Component

Intestinal free-thiamine uptake

Uptake of free thiamine in intestinal cells or loops.

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

Read recorded mechanisms Open recursive mind map

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

    Mouse Slc19a3-null genotype → Intestinal free-thiamine uptake source_derived_draftungraded
    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

  2. SLC19A2-directed siRNA reduced carrier-mediated Caco-2 thiamine uptake by 56%.

    Human thiamine transporter 1 / SLC19A2 → Intestinal free-thiamine uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-scope
    Small-intestinal membranes; Caco-2 cells
    evidence_locator
    Single-transporter siRNA experiment
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/said-2004-intestinal-transport-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1710}]
    experimental_model
    Native human enterocyte membranes and polarized Caco-2 cells; imaging, immunoblotting and siRNA.
    exposure
    Experimental siRNA knockdown; not nutritional deficiency.
    limitations
    Knockdown fraction is assay-specific.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Homo sapiens
    plain_language
    Removing transporter 1 reduced B1 entry.
    primary_references
    [said-2004-intestinal-transport] Expression and functional contribution of hTHTR-2 in thiamin absorption in human intestine (2004). https://pubmed.ncbi.nlm.nih.gov/14615284/ DOI: 10.1152/ajpgi.00361.2003
    tissue_or_cell_type
    Small-intestinal membranes; Caco-2 cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 208–221

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Native human enterocyte membranes and polarized Caco-2 cells; imaging, immunoblotting and siRNA. · source_derived_draft · unverified_draft

    ### b1-slc19a2-caco2-silencing SLC19A2-directed siRNA reduced carrier-mediated Caco-2 thiamine uptake by 56%. Condition category: machinery_impairment nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing transporter 1 reduced B1 entry. organism: Homo sapiens tissue_or_cell_type: Small-intestinal membranes; Caco-2 cells experimental_model: Native human enterocyte membranes and polarized Caco-2 cells; imaging, immunoblotting and siRNA. limitations: Knockdown fraction is assay-specific. evidence_locator: Single-transporter siRNA experiment exposure: Experimental siRNA knockdown; not nutritional deficiency. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/said-2004-intestinal-transport-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1710}] evidence-scope: Small-intestinal membranes; Caco-2 cells [said-2004-intestinal-transport] Expression and functional contribution of hTHTR-2 in thiamin absorption in human intestine (2004). https://pubmed.ncbi.nlm.nih.gov/14615284/ DOI: 10.1152/ajpgi.00361.2003
    Complete structured claim and evidence

  3. SLC19A3-directed siRNA reduced carrier-mediated Caco-2 thiamine uptake by 48%.

    Human thiamine transporter 2 / SLC19A3 → Intestinal free-thiamine uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-scope
    Small-intestinal membranes; Caco-2 cells
    evidence_locator
    Single-transporter siRNA experiment
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/said-2004-intestinal-transport-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1710}]
    experimental_model
    Native human enterocyte membranes and polarized Caco-2 cells; imaging, immunoblotting and siRNA.
    exposure
    Experimental siRNA knockdown; not nutritional deficiency.
    limitations
    Overlapping contributions are not additive clinical percentages.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Homo sapiens
    plain_language
    Removing transporter 2 also reduced B1 entry.
    primary_references
    [said-2004-intestinal-transport] Expression and functional contribution of hTHTR-2 in thiamin absorption in human intestine (2004). https://pubmed.ncbi.nlm.nih.gov/14615284/ DOI: 10.1152/ajpgi.00361.2003
    tissue_or_cell_type
    Small-intestinal membranes; Caco-2 cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 223–236

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Native human enterocyte membranes and polarized Caco-2 cells; imaging, immunoblotting and siRNA. · source_derived_draft · unverified_draft

    ### b1-slc19a3-caco2-silencing SLC19A3-directed siRNA reduced carrier-mediated Caco-2 thiamine uptake by 48%. Condition category: machinery_impairment nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing transporter 2 also reduced B1 entry. organism: Homo sapiens tissue_or_cell_type: Small-intestinal membranes; Caco-2 cells experimental_model: Native human enterocyte membranes and polarized Caco-2 cells; imaging, immunoblotting and siRNA. limitations: Overlapping contributions are not additive clinical percentages. evidence_locator: Single-transporter siRNA experiment exposure: Experimental siRNA knockdown; not nutritional deficiency. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/said-2004-intestinal-transport-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1710}] evidence-scope: Small-intestinal membranes; Caco-2 cells [said-2004-intestinal-transport] Expression and functional contribution of hTHTR-2 in thiamin absorption in human intestine (2004). https://pubmed.ncbi.nlm.nih.gov/14615284/ DOI: 10.1152/ajpgi.00361.2003
    Complete structured claim and evidence

  4. Metformin, along with phenformin, chloroquine, verapamil, famotidine and amprolium, inhibited hTHTR-2-mediated uptake of both thiamine and metformin.

    Metformin → Intestinal free-thiamine uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    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
    Because they share the carrier, the drug gets in the vitamin’s way.
    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
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 1295–1306

    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-metformin-inhibits-thtr2 Metformin, along with phenformin, chloroquine, verapamil, famotidine and amprolium, inhibited hTHTR-2-mediated uptake of both thiamine and metformin. Condition category: nutrient_deficiency nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: Because they share the carrier, the drug gets in the vitamin’s way. 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. Of 1360 screened compounds, 146 inhibited ThTR-2, and several oral drugs including metformin were predicted to reach intestinal concentrations that may result in ThTR-2-mediated drug-nutrient interactions.

    Metformin → Human thiamine transporter 2 / SLC19A3 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/metformin-research/31764942.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "21758b02cd824f37a6e1e076657c0cf72d08cc6babcb66773613f129dc13f15b", "start_char": 0, "end_char": 1829, "text_sha256": "21758b02cd824f37a6e1e076657c0cf72d08cc6babcb66773613f129dc13f15b"}
    experimental_model
    High-throughput screen of 1360 compounds, in-silico modelling and electronic health record analysis
    exposure
    Inhibition kinetics with IC50 values and predicted intestinal concentrations
    limitations
    A screen plus a records analysis, not a trial. The trial termination cited as motivation involved a different, more potent inhibitor.
    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 transporter and human health records
    plain_language
    Among many drugs tested, this one is expected to reach gut levels high enough to matter.
    primary_references
    [metformin-p31764942] Drug-nutrient interactions: discovering prescription drug inhibitors of the thiamine transporter ThTR-2 (SLC19A3). (2020). https://pubmed.ncbi.nlm.nih.gov/31764942/ DOI: 10.1093/ajcn/nqz255
    tissue_or_cell_type
    Intestinal thiamine absorption
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 1321–1332

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-throughput screen of 1360 compounds, in-silico modelling and electronic health record analysis · source_derived_draft · unverified_draft

    ### metformin-thtr2-drug-screen Of 1360 screened compounds, 146 inhibited ThTR-2, and several oral drugs including metformin were predicted to reach intestinal concentrations that may result in ThTR-2-mediated drug-nutrient interactions. Condition category: nutrient_deficiency nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: Among many drugs tested, this one is expected to reach gut levels high enough to matter. organism: Human transporter and human health records tissue_or_cell_type: Intestinal thiamine absorption experimental_model: High-throughput screen of 1360 compounds, in-silico modelling and electronic health record analysis limitations: A screen plus a records analysis, not a trial. The trial termination cited as motivation involved a different, more potent inhibitor. exposure: Inhibition kinetics with IC50 values and predicted intestinal concentrations evidence_span: {"source_cache": "artifacts/metformin-research/31764942.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "21758b02cd824f37a6e1e076657c0cf72d08cc6babcb66773613f129dc13f15b", "start_char": 0, "end_char": 1829, "text_sha256": "21758b02cd824f37a6e1e076657c0cf72d08cc6babcb66773613f129dc13f15b"} [metformin-p31764942] Drug-nutrient interactions: discovering prescription drug inhibitors of the thiamine transporter ThTR-2 (SLC19A3). (2020). https://pubmed.ncbi.nlm.nih.gov/31764942/ DOI: 10.1093/ajcn/nqz255
    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