PMID- 24213682
OWN - NLM
STAT- MEDLINE
DCOM- 20140926
LR  - 20211021
IS  - 1573-4919 (Electronic)
IS  - 0300-8177 (Linking)
VI  - 387
IP  - 1-2
DP  - 2014 Feb
TI  - Nutriepigenetic regulation by folate-homocysteine-methionine axis: a review.
PG  - 55-61
LID - 10.1007/s11010-013-1869-2 [doi]
AB  - Although normally folic acid is given during pregnancy, presumably to prevent 
      neural tube defects, the mechanisms of this protection are unknown. More 
      importantly it is unclear whether folic acid has other function during 
      development. It is known that folic acid re-methylates homocysteine (Hcy) to 
      methionine by methylene tetrahydrofolate reductase-dependent pathways. Folic acid 
      also generates high-energy phosphates, behaves as an antioxidant and improves 
      nitric oxide (NO) production by endothelial NO synthase. Interestingly, during 
      epigenetic modification, methylation of DNA/RNA generate homocysteine 
      unequivocally. The enhanced overexpression of methyl transferase lead to 
      increased yield of Hcy. The accumulation of Hcy causes vascular dysfunction, 
      reduces perfusion in the muscles thereby causing musculopathy. Another 
      interesting fact is that children with severe hyperhomocysteinaemia (HHcy) have 
      skeletal deformities, and do not live past teenage. HHcy is also associated with 
      the progeria syndrome. Epilepsy is primarily caused by inhibition of 
      gamma-amino-butyric-acid (GABA) receptor, an inhibitory neurotransmitter in the 
      neuronal synapse. Folate deficiency leads to HHcy which then competes with GABA 
      for binding on the GABA receptors. With so many genetic and clinical 
      manifestations associated with folate deficiency, we propose that folate 
      deficiency induces epigenetic alterations in the genes and thereby results in 
      disease.
FAU - Bhargava, Seema
AU  - Bhargava S
AD  - Department of Biochemistry, Sir Ganga Ram Hospital, New Delhi, India, 
      bhargavaseema6@gmail.com.
FAU - Tyagi, S C
AU  - Tyagi SC
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20131110
PL  - Netherlands
TA  - Mol Cell Biochem
JT  - Molecular and cellular biochemistry
JID - 0364456
RN  - 0LVT1QZ0BA (Homocysteine)
RN  - 935E97BOY8 (Folic Acid)
RN  - AE28F7PNPL (Methionine)
SB  - IM
MH  - Animals
MH  - *Epigenesis, Genetic
MH  - Fatigue Syndrome, Chronic/genetics
MH  - Folic Acid/administration & dosage/physiology
MH  - Folic Acid Deficiency/*genetics
MH  - Gene-Environment Interaction
MH  - Homocysteine/*physiology
MH  - Humans
MH  - Methionine/*physiology
MH  - Neural Tube Defects/genetics
MH  - Progeria/genetics
EDAT- 2013/11/12 06:00
MHDA- 2014/09/27 06:00
CRDT- 2013/11/12 06:00
PHST- 2013/08/24 00:00 [received]
PHST- 2013/10/17 00:00 [accepted]
PHST- 2013/11/12 06:00 [entrez]
PHST- 2013/11/12 06:00 [pubmed]
PHST- 2014/09/27 06:00 [medline]
AID - 10.1007/s11010-013-1869-2 [doi]
PST - ppublish
SO  - Mol Cell Biochem. 2014 Feb;387(1-2):55-61. doi: 10.1007/s11010-013-1869-2. Epub 
      2013 Nov 10.