Component

Cellular free-thiamine uptake

Measured movement of free thiamine from medium into cells.

7 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. 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

  2. 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

  3. SLC19A3-transfected HeLa cells accumulated more radiolabeled thiamine than vector controls.

    Human thiamine transporter 2 / SLC19A3 → 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/rajgopal-2001-slc19a3-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1133}]
    experimental_model
    Transient human SLC19A3 transfection in HeLa cells.
    limitations
    Heterologous expression; contribution varies across tissues.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Homo sapiens
    plain_language
    A second human membrane transporter imports free B1.
    primary_references
    [rajgopal-2001-slc19a3] SLC19A3 encodes a second thiamine transporter ThTr2 (2001). https://pubmed.ncbi.nlm.nih.gov/11731220/ DOI: 10.1016/S0925-4439(01)00073-4
    tissue_or_cell_type
    HeLa cells
    transport_direction
    Extracellular medium to cell interior.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 163–176

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transient human SLC19A3 transfection in HeLa cells. · source_derived_draft · unverified_draft

    ### b1-slc19a3-free-thiamine-uptake SLC19A3-transfected HeLa cells accumulated more radiolabeled thiamine than vector controls. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second human membrane transporter imports free B1. organism: Homo sapiens tissue_or_cell_type: HeLa cells experimental_model: Transient human SLC19A3 transfection in HeLa cells. limitations: Heterologous expression; contribution varies across tissues. transport_direction: Extracellular medium to cell interior. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/rajgopal-2001-slc19a3-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1133}] evidence_locator: Abstract evidence-scope: HeLa cells [rajgopal-2001-slc19a3] SLC19A3 encodes a second thiamine transporter ThTr2 (2001). https://pubmed.ncbi.nlm.nih.gov/11731220/ DOI: 10.1016/S0925-4439(01)00073-4
    Complete structured claim and evidence

  4. G23V abolished detectable SLC19A3 thiamine transport without preventing cell-surface targeting.

    Human SLC19A3 G23V variant → Cellular free-thiamine uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-scope
    Caco-2 and MDCK epithelial models
    evidence_locator
    Abstract
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/subramanian-2006-biotin-specificity-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1656}]
    experimental_model
    Human transporter constructs in epithelial cell lines; uptake and surface targeting.
    limitations
    Expression assay, not direct brain flux.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Human proteins in human and canine cell lines
    plain_language
    A correctly positioned transporter can still fail to move B1.
    primary_references
    [subramanian-2006-biotin-specificity] Biotin-responsive basal ganglia disease-linked mutations inhibit thiamine transport via hTHTR2: biotin is not a substrate for hTHTR2 (2006). https://pubmed.ncbi.nlm.nih.gov/16790503/ DOI: 10.1152/ajpcell.00105.2006
    tissue_or_cell_type
    Caco-2 and MDCK epithelial models
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 266–278

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human transporter constructs in epithelial cell lines; uptake and surface targeting. · source_derived_draft · unverified_draft

    ### b1-slc19a3-g23v-transport G23V abolished detectable SLC19A3 thiamine transport without preventing cell-surface targeting. Condition category: machinery_impairment nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A correctly positioned transporter can still fail to move B1. organism: Human proteins in human and canine cell lines tissue_or_cell_type: Caco-2 and MDCK epithelial models experimental_model: Human transporter constructs in epithelial cell lines; uptake and surface targeting. limitations: Expression assay, not direct brain flux. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/subramanian-2006-biotin-specificity-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1656}] evidence_locator: Abstract evidence-scope: Caco-2 and MDCK epithelial models [subramanian-2006-biotin-specificity] Biotin-responsive basal ganglia disease-linked mutations inhibit thiamine transport via hTHTR2: biotin is not a substrate for hTHTR2 (2006). https://pubmed.ncbi.nlm.nih.gov/16790503/ DOI: 10.1152/ajpcell.00105.2006
    Complete structured claim and evidence

  5. T422A abolished detectable SLC19A3 thiamine transport without preventing cell-surface targeting.

    Human SLC19A3 T422A variant → Cellular free-thiamine uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence-scope
    Caco-2 and MDCK epithelial models
    evidence_locator
    Abstract
    evidence_spans
    [{"source_document": "artifacts/thiamine_transport_sources/subramanian-2006-biotin-specificity-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1656}]
    experimental_model
    Human transporter constructs in epithelial cell lines; uptake and surface targeting.
    limitations
    Expression assay, not direct brain flux.
    nutrient_topic
    Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
    organism
    Human proteins in human and canine cell lines
    plain_language
    This second disease variant disrupts transport function.
    primary_references
    [subramanian-2006-biotin-specificity] Biotin-responsive basal ganglia disease-linked mutations inhibit thiamine transport via hTHTR2: biotin is not a substrate for hTHTR2 (2006). https://pubmed.ncbi.nlm.nih.gov/16790503/ DOI: 10.1152/ajpcell.00105.2006
    tissue_or_cell_type
    Caco-2 and MDCK epithelial models
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 280–292

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human transporter constructs in epithelial cell lines; uptake and surface targeting. · source_derived_draft · unverified_draft

    ### b1-slc19a3-t422a-transport T422A abolished detectable SLC19A3 thiamine transport without preventing cell-surface targeting. Condition category: machinery_impairment nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: This second disease variant disrupts transport function. organism: Human proteins in human and canine cell lines tissue_or_cell_type: Caco-2 and MDCK epithelial models experimental_model: Human transporter constructs in epithelial cell lines; uptake and surface targeting. limitations: Expression assay, not direct brain flux. evidence_spans: [{"source_document": "artifacts/thiamine_transport_sources/subramanian-2006-biotin-specificity-source-record.json", "source_field": "resultList.result[0].abstractText", "start_char": 0, "end_char": 1656}] evidence_locator: Abstract evidence-scope: Caco-2 and MDCK epithelial models [subramanian-2006-biotin-specificity] Biotin-responsive basal ganglia disease-linked mutations inhibit thiamine transport via hTHTR2: biotin is not a substrate for hTHTR2 (2006). https://pubmed.ncbi.nlm.nih.gov/16790503/ DOI: 10.1152/ajpcell.00105.2006
    Complete structured claim and evidence

  6. Metformin and the biguanide analogue phenformin competitively inhibited OCT1-mediated thiamine uptake.

    Metformin → Cellular 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/24961373.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77be4a228b3d067ca1e7ba44e8148f5fbda7956a23b42fb8281e9faf451a0e70", "start_char": 0, "end_char": 1270, "text_sha256": "77be4a228b3d067ca1e7ba44e8148f5fbda7956a23b42fb8281e9faf451a0e70"}
    experimental_model
    Oct1-knockout and human OCT1 transgenic mice, metabolomics and isotopic uptake
    exposure
    Metformin and phenformin against thiamine uptake; acute metformin in wild-type mice
    limitations
    Identifies thiamine as an endogenous OCT1 substrate and shows competitive inhibition by metformin. The steatosis phenotype is a mouse phenotype.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Mouse and human transporter
    plain_language
    The drug and the vitamin compete for the same door.
    primary_references
    [metformin-p24961373] OCT1 is a high-capacity thiamine transporter that regulates hepatic steatosis and is a target of metformin. (2014). https://pubmed.ncbi.nlm.nih.gov/24961373/ DOI: 10.1073/pnas.1314939111
    tissue_or_cell_type
    Liver and intestine
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 1243–1254

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oct1-knockout and human OCT1 transgenic mice, metabolomics and isotopic uptake · source_derived_draft · unverified_draft

    ### metformin-metformin-thiamine-competition Metformin and the biguanide analogue phenformin competitively inhibited OCT1-mediated thiamine uptake. 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: The drug and the vitamin compete for the same door. organism: Mouse and human transporter tissue_or_cell_type: Liver and intestine experimental_model: Oct1-knockout and human OCT1 transgenic mice, metabolomics and isotopic uptake limitations: Identifies thiamine as an endogenous OCT1 substrate and shows competitive inhibition by metformin. The steatosis phenotype is a mouse phenotype. exposure: Metformin and phenformin against thiamine uptake; acute metformin in wild-type mice evidence_span: {"source_cache": "artifacts/metformin-research/24961373.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77be4a228b3d067ca1e7ba44e8148f5fbda7956a23b42fb8281e9faf451a0e70", "start_char": 0, "end_char": 1270, "text_sha256": "77be4a228b3d067ca1e7ba44e8148f5fbda7956a23b42fb8281e9faf451a0e70"} [metformin-p24961373] OCT1 is a high-capacity thiamine transporter that regulates hepatic steatosis and is a target of metformin. (2014). https://pubmed.ncbi.nlm.nih.gov/24961373/ DOI: 10.1073/pnas.1314939111
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Metabolomic and isotopic uptake methods identified thiamine as a principal endogenous substrate of OCT1.

    Human organic cation transporter 1 / OCT1 / SLC22A1 → Thiamine (vitamin B1) source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/24961373.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77be4a228b3d067ca1e7ba44e8148f5fbda7956a23b42fb8281e9faf451a0e70", "start_char": 0, "end_char": 1270, "text_sha256": "77be4a228b3d067ca1e7ba44e8148f5fbda7956a23b42fb8281e9faf451a0e70"}
    experimental_model
    Oct1-knockout and human OCT1 transgenic mice, metabolomics and isotopic uptake
    exposure
    Metformin and phenformin against thiamine uptake; acute metformin in wild-type mice
    limitations
    Identifies thiamine as an endogenous OCT1 substrate and shows competitive inhibition by metformin. The steatosis phenotype is a mouse phenotype.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Mouse and human transporter
    plain_language
    The transporter that carries the drug into the liver normally carries vitamin B1.
    primary_references
    [metformin-p24961373] OCT1 is a high-capacity thiamine transporter that regulates hepatic steatosis and is a target of metformin. (2014). https://pubmed.ncbi.nlm.nih.gov/24961373/ DOI: 10.1073/pnas.1314939111
    tissue_or_cell_type
    Liver and intestine
    transport_effect
    raises Identified by isotopic uptake as a principal endogenous substrate.
    transport_pool
    the expressing cell Identified by isotopic uptake as a principal endogenous substrate.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 1230–1241

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oct1-knockout and human OCT1 transgenic mice, metabolomics and isotopic uptake · source_derived_draft · unverified_draft

    ### metformin-oct1-thiamine-substrate Metabolomic and isotopic uptake methods identified thiamine as a principal endogenous substrate of OCT1. 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 transporter that carries the drug into the liver normally carries vitamin B1. organism: Mouse and human transporter tissue_or_cell_type: Liver and intestine experimental_model: Oct1-knockout and human OCT1 transgenic mice, metabolomics and isotopic uptake limitations: Identifies thiamine as an endogenous OCT1 substrate and shows competitive inhibition by metformin. The steatosis phenotype is a mouse phenotype. exposure: Metformin and phenformin against thiamine uptake; acute metformin in wild-type mice evidence_span: {"source_cache": "artifacts/metformin-research/24961373.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77be4a228b3d067ca1e7ba44e8148f5fbda7956a23b42fb8281e9faf451a0e70", "start_char": 0, "end_char": 1270, "text_sha256": "77be4a228b3d067ca1e7ba44e8148f5fbda7956a23b42fb8281e9faf451a0e70"} [metformin-p24961373] OCT1 is a high-capacity thiamine transporter that regulates hepatic steatosis and is a target of metformin. (2014). https://pubmed.ncbi.nlm.nih.gov/24961373/ DOI: 10.1073/pnas.1314939111
    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