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dc.contributor.authorvan Wijk, Nick
dc.contributor.authorWatkins, Carol J.
dc.contributor.authorHageman, Robert J. J.
dc.contributor.authorSijben, John C. W.
dc.contributor.authorKamphuis, Patrick G. H. J.
dc.contributor.authorWurtman, Richard Jay
dc.contributor.authorBroersen, Laus M.
dc.date.accessioned2012-08-16T18:33:57Z
dc.date.available2012-08-16T18:33:57Z
dc.date.issued2012-05
dc.identifier.issn1743-7075
dc.identifier.urihttp://hdl.handle.net/1721.1/72173
dc.description.abstractBackground: Folate, vitamin B-12, and vitamin B-6 are essential nutritional components in one-carbon metabolism and are required for methylation capacity. The availability of these vitamins may therefore modify methylation of phosphatidylethanolamine (PE) to phosphatidylcholine (PC) by PE-N-methyltransferase (PEMT) in the liver. It has been suggested that PC synthesis by PEMT plays an important role in the transport of polyunsaturated fatty acids (PUFAs) like docosahexaenoic acid (DHA) from the liver to plasma and possibly other tissues. We hypothesized that if B-vitamin supplementation enhances PEMT activity, then supplementation could also increase the concentration of plasma levels of PUFAs such as DHA. To test this hypothesis, we determined the effect of varying the combined dietary intake of these three B-vitamins on plasma DHA concentration in rats. Methods: In a first experiment, plasma DHA and plasma homocysteine concentrations were measured in rats that had consumed a B-vitamin-poor diet for 4 weeks after which they were either continued on the B-vitamin-poor diet or switched to a B-vitamin-enriched diet for another 4 weeks. In a second experiment, plasma DHA and plasma homocysteine concentrations were measured in rats after feeding them one of four diets with varying levels of B-vitamins for 4 weeks. The diets provided 0% (poor), 100% (normal), 400% (enriched), and 1600% (high) of the laboratory rodent requirements for each of the three B-vitamins. Results: Plasma DHA concentration was higher in rats fed the B-vitamin-enriched diet than in rats that were continued on the B-vitamin-poor diet (P = 0.005; experiment A). Varying dietary B-vitamin intake from deficient to supra-physiologic resulted in a non-linear dose-dependent trend for increasing plasma DHA (P = 0.027; experiment B). Plasma DHA was lowest in rats consuming the B-vitamin-poor diet (P > 0.05 vs. normal, P < 0.05 vs. enriched and high) and highest in rats consuming the B-vitamin-high diet (P < 0.05 vs. poor and normal, P > 0.05 vs. enriched). B-vitamin deficiency significantly increased plasma total homocysteine but increasing intake above normal did not significantly reduce it. Nevertheless, in both experiments plasma DHA was inversely correlated with plasma total homocysteine. Conclusion: These data demonstrate that dietary folate, vitamin B-12, and vitamin B-6 intake can influence plasma concentration of DHA.en_US
dc.description.sponsorshipNutricia Advanced Medical Nutritionen_US
dc.description.sponsorshipDanone Researchen_US
dc.publisherBioMed Central Ltden_US
dc.relation.isversionofhttp://dx.doi.org/10.1186/1743-7075-9-49en_US
dc.rightsCreative Commons Attributionen_US
dc.rights.urihttp://creativecommons.org/licenses/by/2.0en_US
dc.sourceBioMed Central Ltden_US
dc.titleCombined dietary folate, vitamin B-12, and vitamin B-6 intake influences plasma docosahexaenoic acid concentration in ratsen_US
dc.typeArticleen_US
dc.identifier.citationvan Wijk, Nick et al. “Combined Dietary Folate, Vitamin B-12, and Vitamin B-6 Intake Influences Plasma Docosahexaenoic Acid Concentration in Rats.” Nutrition & Metabolism 9.1 (2012): 49. Web.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Brain and Cognitive Sciencesen_US
dc.contributor.mitauthorWurtman, Richard Jay
dc.contributor.mitauthorWatkins, Carol J.
dc.relation.journalNutrition and Metabolismen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dc.date.updated2012-08-16T15:06:05Z
dc.language.rfc3066en
dc.rights.holderNick van Wijk et al.; licensee BioMed Central Ltd.
dspace.orderedauthorsvan Wijk, Nick; Watkins, Carol J; Hageman, Robert J J; Sijben, John C W; Kamphuis, Patrick G H J; Wurtman, Richard J; Broersen, Laus Men
dc.identifier.orcidhttps://orcid.org/0000-0001-8286-6825
mit.licensePUBLISHER_CCen_US
mit.metadata.statusComplete


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