Folate And Fetal Programming Essay

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Pages: 5

Folate and fetal programming: a play in epigenomics?

Introduction
Epigenetics is described as chances occurring in gene expression that does not affect the sequence of DNA. The folate cycle plays can cause such changes and plays a crucial part in the synthesis of DNA, methylation groups and amino acid metabolism. Folate deficiency creates these changes to DNA by not providing methyl group donations to the methylation of DNA. This DNA methylation silences genes and helps to keep the genes regulated without causing any lasting effects on the DNA sequence. Extensive studies have shown a direct link between folate deficiency and birth defects. However the underlying cause of why folate deficiency causes these birth defects is not completely known and there is conflicting evidence. To understand fully the effect folate has on fetal programming the mechanisms must be known and analysed.

Cycles (Folate and Methionine)
Folate consumed through the diet enters the folate cycle, here the dietary folate is reduced to tetrahydrofolate (THF). This THF is then converted by serine hydroxymethyl
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For the methionine cycle to function there must be appropriate levels of folate being converted into 5-methylTHF to donate methyl group to methionine cycle. Without this donation HCY is not converted to methionine and an accumulation of HCY occurs. This accumulation not only causes insufficient amounts of SAM being produced it also creates more SAH because the excess HCY will be converted into SAH. SAH is a known inhibitor of cellular methylation (Natalie C. Chen, 2010). This creates a distorted SAM:SAH ratio which diminishes the cells ability for transmethylation reactions of DNA, RNA and histones, all of which play a major part in epigenetic mechanisms (Stover,