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Effect of riboflavin status on the homocysteine-lowering effect of folate in relation to the MTHFR (C677T) genotype

Moat, Stuart James, Ashfield-Watt, Pauline Annie L., Powers, Hilary J., Newcombe, Robert Gordon and McDowell, Ian Frederick 2003. Effect of riboflavin status on the homocysteine-lowering effect of folate in relation to the MTHFR (C677T) genotype. Clinical chemistry 49 (2) , pp. 295-302. 10.1373/49.2.295

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Abstract

Background: Riboflavin (vitamin B2) is the precursor for FAD, the cofactor for methylenetetrahydrofolate reductase (MTHFR). MTHFR catalyzes the formation of 5-methyltetrahydrofolate, which acts as a methyl donor for homocysteine remethylation. Individuals with the MTHFR 677CT mutation have increased plasma total homocysteine (tHcy) concentrations, particularly in association with low folate status. It has been proposed that riboflavin may act together with folate to lower plasma tHcy, particularly in individuals with the thermolabile MTHFR T variant. Methods: We measured B-vitamin status and plasma tHcy in 126 healthy individuals 20–63 years of age (42 CC, 42 CT, and 42 TT MTHFR genotypes) at baseline and after three interventions (4 months): placebo plus natural diet; daily 400 µg folic acid supplement plus natural diet; and increased dietary folate to 400 µg/day. Results: At baseline and after nutritional intervention, lower riboflavin status was associated with increased plasma tHcy concentrations. Plasma tHcy was 2.6 µmol/L higher in the lowest plasma riboflavin quartile compared with the highest (P <0.02) and was 4.2 µmol/L higher in the highest erythrocyte glutathione reductase activation coefficient (EGRAC) quartile compared with the lowest (P <0.001). This effect was not restricted to those with the T allele. Folic acid given as a 400 µg/day supplement appeared to exacerbate a tendency toward riboflavin deficiency, as suggested by an increase in the proportion of individuals with EGRAC 1.4 from 52% to 65% after supplementation (P <0.05). Conclusions: Folate and riboflavin interact to lower plasma tHcy, possibly by maximizing the catalytic activity of MTHFR. The effect may be unrelated to MTHFR genotype.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Publisher: American Association for Clinical Chemistry
ISSN: 15308561
Related URLs:
Last Modified: 30 Jun 2017 01:30
URI: http://orca.cf.ac.uk/id/eprint/45

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