Component

Plasma riboflavin, FMN and FAD concentrations

Measured plasma flavins, not a universal intracellular sufficiency threshold.

1 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. The child with compound SLC52A2 L123P/L339P variants had normal measured plasma riboflavin, FMN and FAD despite a transport-associated neurologic disorder.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_location
    Table 3 and Methods/results
    experimental_model
    Single genetic case; plasma flavin assay
    exposure
    Pretreatment plasma measurements.
    limitations
    One case; normal plasma measurements are not direct measurements of neuronal flavin sufficiency.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Homo sapiens
    plain_language
    Normal plasma flavins did not exclude a cellular transport defect.
    primary_references
    [transport-slc52a2-disease-2012] Impaired riboflavin transport due to missense mutations in SLC52A2 causes Brown-Vialetto-Van Laere syndrome (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3470687/ DOI: 10.1007/s10545-012-9513-y
    tissue_or_cell_type
    Plasma and clinical nervous-system phenotype
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 451–462

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single genetic case; plasma flavin assay · source_derived_draft · unverified_draft

    ### transport-slc52a2-normal-plasma The child with compound SLC52A2 L123P/L339P variants had normal measured plasma riboflavin, FMN and FAD despite a transport-associated neurologic disorder. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Normal plasma flavins did not exclude a cellular transport defect. organism: Homo sapiens tissue_or_cell_type: Plasma and clinical nervous-system phenotype experimental_model: Single genetic case; plasma flavin assay limitations: One case; normal plasma measurements are not direct measurements of neuronal flavin sufficiency. exposure: Pretreatment plasma measurements. evidence_location: Table 3 and Methods/results [transport-slc52a2-disease-2012] Impaired riboflavin transport due to missense mutations in SLC52A2 causes Brown-Vialetto-Van Laere syndrome (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3470687/ DOI: 10.1007/s10545-012-9513-y
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards