diet might not only affect the overall improvement of the DNA methylation profile, but, to some extent, also reduce the risk of cancer, the effect of which can depend on the content of folic acid in the body. Research results on the effect of supplementation of methyl nutrients on the DNA methylation process are inconclusive. It is therefore necessary to conduct further research in this area to draw clear conclusions.

scholarly journals FOLIC ACID, VITAMIN B12, AND DNA METHYLATION: AN UPDATE.

2018 ◽  
Vol 11 (1) ◽  
pp. 17 ◽  
Author(s):  
Bhongir Aparna Varma ◽  
Srilatha Bashetti ◽  
Rajagopalan Vijayaraghavan ◽  
Kumar Sai Sailesh
Keyword(s):  
Dna Methylation ◽  
Folic Acid ◽  
Vitamin B12 ◽  
The Body ◽  
Aberrant Methylation ◽  
Restricted Diet ◽  
Current Review ◽  
Folate And Vitamin B12 ◽  
Methylation Patterns

 Epigenetics is one of the exciting and fastest expanding fields of biology; this is above genetics. Methylation is the process involved in the transfer of methyl group to amino acids, proteins, enzymes and DNA of all the cells, and tissues of the body. During cell-division low folate availability may result in decreased production of thymidine wherein uracil may be substituted in the place of thymidine in the DNA sequence. It was reported that folate and Vitamin B12 restricted diet resulted in aberrant methylation patterns. The current review was undertaken to explore the role of folic acid and Vitamin B12 in DNA methylation.

scholarly journals FOLIC ACID, VITAMIN B12, AND DNA METHYLATION: AN UPDATE.

2018 ◽  
Vol 11 (1) ◽  
pp. 17
Author(s):  
Bhongir Aparna Varma ◽  
Srilatha Bashetti ◽  
Rajagopalan Vijayaraghavan ◽  
Kumar Sai Sailesh
Keyword(s):  
Dna Methylation ◽  
Folic Acid ◽  
Vitamin B12 ◽  
The Body ◽  
Aberrant Methylation ◽  
Restricted Diet ◽  
Current Review ◽  
Folate And Vitamin B12 ◽  
Methylation Patterns

 Epigenetics is one of the exciting and fastest expanding fields of biology; this is above genetics. Methylation is the process involved in the transfer of methyl group to amino acids, proteins, enzymes and DNA of all the cells, and tissues of the body. During cell-division low folate availability may result in decreased production of thymidine wherein uracil may be substituted in the place of thymidine in the DNA sequence. It was reported that folate and Vitamin B12 restricted diet resulted in aberrant methylation patterns. The current review was undertaken to explore the role of folic acid and Vitamin B12 in DNA methylation.

scholarly journals The Impact of Natural Dietary Compounds and Food-Borne Mycotoxins on DNA Methylation and Cancer

Cells ◽  
2020 ◽  
Vol 9 (9) ◽  
pp. 2004 ◽  
Author(s):  
Terisha Ghazi ◽  
Thilona Arumugam ◽  
Ashmika Foolchand ◽  
Anil A. Chuturgoon
Keyword(s):  
Dna Methylation ◽  
Bioactive Compounds ◽  
Epigenetic Modification ◽  
Bioactive Molecules ◽  
Methyl Donors ◽  
Food Borne ◽  
One Carbon Metabolism ◽  
Aberrant Dna Methylation ◽  
Methylation Patterns ◽  
The Impact

Cancer initiation and progression is an accumulation of genetic and epigenetic modifications. DNA methylation is a common epigenetic modification that regulates gene expression, and aberrant DNA methylation patterns are considered a hallmark of cancer. The human diet is a source of micronutrients, bioactive molecules, and mycotoxins that have the ability to alter DNA methylation patterns and are thus a contributing factor for both the prevention and onset of cancer. Micronutrients such as betaine, choline, folate, and methionine serve as cofactors or methyl donors for one-carbon metabolism and other DNA methylation reactions. Dietary bioactive compounds such as curcumin, epigallocatechin-3-gallate, genistein, quercetin, resveratrol, and sulforaphane reactivate essential tumor suppressor genes by reversing aberrant DNA methylation patterns, and therefore, they have shown potential against various cancers. In contrast, fungi-contaminated agricultural foods are a source of potent mycotoxins that induce carcinogenesis. In this review, we summarize the existing literature on dietary micronutrients, bioactive compounds, and food-borne mycotoxins that affect DNA methylation patterns and identify their potential in the onset and treatment of cancer.

scholarly journals Overall and sex-specific associations between methylation of the ABCG1 and APOE genes and ischemic stroke or other atherosclerosis-related traits in a sibling study of Chinese population

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Xueying Qin ◽  
Jin Li ◽  
Tao Wu ◽  
Yiqun Wu ◽  
Xun Tang ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Ischemic Stroke ◽  
Environmental Risk ◽  
Epigenetic Modification ◽  
Previous History ◽  
Ankle Brachial Index ◽  
Blood Lipid ◽  
The Body ◽  
Lipid Levels ◽  
Blood Lipid Levels

Abstract Background Identifying subjects with a high risk of ischemic stroke is fundamental for prevention of the disease. Both genetic and environmental risk factors contribute to ischemic stroke, but the underlying epigenetic mechanisms which mediate genetic and environmental risk effects are not fully understood. The aim of this study was to explore whether DNA methylation loci located in the ATP-binding cassette G1 (ABCG1) and apolipoprotein E (APOE) genes, both involved in the metabolism of lipids in the body, are related to ischemic stroke, using the Fangshan/Family-based Ischemic Stroke Study in China. We also tested if these CpG sites were associated with early signs of cardiovascular atherosclerosis (carotid intima–media thickness (cIMT), ankle–brachial index (ABI), and brachial–ankle pulse wave velocity (baPWV)). Results DNA methylation at the cg02494239 locus in ABCG1 was correlated with ischemic stroke after adjusting for gender, previous history of diabetes and hypertension, smoking, drinking, body mass index, and blood lipid levels (above vs below mean, OR = 2.416, 95% CI 1.024–5.700, P = 0.044; 75–100% percentile vs 0–25% percentile, OR = 4.461, 95% CI 1.226–16.225, P = 0.023). No statistically significant associations were observed for the cg06500161 site in ABCG1 and the cg14123992 site in APOE with ischemic stroke. The study detected that hypermethylation of the ABCG1 gene was significantly associated with cIMT, hypermethylation of the APOE gene was significantly related to ABI, and methylation of the APOE gene was statistically negatively correlated with baPWV. The above relationships demonstrated gender differences. Conclusions These findings suggest that epigenetic modification of ABCG1 and APOE may play a role in the pathway from disturbed blood lipid levels to the development of cardiovascular diseases. Future prospective validation of these findings is warranted.

Levels of Folate and Vitamin B12, and Genetic Polymorphisms Involved in One-Carbon Metabolism May Increase the Risk of Cervical Cytological Abnormalities

2021 ◽  
pp. 1-10
Author(s):  
Nayara Nascimento Toledo Silva ◽  
Ana Carolina Silva Santos ◽  
Maria de Fátima Dias de Sousa Brito ◽  
Diama Bradha Andrade Peixoto do Vale ◽  
Cláudia Martins Carneiro ◽  
...  
Keyword(s):  
Vitamin B12 ◽  
Genetic Polymorphisms ◽  
Carbon Metabolism ◽  
Cytological Abnormalities ◽  
One Carbon Metabolism ◽  
Folate And Vitamin B12

scholarly journals Effect of imbalance in folate and vitamin B12 in maternal/parental diet on global methylation and regulatory miRNAs

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Aatish Mahajan ◽  
Divika Sapehia ◽  
Shilpa Thakur ◽  
Palani Selvam Mohanraj ◽  
Rashmi Bagga ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Vitamin B12 ◽  
Dna Methyltransferases ◽  
Central Component ◽  
Global Methylation ◽  
Altered Expression ◽  
Carbon Carrier ◽  
B12 Deficiency ◽  
Folate And Vitamin B12 ◽  
F1 Generation

AbstractDNA methylation, a central component of the epigenetic network is altered in response to nutritional influences. In one-carbon cycle, folate acts as a one-carbon carrier and vitamin B12 acts as co-factor for the enzyme methionine synthase. Both folate and vitamin B12 are the important regulators of DNA methylation which play an important role in development in early life. Previous studies carried out in this regard have shown the individual effects of these vitamins but recently the focus has been to study the combined effects of both the vitamins during pregnancy. Therefore, this study was planned to elucidate the effect of the altered dietary ratio of folate and B12 on the expression of transporters, related miRNAs and DNA methylation in C57BL/6 mice. Female mice were fed diets with 9 combinations of folate and B12 for 4 weeks. They were mated and off-springs born (F1) were continued on the same diet for 6 weeks post-weaning. Maternal and fetal (F2) tissues were collected at day 20 of gestation. Deficient state of folate led to an increase in the expression of folate transporters in both F1 and F2 generations, however, B12 deficiency (BDFN) also led to an increase in the expression in both the generations. B12 transporters/proteins were found to be increased with B12 deficiency in F1 and F2 generations except for TC-II in the kidney which was found to be decreased in the F1 generation. miR-483 was found to be increased with all conditions of folate and B12 in both F1 and F2 generations, however, deficient conditions of B12 led to an increase in the expression of miR-221 in both F1 and F2 generations. The level of miR-133 was found to be increased in BDFN group in F1 generation however; in F2 generation the change in expression was tissue and sex-specific. Global DNA methylation was decreased with deficiency of both folate and B12 in maternal tissues (F1) but increased with folate deficiency in placenta (F1) and under all conditions in fetal tissues (F2). DNA methyltransferases were overall found to be increased with deficiency of folate and B12 in both F1 and F2 generations. Results suggest that the dietary ratio of folate and B12 resulted in altered expression of transporters, miRNAs, and genomic DNA methylation in association with DNMTs.

scholarly journals Regular, Intense Exercise Training as a Healthy Aging Lifestyle Strategy: Preventing DNA Damage, Telomere Shortening and Adverse DNA Methylation Changes Over a Lifetime

2021 ◽  
Vol 12 ◽  
Author(s):  
Maha Sellami ◽  
Nicola Bragazzi ◽  
Mohammad Shoaib Prince ◽  
Joshua Denham ◽  
Mohamed Elrayess
Keyword(s):  
Dna Methylation ◽  
Dna Damage ◽  
Exercise Training ◽  
Epigenetic Modification ◽  
Methylation Status ◽  
The Body ◽  
Training Load ◽  
Activity Level ◽  
Biological Aging ◽  
Age Related

Exercise training is one of the few therapeutic interventions that improves health span by delaying the onset of age-related diseases and preventing early death. The length of telomeres, the 5′-TTAGGGn-3′ tandem repeats at the ends of mammalian chromosomes, is one of the main indicators of biological age. Telomeres undergo shortening with each cellular division. This subsequently leads to alterations in the expression of several genes that encode vital proteins with critical functions in many tissues throughout the body, and ultimately impacts cardiovascular, immune and muscle physiology. The sub-telomeric DNA is comprised of heavily methylated, heterochromatin. Methylation and histone acetylation are two of the most well-studied examples of the epigenetic modifications that occur on histone proteins. DNA methylation is the type of epigenetic modification that alters gene expression without modifying gene sequence. Although diet, genetic predisposition and a healthy lifestyle seem to alter DNA methylation and telomere length (TL), recent evidence suggests that training status or physical fitness are some of the major factors that control DNA structural modifications. In fact, TL is positively associated with cardiorespiratory fitness, physical activity level (sedentary, active, moderately trained, or elite) and training intensity, but is shorter in over-trained athletes. Similarly, somatic cells are vulnerable to exercise-induced epigenetic modification, including DNA methylation. Exercise-training load, however, depends on intensity and volume (duration and frequency). Training load-dependent responses in genomic profiles could underpin the discordant physiological and physical responses to exercise. In the current review, we will discuss the role of various forms of exercise training in the regulation of DNA damage, TL and DNA methylation status in humans, to provide an update on the influence exercise training has on biological aging.

scholarly journals Plasma Homocysteine and Polymorphisms of Genes Involved in Folate Metabolism Correlate with DNMT1 Gene Methylation Levels

Metabolites ◽  
2019 ◽  
Vol 9 (12) ◽  
pp. 298
Author(s):  
Fabio Coppedè ◽  
Andrea Stoccoro ◽  
Pierpaola Tannorella ◽  
Lucia Migliore
Keyword(s):  
Dna Methylation ◽  
Vitamin B12 ◽  
Promoter Methylation ◽  
Dna Methyltransferase ◽  
Tandem Repeats ◽  
Inverse Correlation ◽  
Plasma Homocysteine ◽  
Gene Methylation ◽  
Folate And Vitamin B12 ◽  
Methylation Patterns

DNA methyltransferase 1 (DNMT1) is responsible for the maintenance of DNA methylation patterns during cell division. Several human diseases are characterized by impaired DNMT1 gene methylation, but less is known about the factors that regulate DNMT1 promoter methylation levels. Dietary folates and related B-vitamins are essential micronutrients for DNA methylation processes, and we performed the present study to investigate the contribution of circulating folate, vitamin B12, homocysteine, and common polymorphisms in folate pathway genes to the DNMT1 gene methylation levels. We investigated DNMT1 gene methylation levels in peripheral blood DNA samples from 215 healthy individuals. All the DNA samples were genotyped for MTHFR 677C > T (rs1801133) and 1298A > C (rs1801131), MTRR 66A > G (rs1801394), MTR 2756A > G (rs1805087), SLC19A1 (RFC1) 80G > A (rs1051266), TYMS 28-bp tandem repeats (rs34743033) and 1494 6-bp insertion/deletion (indel) (rs34489327), DNMT3A -448A > G (rs1550117), and DNMT3B -149C > T (rs2424913) polymorphisms. Circulating homocysteine, folate, and vitamin B12 levels were available from 158 of the recruited individuals. We observed an inverse correlation between plasma homocysteine and DNMT1 methylation levels. Furthermore, both MTR rs1805087 and TYMS rs34743033 polymorphisms showed a statistically significant effect on DNMT1 methylation levels. The present study revealed several correlations between the folate metabolic pathway and DNMT1 promoter methylation that could be of relevance for those disorders characterized by altered DNA methylation.

scholarly journals A Complex Case of Haemoglobin E Disease with Immune Thrombocytopenia and Combined Iron, Folate and Vit B12 Deficiency

2013 ◽  
Vol 6 (1) ◽  
pp. 31-33
Author(s):  
Md Sirazul Islam ◽  
Tashmim Farhana Dipta ◽  
Gazi Sharmin Sultana
Keyword(s):  
Case Report ◽  
Vitamin B12 ◽  
Immune Thrombocytopenia ◽  
Severe Anaemia ◽  
The Body ◽  
Complex Case ◽  
B12 Deficiency ◽  
Folate And Vitamin B12

This is a case report of a 13 years old indigenous ‘Garo’ girl who presented with purpuric spots and ecchymotic patches all over the body with menorrhagia, mild jaundice, severe anaemia, marked thrombocytopenia, moderate neutrophil leucocytosis and reticulocytosis. Investigations revealed this as a complex case of Haemoglobin E disease with immune thrombocytopenia (ITP) and combined iron, folate and vitamin B12 DOI: http://dx.doi.org/10.3329/imcj.v6i1.14723 Ibrahim Med. Coll. J. 2012; 6(1): 31-33

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