Ontology highlight
ABSTRACT: Background
Increased consumption of folic acid is prevalent, leading to concerns about negative consequences. The effects of folic acid on the liver, the primary organ for folate metabolism, are largely unknown. Methylenetetrahydrofolate reductase (MTHFR) provides methyl donors for S-adenosylmethionine (SAM) synthesis and methylation reactions.Objective
Our goal was to investigate the impact of high folic acid intake on liver disease and methyl metabolism.Design
Folic acid-supplemented diet (FASD, 10-fold higher than recommended) and control diet were fed to male Mthfr(+/+) and Mthfr(+/-) mice for 6 mo to assess gene-nutrient interactions. Liver pathology, folate and choline metabolites, and gene expression in folate and lipid pathways were examined.Results
SUBMITTER: Christensen KE
PROVIDER: S-EPMC4340065 | biostudies-literature | 2015 Mar
REPOSITORIES: biostudies-literature