Component

Mouse thiamine transporter 2 / Slc19a3

Mouse ortholog; kept distinct from human SLC19A3.

3 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. Slc19a2-null mouse intestine increased Slc19a3 expression while thiamine uptake remained comparable to controls.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-scope
    Intestine
    evidence_locator
    Abstract
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/reidling-2010-slc19a3-knockout-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1719}]
    experimental_model
    Slc19a3-null or Slc19a2-null mice versus littermates; cells, intestinal loops and expression assays.
    limitations
    Association supports compensation; not a universal redundancy rule.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Mus musculus
    plain_language
    The second transporter can compensate in this mouse tissue.
    primary_references
    [reidling-2010-slc19a3-knockout] Impaired intestinal vitamin B1 (thiamin) uptake in thiamin transporter-2-deficient mice (2010). https://pubmed.ncbi.nlm.nih.gov/19879271/ DOI: 10.1053/j.gastro.2009.10.042
    tissue_or_cell_type
    Intestine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 252–264

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc19a3-null or Slc19a2-null mice versus littermates; cells, intestinal loops and expression assays. · source_derived_draft · unverified_draft

    ### b1-mouse-slc19a2-compensation Slc19a2-null mouse intestine increased Slc19a3 expression while thiamine uptake remained comparable to controls. Condition category: machinery_impairment nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The second transporter can compensate in this mouse tissue. organism: Mus musculus tissue_or_cell_type: Intestine experimental_model: Slc19a3-null or Slc19a2-null mice versus littermates; cells, intestinal loops and expression assays. limitations: Association supports compensation; not a universal redundancy rule. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/reidling-2010-slc19a3-knockout-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1719}] evidence_locator: Abstract evidence-scope: Intestine [reidling-2010-slc19a3-knockout] Impaired intestinal vitamin B1 (thiamin) uptake in thiamin transporter-2-deficient mice (2010). https://pubmed.ncbi.nlm.nih.gov/19879271/ DOI: 10.1053/j.gastro.2009.10.042
    Complete structured claim and evidence
  2. Species differences in the substrate specificity of THTR-2 between the human and mouse orthologues were observed.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/26528626.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "67707c1e73b51b8db54bf2ffdfbb07210b877ce242d62840836f3e546dd4c6a9", "start_char": 0, "end_char": 1436, "text_sha256": "67707c1e73b51b8db54bf2ffdfbb07210b877ce242d62840836f3e546dd4c6a9"}
    experimental_model
    Transporter uptake assays in cells expressing human THTR-1 and THTR-2
    exposure
    Metformin against thiamine uptake by SLC19A2 and SLC19A3
    limitations
    In-vitro transport with a millimolar Km. The authors propose intestinal relevance; they do not measure human thiamine status.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Human transporters, with mouse orthologue comparison
    plain_language
    The mouse version of this carrier does not behave like the human one.
    primary_references
    [metformin-p26528626] Metformin Is a Substrate and Inhibitor of the Human Thiamine Transporter, THTR-2 (SLC19A3). (2015). https://pubmed.ncbi.nlm.nih.gov/26528626/ DOI: 10.1021/acs.molpharmaceut.5b00501
    tissue_or_cell_type
    Small-intestinal absorption

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 1308–1319

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter uptake assays in cells expressing human THTR-1 and THTR-2 · source_derived_draft · unverified_draft

    ### metformin-thtr2-species-difference Species differences in the substrate specificity of THTR-2 between the human and mouse orthologues were observed. Condition category: normal nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: The mouse version of this carrier does not behave like the human one. organism: Human transporters, with mouse orthologue comparison tissue_or_cell_type: Small-intestinal absorption experimental_model: Transporter uptake assays in cells expressing human THTR-1 and THTR-2 limitations: In-vitro transport with a millimolar Km. The authors propose intestinal relevance; they do not measure human thiamine status. exposure: Metformin against thiamine uptake by SLC19A2 and SLC19A3 evidence_span: {"source_cache": "artifacts/metformin-research/26528626.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "67707c1e73b51b8db54bf2ffdfbb07210b877ce242d62840836f3e546dd4c6a9", "start_char": 0, "end_char": 1436, "text_sha256": "67707c1e73b51b8db54bf2ffdfbb07210b877ce242d62840836f3e546dd4c6a9"} [metformin-p26528626] Metformin Is a Substrate and Inhibitor of the Human Thiamine Transporter, THTR-2 (SLC19A3). (2015). https://pubmed.ncbi.nlm.nih.gov/26528626/ DOI: 10.1021/acs.molpharmaceut.5b00501
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Slc19a3-null mice had lower thiamine uptake in isolated intestinal cells and intact loops.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-scope
    Intestine
    evidence_locator
    Abstract
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/reidling-2010-slc19a3-knockout-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1719}]
    experimental_model
    Slc19a3-null or Slc19a2-null mice versus littermates; cells, intestinal loops and expression assays.
    limitations
    Cannot assign the same quantitative effect to humans.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Mus musculus
    plain_language
    Loss of transporter 2 reduced intestinal B1 entry in mice.
    primary_references
    [reidling-2010-slc19a3-knockout] Impaired intestinal vitamin B1 (thiamin) uptake in thiamin transporter-2-deficient mice (2010). https://pubmed.ncbi.nlm.nih.gov/19879271/ DOI: 10.1053/j.gastro.2009.10.042
    tissue_or_cell_type
    Intestine
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 238–250

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Slc19a3-null or Slc19a2-null mice versus littermates; cells, intestinal loops and expression assays. · source_derived_draft · unverified_draft

    ### b1-mouse-slc19a3-absorption-loss Slc19a3-null mice had lower thiamine uptake in isolated intestinal cells and intact loops. Condition category: machinery_impairment nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of transporter 2 reduced intestinal B1 entry in mice. organism: Mus musculus tissue_or_cell_type: Intestine experimental_model: Slc19a3-null or Slc19a2-null mice versus littermates; cells, intestinal loops and expression assays. limitations: Cannot assign the same quantitative effect to humans. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/reidling-2010-slc19a3-knockout-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1719}] evidence_locator: Abstract evidence-scope: Intestine [reidling-2010-slc19a3-knockout] Impaired intestinal vitamin B1 (thiamin) uptake in thiamin transporter-2-deficient mice (2010). https://pubmed.ncbi.nlm.nih.gov/19879271/ DOI: 10.1053/j.gastro.2009.10.042
    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