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Effect of riboflavin status on the homocysteine-lowering effect of folate in relation to the MTHFR (C677T) genotype.
Clin Chem 2003; 49(2):295-302CC

Abstract

BACKGROUND

Riboflavin (vitamin B(2)) 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 677C-->T 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 microg folic acid supplement plus natural diet; and increased dietary folate to 400 microg/day.

RESULTS

At baseline and after nutritional intervention, lower riboflavin status was associated with increased plasma tHcy concentrations. Plasma tHcy was 2.6 micromol/L higher in the lowest plasma riboflavin quartile compared with the highest (P <0.02) and was 4.2 micromol/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 microg/day supplement appeared to exacerbate a tendency toward riboflavin deficiency, as suggested by an increase in the proportion of individuals with EGRAC > or =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.

Authors+Show Affiliations

Cardiovascular Sciences Research Group, Wales Heart Research Institute, University of Wales College of Medicine, Cardiff, Wales CF14 4XN, United Kingdom. moatsj@cardiff.ac.ukNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Clinical Trial
Controlled Clinical Trial
Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

12560354

Citation

Moat, Stuart J., et al. "Effect of Riboflavin Status On the Homocysteine-lowering Effect of Folate in Relation to the MTHFR (C677T) Genotype." Clinical Chemistry, vol. 49, no. 2, 2003, pp. 295-302.
Moat SJ, Ashfield-Watt PA, Powers HJ, et al. Effect of riboflavin status on the homocysteine-lowering effect of folate in relation to the MTHFR (C677T) genotype. Clin Chem. 2003;49(2):295-302.
Moat, S. J., Ashfield-Watt, P. A., Powers, H. J., Newcombe, R. G., & McDowell, I. F. (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.
Moat SJ, et al. Effect of Riboflavin Status On the Homocysteine-lowering Effect of Folate in Relation to the MTHFR (C677T) Genotype. Clin Chem. 2003;49(2):295-302. PubMed PMID: 12560354.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Effect of riboflavin status on the homocysteine-lowering effect of folate in relation to the MTHFR (C677T) genotype. AU - Moat,Stuart J, AU - Ashfield-Watt,Pauline A L, AU - Powers,Hilary J, AU - Newcombe,Robert G, AU - McDowell,Ian F W, PY - 2003/2/1/pubmed PY - 2003/2/28/medline PY - 2003/2/1/entrez SP - 295 EP - 302 JF - Clinical chemistry JO - Clin. Chem. VL - 49 IS - 2 N2 - BACKGROUND: Riboflavin (vitamin B(2)) 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 677C-->T 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 microg folic acid supplement plus natural diet; and increased dietary folate to 400 microg/day. RESULTS: At baseline and after nutritional intervention, lower riboflavin status was associated with increased plasma tHcy concentrations. Plasma tHcy was 2.6 micromol/L higher in the lowest plasma riboflavin quartile compared with the highest (P <0.02) and was 4.2 micromol/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 microg/day supplement appeared to exacerbate a tendency toward riboflavin deficiency, as suggested by an increase in the proportion of individuals with EGRAC > or =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. SN - 0009-9147 UR - https://www.unboundmedicine.com/medline/citation/12560354/Effect_of_riboflavin_status_on_the_homocysteine_lowering_effect_of_folate_in_relation_to_the_MTHFR__C677T__genotype_ L2 - http://www.clinchem.org/cgi/pmidlookup?view=long&amp;pmid=12560354 DB - PRIME DP - Unbound Medicine ER -