Component
Intestinal pyridoxine uptake
Uptake of unphosphorylated pyridoxine by enterocytes.
1 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
Caco-2 pyridoxine uptake was energy-dependent and sodium-independent; saturation occurred at pH 5.5 (apparent Km 11.99 micromolar), but not pH 7.4.
Experimental context and source evidence
- evidence_location
- Indexed abstract: pH-dependent saturation and sodium independence
- experimental_model
- Human Caco-2 intestinal epithelial cells.
- exposure
- Radiotracer uptake at controlled extracellular pH.
- limitations
- Carrier identity was not established; uptake behavior alone does not identify a transporter gene.
- nutrient_topic
- Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
- organism
- Homo sapiens
- plain_language
- Acidic conditions exposed a saturable uptake component.
- primary_references
- [said2003] A carrier-mediated mechanism for pyridoxine uptake by human intestinal epithelial Caco-2 cells: regulation by a PKA-mediated pathway. (2003). https://pubmed.ncbi.nlm.nih.gov/12867360/ DOI: 10.1152/ajpcell.00204.2003
- tissue_or_cell_type
- Caco-2 cells
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 111–122
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human Caco-2 intestinal epithelial cells. · source_derived_draft · unverified_draft
### b6-transport-caco2-pn-uptake Caco-2 pyridoxine uptake was energy-dependent and sodium-independent; saturation occurred at pH 5.5 (apparent Km 11.99 micromolar), but not pH 7.4. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Acidic conditions exposed a saturable uptake component. organism: Homo sapiens tissue_or_cell_type: Caco-2 cells experimental_model: Human Caco-2 intestinal epithelial cells. limitations: Carrier identity was not established; uptake behavior alone does not identify a transporter gene. exposure: Radiotracer uptake at controlled extracellular pH. evidence_location: Indexed abstract: pH-dependent saturation and sodium independence [said2003] A carrier-mediated mechanism for pyridoxine uptake by human intestinal epithelial Caco-2 cells: regulation by a PKA-mediated pathway. (2003). https://pubmed.ncbi.nlm.nih.gov/12867360/ DOI: 10.1152/ajpcell.00204.2003
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.