Methyl donor deficiency impairs fatty acid oxidation through PGC-1α hypomethylation and decreased ER-α, ERR-α, and HNF-4α in the rat liver.
Fiche publication
Date publication
août 2012
Journal
Journal of hepatology
Auteurs
Membres identifiés du Cancéropôle Est :
Dr BLAISE Sébastien, Pr BRONOWICKI Jean-Pierre, Pr GUEANT Jean-Louis, Pr PEYRIN-BIROULET Laurent
Tous les auteurs :
Pooya S, Blaise S, Moreno Garcia M, Giudicelli J, Alberto JM, Guéant-Rodriguez RM, Jeannesson E, Gueguen N, Bressenot A, Nicolas B, Malthiery Y, Daval JL, Peyrin-Biroulet L, Bronowicki JP, Guéant JL
Lien Pubmed
Résumé
Folate and cobalamin are methyl donors needed for the synthesis of methionine, which is the precursor of S-adenosylmethionine, the substrate of methylation in epigenetic, and epigenomic pathways. Methyl donor deficiency produces liver steatosis and predisposes to metabolic syndrome. Whether impaired fatty acid oxidation contributes to this steatosis remains unknown.
Mots clés
Animals, Electron Transport, Endoplasmic Reticulum Stress, Energy Metabolism, Estrogen Receptor alpha, analysis, Fatty Acids, metabolism, Fatty Liver, etiology, Folic Acid, blood, Hepatocyte Nuclear Factor 4, analysis, Liver, metabolism, Methylation, Oxidation-Reduction, Oxidative Stress, Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha, RNA-Binding Proteins, metabolism, Rats, Rats, Wistar, Receptors, Estrogen, analysis, Transcription Factors, metabolism, Vitamin B 12, blood
Référence
J. Hepatol.. 2012 Aug;57(2):344-51