First Author | Mandaviya PR | Year | 2014 |
Journal | Mol Genet Metab | Volume | 113 |
Issue | 4 | Pages | 243-52 |
PubMed ID | 25456744 | Mgi Jnum | J:220262 |
Mgi Id | MGI:5634046 | Doi | 10.1016/j.ymgme.2014.10.006 |
Citation | Mandaviya PR, et al. (2014) Homocysteine and DNA methylation: a review of animal and human literature. Mol Genet Metab 113(4):243-52 |
abstractText | Homocysteine (Hcy) is a sulfur-containing non-protein forming amino acid, which is synthesized from methionine as an important intermediate in the one-carbon pathway. High concentrations of Hcy in a condition called hyperhomocysteinemia (HHcy) are an independent risk factor for several disorders including cardiovascular diseases and osteoporotic fractures. Since Hcy is produced as a byproduct of the methyltransferase reaction, alteration in DNA methylation is studied as one of the underlying mechanisms of HHcy-associated disorders. In animal models, elevated Hcy concentrations are induced either by diet (high methionine, low B-vitamins, or both), gene knockouts (Mthfr, Cbs, Mtrr or Mtr) or combination of both to investigate their effects on DNA methylation or its markers. In humans, most of the literature involves case-control studies concerning patients. The focus of this review is to study existing literature on HHcy and its role in relation to DNA methylation. Apart from this, a few studies investigated the effect of Hcy-lowering trials on restoring DNA methylation patterns, by giving a folic acid or B-vitamin supplemented diet. These studies which were conducted in animal models as well as humans were included in this review. |