Component

Human thiamine transporter 1 / SLC19A2

Human plasma membrane transporter for free thiamine.

9 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 it acts on

  1. 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

  2. Human SLC19A2 expression increased thiamine uptake in HeLa cells, with apparent Kt 2.5 +/- 0.6 micromolar.

    Human thiamine transporter 1 / SLC19A2 → Cellular free-thiamine uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence-scope
    HeLa cells
    evidence_locator
    Abstract
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/dutta-1999-slc19a2-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1275}]
    experimental_model
    Human placental cDNA expressed in HeLa cells; radiotracer uptake.
    limitations
    Expression-system affinity is not a blood sufficiency threshold.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Homo sapiens
    plain_language
    This membrane protein brings free B1 into cells.
    primary_references
    [dutta-1999-slc19a2] Cloning of the human thiamine transporter, a member of the folate transporter family (1999). https://pubmed.ncbi.nlm.nih.gov/10542220/ DOI: 10.1074/jbc.274.45.31925
    tissue_or_cell_type
    HeLa cells
    transport_direction
    Extracellular medium to cell interior.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 120–133

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human placental cDNA expressed in HeLa cells; radiotracer uptake. · source_derived_draft · unverified_draft

    ### b1-slc19a2-free-thiamine-uptake Human SLC19A2 expression increased thiamine uptake in HeLa cells, with apparent Kt 2.5 +/- 0.6 micromolar. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: This membrane protein brings free B1 into cells. organism: Homo sapiens tissue_or_cell_type: HeLa cells experimental_model: Human placental cDNA expressed in HeLa cells; radiotracer uptake. limitations: Expression-system affinity is not a blood sufficiency threshold. transport_direction: Extracellular medium to cell interior. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/dutta-1999-slc19a2-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1275}] evidence_locator: Abstract evidence-scope: HeLa cells [dutta-1999-slc19a2] Cloning of the human thiamine transporter, a member of the folate transporter family (1999). https://pubmed.ncbi.nlm.nih.gov/10542220/ DOI: 10.1074/jbc.274.45.31925
    Complete structured claim and evidence

  3. SLC19A2-mediated uptake did not require extracellular sodium and increased with an outward proton gradient.

    Human thiamine transporter 1 / SLC19A2 → Cellular free-thiamine uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence-scope
    HeLa cells
    evidence_locator
    Abstract
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/dutta-1999-slc19a2-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1275}]
    experimental_model
    Human placental cDNA expressed in HeLa cells; radiotracer uptake.
    limitations
    Does not establish an exact proton stoichiometry.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Homo sapiens
    plain_language
    B1 entry in this assay depended on proton conditions without sodium cotransport.
    primary_references
    [dutta-1999-slc19a2] Cloning of the human thiamine transporter, a member of the folate transporter family (1999). https://pubmed.ncbi.nlm.nih.gov/10542220/ DOI: 10.1074/jbc.274.45.31925
    tissue_or_cell_type
    HeLa cells

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 135–147

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human placental cDNA expressed in HeLa cells; radiotracer uptake. · source_derived_draft · unverified_draft

    ### b1-slc19a2-sodium-independence SLC19A2-mediated uptake did not require extracellular sodium and increased with an outward proton gradient. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: B1 entry in this assay depended on proton conditions without sodium cotransport. organism: Homo sapiens tissue_or_cell_type: HeLa cells experimental_model: Human placental cDNA expressed in HeLa cells; radiotracer uptake. limitations: Does not establish an exact proton stoichiometry. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/dutta-1999-slc19a2-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1275}] evidence_locator: Abstract evidence-scope: HeLa cells [dutta-1999-slc19a2] Cloning of the human thiamine transporter, a member of the folate transporter family (1999). https://pubmed.ncbi.nlm.nih.gov/10542220/ DOI: 10.1074/jbc.274.45.31925
    Complete structured claim and evidence

What acts on it

  1. SLC19A2 mRNA fell 76% and THTR-1 protein 77% under high glucose.

    D-glucose → Human thiamine transporter 1 / SLC19A2 source_derived_draftungraded
    Experimental context and source evidence
    curation_topic
    thiamine · Thiamine (vitamin B1)
    experimental_condition
    5 mM glucose 26 mM glucose · D-glucose Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "26 mM glucose", "comparator": "5 mM glucose", "endpoint": "Transporter abundance", "effect_direction": "decrease", "combination": "single", "conditions": [{"entity_slug": "glucose", "state": "26 mM glucose"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Human primary proximal-tubule epithelial cells; 5-day culture
    limitations
    Cell culture; does not by itself establish patient-level thiamine loss.
    primary_references
    Larkin et al. 2012; DOI:10.1371/journal.pone.0053175; PMCID:PMC3532206; https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0053175

    Diabetes cascade: targeted primary-source supplement · lines 18–18

    See claim-local references; curated paraphrases reviewed 2026-09-20. · supports · Human primary proximal-tubule epithelial cells; 5-day culture · source_derived_draft · unverified_draft

    SLC19A2 mRNA fell 76% and THTR-1 protein 77% under high glucose. Model: Human primary proximal-tubule epithelial cells; 5-day culture. Limits: Cell culture; does not by itself establish patient-level thiamine loss. Primary reference: Larkin et al. 2012; DOI:10.1371/journal.pone.0053175; PMCID:PMC3532206; https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0053175
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. High glucose reduced apical-to-basolateral thiamine transport across proximal-tubule monolayers by 37%.

    D-glucose → Human proximal-tubule thiamine reabsorption source_derived_draftungraded
    Experimental context and source evidence
    curation_topic
    thiamine · Thiamine (vitamin B1)
    experimental_condition
    5 mM glucose 26 mM glucose · D-glucose Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "26 mM glucose", "comparator": "5 mM glucose", "endpoint": "Directional thiamine transport", "effect_direction": "decrease", "combination": "single", "conditions": [{"entity_slug": "glucose", "state": "26 mM glucose"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Human primary proximal-tubule epithelial cells; 5-day culture
    limitations
    Transport assay; transporter-expression changes accompany the effect without proving exclusive mediation.
    primary_references
    Larkin et al. 2012; DOI:10.1371/journal.pone.0053175; PMCID:PMC3532206; https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0053175

    Diabetes cascade: targeted primary-source supplement · lines 24–24

    See claim-local references; curated paraphrases reviewed 2026-09-20. · supports · Human primary proximal-tubule epithelial cells; 5-day culture · source_derived_draft · unverified_draft

    High glucose reduced apical-to-basolateral thiamine transport across proximal-tubule monolayers by 37%. Model: Human primary proximal-tubule epithelial cells; 5-day culture. Limits: Transport assay; transporter-expression changes accompany the effect without proving exclusive mediation. Primary reference: Larkin et al. 2012; DOI:10.1371/journal.pone.0053175; PMCID:PMC3532206; https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0053175
    Complete structured claim and evidence

  2. Two exon-2 frameshifting SLC19A2 variants were identified among four Iranian TRMA families.

    SLC19A2 frameshift genotypes in TRMA families → Thiamine-responsive megaloblastic anemia syndrome phenotype source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-scope
    Clinical genetics
    evidence_locator
    Abstract
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/diaz-1999-trma-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1218}]
    experimental_model
    Four Iranian TRMA families; linkage and SLC19A2 sequencing.
    limitations
    Family genetics; individual tissue mechanisms were not directly tested.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Homo sapiens
    plain_language
    Inherited disruption of B1 transport accompanies anemia, diabetes and deafness.
    primary_references
    [diaz-1999-trma] Mutations in a new gene encoding a thiamine transporter cause thiamine-responsive megaloblastic anaemia syndrome (1999). https://www.nature.com/articles/ng0799_309 DOI: 10.1038/10385
    tissue_or_cell_type
    Clinical genetics
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 149–161

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Four Iranian TRMA families; linkage and SLC19A2 sequencing. · source_derived_draft · unverified_draft

    ### b1-slc19a2-frameshift-trma Two exon-2 frameshifting SLC19A2 variants were identified among four Iranian TRMA families. Condition category: machinery_impairment nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Inherited disruption of B1 transport accompanies anemia, diabetes and deafness. organism: Homo sapiens tissue_or_cell_type: Clinical genetics experimental_model: Four Iranian TRMA families; linkage and SLC19A2 sequencing. limitations: Family genetics; individual tissue mechanisms were not directly tested. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/diaz-1999-trma-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1218}] evidence_locator: Abstract evidence-scope: Clinical genetics [diaz-1999-trma] Mutations in a new gene encoding a thiamine transporter cause thiamine-responsive megaloblastic anaemia syndrome (1999). https://www.nature.com/articles/ng0799_309 DOI: 10.1038/10385
    Complete structured claim and evidence

  3. Human SLC19A3 expression increased pyridoxine uptake at pH 5.5; transport favored acidic over neutral/basic conditions.

    Human thiamine transporter 2 / SLC19A3 → Cellular pyridoxine uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    A pH-dependent shared transport route links B1 and the pyridoxine form of B6.
    evidence-scope
    Cultured epithelial cells
    evidence_locator
    Figures 1-3, 6 and 9
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/yamashiro-2020-pyridoxine-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1718}]
    experimental_model
    Human transporter constructs in MDCKII/HEK293 cells; radiotracer uptake at pH 5.5.
    extracellular-pH
    5.5
    limitations
    No systemic B6 transport fraction or supplementation benefit established.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Human proteins; canine and human cell hosts
    plain_language
    The B1 carrier can also carry one B6 form under acidic conditions.
    primary_references
    [yamashiro-2020-pyridoxine] pH-dependent pyridoxine transport by SLC19A2 and SLC19A3: Implications for absorption in acidic microclimates (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7863892/ DOI: 10.1074/jbc.RA120.013610
    tissue_or_cell_type
    Cultured epithelial cells

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 631–645

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human transporter constructs in MDCKII/HEK293 cells; radiotracer uptake at pH 5.5. · source_derived_draft · unverified_draft

    ### b1-slc19a3-pyridoxine-transport Human SLC19A3 expression increased pyridoxine uptake at pH 5.5; transport favored acidic over neutral/basic conditions. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The B1 carrier can also carry one B6 form under acidic conditions. organism: Human proteins; canine and human cell hosts tissue_or_cell_type: Cultured epithelial cells experimental_model: Human transporter constructs in MDCKII/HEK293 cells; radiotracer uptake at pH 5.5. limitations: No systemic B6 transport fraction or supplementation benefit established. cross_nutrient: A pH-dependent shared transport route links B1 and the pyridoxine form of B6. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/yamashiro-2020-pyridoxine-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1718}] evidence_locator: Figures 1-3, 6 and 9 extracellular-pH: 5.5 evidence-scope: Cultured epithelial cells [yamashiro-2020-pyridoxine] pH-dependent pyridoxine transport by SLC19A2 and SLC19A3: Implications for absorption in acidic microclimates (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7863892/ DOI: 10.1074/jbc.RA120.013610
    Complete structured claim and evidence

  4. Thiamine inhibited SLC19A2- and SLC19A3-mediated pyridoxine uptake in acidic-pH transfectant assays.

    Thiamine (vitamin B1) → Cellular pyridoxine uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Direct B1-to-pyridoxine transport inhibition is demonstrated in vitro, with pH and exposure limitations.
    evidence-scope
    Cultured epithelial cells
    evidence_locator
    Figures 1-3, 6 and 9
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/yamashiro-2020-pyridoxine-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1718}]
    experimental_model
    Human transporter constructs in MDCKII/HEK293 cells; radiotracer uptake at pH 5.5.
    extracellular-pH
    5.5
    limitations
    Assay inhibition does not show clinical B6 deficiency from dietary thiamine.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Human proteins; canine and human cell hosts
    plain_language
    B1 reduced uptake of a B6 form in these transporter experiments.
    primary_references
    [yamashiro-2020-pyridoxine] pH-dependent pyridoxine transport by SLC19A2 and SLC19A3: Implications for absorption in acidic microclimates (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7863892/ DOI: 10.1074/jbc.RA120.013610
    tissue_or_cell_type
    Cultured epithelial cells

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 647–661

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human transporter constructs in MDCKII/HEK293 cells; radiotracer uptake at pH 5.5. · source_derived_draft · unverified_draft

    ### b1-thiamine-inhibits-pyridoxine-uptake Thiamine inhibited SLC19A2- and SLC19A3-mediated pyridoxine uptake in acidic-pH transfectant assays. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: B1 reduced uptake of a B6 form in these transporter experiments. organism: Human proteins; canine and human cell hosts tissue_or_cell_type: Cultured epithelial cells experimental_model: Human transporter constructs in MDCKII/HEK293 cells; radiotracer uptake at pH 5.5. limitations: Assay inhibition does not show clinical B6 deficiency from dietary thiamine. cross_nutrient: Direct B1-to-pyridoxine transport inhibition is demonstrated in vitro, with pH and exposure limitations. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/yamashiro-2020-pyridoxine-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1718}] evidence_locator: Figures 1-3, 6 and 9 extracellular-pH: 5.5 evidence-scope: Cultured epithelial cells [yamashiro-2020-pyridoxine] pH-dependent pyridoxine transport by SLC19A2 and SLC19A3: Implications for absorption in acidic microclimates (2020). https://pmc.ncbi.nlm.nih.gov/articles/PMC7863892/ DOI: 10.1074/jbc.RA120.013610
    Complete structured claim and evidence

  5. Human THTR-2 (SLC19A3), highly expressed in the small intestine, transported metformin with a Km of 1.15 mM, whereas THTR-1 did not.

    Human thiamine transporter 2 / SLC19A3 → Metformin source_derived_draftungraded
    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 vitamin B1 transporter in the gut also carries the drug.
    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
    transport_effect
    raises Intestinal THTR-2 transported metformin with a Km of 1.15 mM, which is absorption.
    transport_pool
    the enterocyte interior Intestinal THTR-2 transported metformin with a Km of 1.15 mM, which is absorption.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 1282–1293

    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-transports-metformin Human THTR-2 (SLC19A3), highly expressed in the small intestine, transported metformin with a Km of 1.15 mM, whereas THTR-1 did not. 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 vitamin B1 transporter in the gut also carries the drug. 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

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