Component

Intestinal riboflavin uptake

Entry of free riboflavin into intestinal epithelial cells.

2 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. Intestine-specific Slc52a3 deletion severely reduced carrier-mediated riboflavin uptake in mouse jejunal/colonic loops and isolated enterocytes.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_location
    Effect of loss of RFVT-3 on intestinal RF uptake
    experimental_model
    Conditional knockout with in vivo loops and isolated enterocytes
    exposure
    Intestinal Slc52a3 deletion versus littermate controls.
    limitations
    Residual uptake and species differences limit generalization.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Mus musculus
    plain_language
    Loss of intestinal RFVT3 restricts riboflavin absorption.
    primary_references
    [transport-intestinal-ko-2016] Conditional (intestinal-specific) knockout of the riboflavin transporter-3 (RFVT-3) impairs riboflavin absorption. (2016). https://pubmed.ncbi.nlm.nih.gov/26660539/ DOI: 10.1152/ajpgi.00340.2015
    tissue_or_cell_type
    Jejunum, colon and isolated intestinal epithelium
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 267–278

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Conditional knockout with in vivo loops and isolated enterocytes · source_derived_draft · unverified_draft

    ### transport-intestinal-ko-uptake Intestine-specific Slc52a3 deletion severely reduced carrier-mediated riboflavin uptake in mouse jejunal/colonic loops and isolated enterocytes. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of intestinal RFVT3 restricts riboflavin absorption. organism: Mus musculus tissue_or_cell_type: Jejunum, colon and isolated intestinal epithelium experimental_model: Conditional knockout with in vivo loops and isolated enterocytes limitations: Residual uptake and species differences limit generalization. exposure: Intestinal Slc52a3 deletion versus littermate controls. evidence_location: Effect of loss of RFVT-3 on intestinal RF uptake [transport-intestinal-ko-2016] Conditional (intestinal-specific) knockout of the riboflavin transporter-3 (RFVT-3) impairs riboflavin absorption. (2016). https://pubmed.ncbi.nlm.nih.gov/26660539/ DOI: 10.1152/ajpgi.00340.2015
    Complete structured claim and evidence
  2. RFVT3-directed siRNA decreased apical radiolabeled-riboflavin uptake by human T84 epithelial cells.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_location
    RFVT3 siRNA experiment
    experimental_model
    T84 siRNA and apical tracer-uptake assay
    exposure
    RFVT3-specific siRNA compared with control siRNA.
    limitations
    Partial gene silencing in cultured cells; other uptake routes remain possible.
    nutrient_topic
    Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
    organism
    Homo sapiens
    plain_language
    Reducing RFVT3 lowers intestinal-cell riboflavin uptake.
    primary_references
    [transport-rfvt3-2014] Functional involvement of RFVT3/SLC52A3 in intestinal riboflavin absorption. (2014). https://doi.org/10.1152/ajpgi.00349.2013 DOI: 10.1152/ajpgi.00349.2013
    tissue_or_cell_type
    Intestinal epithelial T84 cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 215–226

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · T84 siRNA and apical tracer-uptake assay · source_derived_draft · unverified_draft

    ### transport-rfvt3-silencing RFVT3-directed siRNA decreased apical radiolabeled-riboflavin uptake by human T84 epithelial cells. Condition category: machinery_impairment nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Reducing RFVT3 lowers intestinal-cell riboflavin uptake. organism: Homo sapiens tissue_or_cell_type: Intestinal epithelial T84 cells experimental_model: T84 siRNA and apical tracer-uptake assay limitations: Partial gene silencing in cultured cells; other uptake routes remain possible. exposure: RFVT3-specific siRNA compared with control siRNA. evidence_location: RFVT3 siRNA experiment [transport-rfvt3-2014] Functional involvement of RFVT3/SLC52A3 in intestinal riboflavin absorption. (2014). https://doi.org/10.1152/ajpgi.00349.2013 DOI: 10.1152/ajpgi.00349.2013
    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