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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
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 evidenceSpecies 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)
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
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.