Modeling folate, one-carbon metabolism, and DNA methylation

2008 ◽  
Vol 66 ◽  
pp. S27-S30 ◽  
Author(s):  
Cornelia M Ulrich ◽  
Michael C Reed ◽  
H Frederik Nijhout
Oncogene ◽  
2017 ◽  
Vol 37 (7) ◽  
pp. 963-970 ◽  
Author(s):  
E Cuyàs ◽  
S Fernández-Arroyo ◽  
S Verdura ◽  
R Á-F García ◽  
J Stursa ◽  
...  

2018 ◽  
Vol 19 (10) ◽  
pp. 3106 ◽  
Author(s):  
Kuniyasu Soda

Recent investigations have revealed that changes in DNA methylation status play an important role in aging-associated pathologies and lifespan. The methylation of DNA is regulated by DNA methyltransferases (DNMT1, DNMT3a, and DNMT3b) in the presence of S-adenosylmethionine (SAM), which serves as a methyl group donor. Increased availability of SAM enhances DNMT activity, while its metabolites, S-adenosyl-l-homocysteine (SAH) and decarboxylated S-adenosylmethionine (dcSAM), act to inhibit DNMT activity. SAH, which is converted from SAM by adding a methyl group to cytosine residues in DNA, is an intermediate precursor of homocysteine. dcSAM, converted from SAM by the enzymatic activity of adenosylmethionine decarboxylase, provides an aminopropyl group to synthesize the polyamines spermine and spermidine. Increased homocysteine levels are a significant risk factor for the development of a wide range of conditions, including cardiovascular diseases. However, successful homocysteine-lowering treatment by vitamins (B6, B12, and folate) failed to improve these conditions. Long-term increased polyamine intake elevated blood spermine levels and inhibited aging-associated pathologies in mice and humans. Spermine reversed changes (increased dcSAM, decreased DNMT activity, aberrant DNA methylation, and proinflammatory status) induced by the inhibition of ornithine decarboxylase. The relation between polyamine metabolism, one-carbon metabolism, DNA methylation, and the biological mechanism of spermine-induced lifespan extension is discussed.


2018 ◽  
Vol 8 (1) ◽  
Author(s):  
Anna K. Knight ◽  
Hea Jin Park ◽  
Dorothy B. Hausman ◽  
Jennifer M. Fleming ◽  
Victoria L. Bland ◽  
...  

2009 ◽  
Vol 19 (4) ◽  
pp. 215-216 ◽  
Author(s):  
Bernd Lenz ◽  
Carmen Soehngen ◽  
Michael Linnebank ◽  
Annemarie Heberlein ◽  
Helge Frieling ◽  
...  

2017 ◽  
Vol 1 (3) ◽  
Author(s):  
Huang Guiling

Esophagus cancer is a common malignant tumor in China, and itsprevalence rate and fatality rate are the highest in the world whoseoccurrence is related to multiple factors, including family heredity,race, gender, region, diet and so on. Esophagus cancer is the diseasewith the most Chinese characteristic. The pathogenesis of esophagus cancer is very complicated, and the epigenetics in the pathogenetic process has become the current research hotspot, and the reversible feature provides a new direction for the early screening, prevention and treatment of esophagus cancer. DNA methylation is the most deep epigenetics in the current study, and the pattern of genome methylation is often abnormal in the cancerization of esophagus cancer. The folate, as the methyl group donor, and B-vitamins related to one-carbon metabolism, shall directly influence the condition of DNA methylation, give rise to the change of epigenetics, affect the occurrence of esophagus cancer. This paper summarizes the relationship among the occurrence of esophagus cancer and folate, several kinds of B-vitamins related to one-carbon metabolism, DNA methylation.


Epigenetics ◽  
2015 ◽  
Vol 10 (8) ◽  
pp. 727-735 ◽  
Author(s):  
Adana A M Llanos ◽  
Catalin Marian ◽  
Theodore M Brasky ◽  
Ramona G Dumitrescu ◽  
Zhenhua Liu ◽  
...  

2016 ◽  
Author(s):  
Min-Ae Song ◽  
Theodore M. Brasky ◽  
Catalin Marian ◽  
Daniel Y. Weng ◽  
Cenny Taslim ◽  
...  

2019 ◽  
Vol 149 (3) ◽  
pp. 372-380 ◽  
Author(s):  
Denise Mafra ◽  
Marta Esgalhado ◽  
Natalia A Borges ◽  
Ludmila F M F Cardozo ◽  
Milena B Stockler-Pinto ◽  
...  

ABSTRACT Epigenetic alterations, such as those linked to DNA methylation, may potentially provide molecular explanations for complications associated with altered gene expression in illnesses, such as chronic kidney disease (CKD). Although both DNA hypo- and hypermethylation have been observed in the uremic milieu, this remains only a single aspect of the epigenetic landscape and, thus, of any biochemical dysregulation associated with CKD. Nevertheless, the role of uremia-promoting alterations on the epigenetic landscape regulating gene expression is still a novel and scarcely studied field. Although few studies have actually reported alterations of DNA methylation via methyl donor nutrient intake, emerging evidence indicates that nutritional modification of the microbiome can affect one-carbon metabolism and the capacity to methylate the genome in CKD. In this review, we discuss the nutritional modifications that may affect one-carbon metabolism and the possible impact of methyl donor nutrients on the microbiome, CKD, and its phenotype.


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