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Title: MTHFR polymorphisms and serum cobalamin affect plasma homocysteine concentrations differentially in females and males
Authors: Nilsson, Torbjörn K.
Böttiger, Anna K.
Henríquez, Patricia 
Majem, Lluís Serra 
UNESCO Clasification: 32 Ciencias médicas
3206 Ciencias de la nutrición
Keywords: Methylenetetrahydrofolate Reductase Mthfr
Genetic Polymorphisms
Folate Status
C677T Polymorphism
Common Mutation, et al
Issue Date: 2014
Journal: Molecular Medicine Reports 
Abstract: A total of 523 subjects (297 females and 226 males) from the Canary Islands Nutrition Study (ENCA) were studied in order to examine the effect of the MTHFR 677C>T, 1298A>C and 1793G>A polymorphisms, adjusted for age, serum (5)-folate and S-cobalamin levels, on total plasma homocysteine concentrations (tHcy). Genotyping was performed with Pyrosequencing(R) technology. The MTHFR 677T-allele was associated with increased tHcy concentrations only in males (P=0.005). The MTHFR 1298C-allele was found to be associated with higher tHcy levels but similarly, only in males (P=0.025). The MTHFR 1793A-allele was associated with decreased tHcy concentrations in the younger males (P=0.042). A haplotype-based approach was marginally superior in explaining the genetic interaction of the MTHFR polymorphisms on tHcy plasma levels (R-2 0.352 vs. 0.342 for a simple genotype-based approach). A nutrigenetic interaction between the MTHFR 677C>T genotype and S-cobalamin on tHcy levels was demonstrated in both genders. The increase in tHcy was more pronounced with decreasing S-cobalamin quintiles in 677TT homozygotes (P=0.005 for males and P=0.015 for females) than with decreasing S-folate quintiles (P for trend not significant). It was concluded that gene-nutrient interactions may differ depending on the sex and age of the subjects. The transferability of gene-nutrient interactions from one community to others may therefore be limited not only by different food patterns but also by different ages, genders and genotype distributions.
ISSN: 1791-2997
DOI: 10.3892/mmr.2014.2521
Source: Molecular Medicine Reports[ISSN 1791-2997],v. 10, p. 2706-2712
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