Vitamin B-12 and liver activity and expression of methionine synthase are decreased in fetuses with neural tube defects.

Date publication

mars 2019

Journal

The American journal of clinical nutrition

Auteurs

Membres identifiés du Cancéropôle Est :
Pr GUEANT Jean-Louis

Tous les auteurs :
Fofou-Caillierez MB, Guéant-Rodriguez RM, Alberto JM, Chéry C, Josse T, Gérard P, Forges T, Foliguet B, Feillet F, Guéant JL

Lien Pubmed

https://www.ncbi.nlm.nih.gov/pubmed/30848279

Résumé

The risk of neural tube defects (NTDs) is influenced by nutritional factors and genetic determinants of one-carbon metabolism. A key pathway of this metabolism is the vitamin B-12- and folate-dependent remethylation of homocysteine, which depends on methionine synthase (MS, encoded by MTR), methionine synthase reductase, and methylenetetrahydrofolate reductase. Methionine, the product of this pathway, is the direct precursor of S-adenosylmethionine (SAM), the universal methyl donor needed for epigenetic mechanisms.

Mots clés

S-adenosylmethionine, gastric intrinsic factor, methionine synthase, methylenetetrahydrofolate reductase, neural tube defects, spina bifida, vitamin B-12

Référence

Am. J. Clin. Nutr.. 2019 Mar 6;: