Homocysteine predicts increased NT-pro-BNP through impaired fatty acid oxidation.

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Date publication

août 2013

Auteurs

Membres identifiés du Cancéropôle Est :
Pr GUEANT Jean-Louis


Tous les auteurs :
Gueant Rodriguez RM, Spada R, Pooya S, Jeannesson E, Moreno Garcia MA, Anello G, Bosco P, Elia M, Romano A, Alberto JM, Juilliere Y, Gueant JL

Résumé

BACKGROUND: The deficiency in methyl donors, folate and vitamin B12, increases homocysteine and produces myocardium hypertrophy with impaired mitochondrial fatty acid oxidation and increased BNP, through hypomethylation of peroxisome-proliferator-activated-receptor gamma co-activator-1alpha, in rat. This may help to understand better the elusive link previously reported between hyperhomocysteinemia and BNP, in human. We investigated therefore the influence of methyl donors on heart mitochondrial fatty acid oxidation and brain natriuretic peptide, in two contrasted populations. METHODS: Biomarkers of heart disease, of one carbon metabolism and of mitochondrial fatty acid oxidation were assessed in 1020 subjects, including patients undergoing coronarography and ambulatory elderly subjects from OASI cohort. RESULTS: Folate deficit was more frequent in the coronarography population than in the elderly ambulatory volunteers and produced a higher concentration of homocysteine (19.3 +/- 6.8 vs. 15.3 +/- 5.6, P/= 18 mumol/L) had higher concentrations of NT-pro-BNP (or BNP in ambulatory subjects) and of short chain-, medium chain-, and long chain-acylcarnitines, compared to those in the lower quartile (

Référence

Int J Cardiol. 2013 Aug 10;167(3):768-75