Component
Intestinal cholecalciferol uptake
Cellular entry of vitamin D3 across intestinal epithelial uptake surfaces.
4 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
Expression of CD36 in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake.
Experimental context and source evidence
- cross_nutrient
- false
- evidence_location
- Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract.
- experimental_model
- Transfected HEK-cell uptake assay; intestinal relevance tested separately
- exposure
- Transporter transfection and selective-inhibitor co-incubation; exact dose/time absent from abstract.
- limitations
- HEK overexpression is not intact human intestine; inhibitors and uptake assays do not establish clinical deficiency. In-vivo ezetimibe effect in mice was nonsignificant.
- nutrient
- Vitamin D2 and D3 · Vitamin D2 and D3
- nutrient_topic
- Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
- organism
- Homo sapiens
- plain_language
- CD36 can contribute to vitamin D3 entry into cells.
- primary_references
- [reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553
- tissue_or_cell_type
- HEK cell model of a candidate intestinal uptake mechanism
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 181–194
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected HEK-cell uptake assay; intestinal relevance tested separately · source_derived_draft · unverified_draft
### vd-act-cd36-uptake Expression of CD36 in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: CD36 can contribute to vitamin D3 entry into cells. organism: Homo sapiens tissue_or_cell_type: HEK cell model of a candidate intestinal uptake mechanism experimental_model: Transfected HEK-cell uptake assay; intestinal relevance tested separately limitations: HEK overexpression is not intact human intestine; inhibitors and uptake assays do not establish clinical deficiency. In-vivo ezetimibe effect in mice was nonsignificant. exposure: Transporter transfection and selective-inhibitor co-incubation; exact dose/time absent from abstract. cross_nutrient: false evidence_location: Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract. nutrient: Vitamin D2 and D3 [reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553
Complete structured claim and evidenceExpression of NPC1L1 in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake.
Experimental context and source evidence
- cross_nutrient
- false
- evidence_location
- Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract.
- experimental_model
- Transfected HEK-cell uptake assay; intestinal relevance tested separately
- exposure
- Transporter transfection and selective-inhibitor co-incubation; exact dose/time absent from abstract.
- limitations
- HEK overexpression is not intact human intestine; inhibitors and uptake assays do not establish clinical deficiency. In-vivo ezetimibe effect in mice was nonsignificant.
- nutrient
- Vitamin D2 and D3 · Vitamin D2 and D3
- nutrient_topic
- Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
- organism
- Homo sapiens
- plain_language
- NPC1L1 can contribute to vitamin D3 entry into cells.
- primary_references
- [reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553
- tissue_or_cell_type
- HEK cell model of a candidate intestinal uptake mechanism
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 196–209
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected HEK-cell uptake assay; intestinal relevance tested separately · source_derived_draft · unverified_draft
### vd-act-npc1l1-uptake Expression of NPC1L1 in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: NPC1L1 can contribute to vitamin D3 entry into cells. organism: Homo sapiens tissue_or_cell_type: HEK cell model of a candidate intestinal uptake mechanism experimental_model: Transfected HEK-cell uptake assay; intestinal relevance tested separately limitations: HEK overexpression is not intact human intestine; inhibitors and uptake assays do not establish clinical deficiency. In-vivo ezetimibe effect in mice was nonsignificant. exposure: Transporter transfection and selective-inhibitor co-incubation; exact dose/time absent from abstract. cross_nutrient: false evidence_location: Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract. nutrient: Vitamin D2 and D3 [reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553
Complete structured claim and evidenceExpression of SR-BI in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake.
Experimental context and source evidence
- cross_nutrient
- false
- evidence_location
- Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract.
- experimental_model
- Transfected HEK-cell uptake assay; intestinal relevance tested separately
- exposure
- Transporter transfection and selective-inhibitor co-incubation; exact dose/time absent from abstract.
- limitations
- HEK overexpression is not intact human intestine; inhibitors and uptake assays do not establish clinical deficiency. In-vivo ezetimibe effect in mice was nonsignificant.
- nutrient
- Vitamin D2 and D3 · Vitamin D2 and D3
- nutrient_topic
- Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
- organism
- Homo sapiens
- plain_language
- SR-BI can contribute to vitamin D3 entry into cells.
- primary_references
- [reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553
- tissue_or_cell_type
- HEK cell model of a candidate intestinal uptake mechanism
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 166–179
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected HEK-cell uptake assay; intestinal relevance tested separately · source_derived_draft · unverified_draft
### vd-act-scarb1-uptake Expression of SR-BI in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: SR-BI can contribute to vitamin D3 entry into cells. organism: Homo sapiens tissue_or_cell_type: HEK cell model of a candidate intestinal uptake mechanism experimental_model: Transfected HEK-cell uptake assay; intestinal relevance tested separately limitations: HEK overexpression is not intact human intestine; inhibitors and uptake assays do not establish clinical deficiency. In-vivo ezetimibe effect in mice was nonsignificant. exposure: Transporter transfection and selective-inhibitor co-incubation; exact dose/time absent from abstract. cross_nutrient: false evidence_location: Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract. nutrient: Vitamin D2 and D3 [reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553
Complete structured claim and evidenceCo-incubation with tocopherol significantly impaired cholecalciferol uptake in Caco-2 cells.
Experimental context and source evidence
- cross_nutrient
- true
- evidence_location
- Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract.
- experimental_model
- Caco-2 apical uptake assay
- exposure
- Tocopherol and cholecalciferol co-incubation; dose/time unavailable in primary abstract.
- limitations
- The primary abstract says tocopherol; the authors' subsequent primary paper identifies it as alpha-tocopherol. No evidence here warrants separating normal oral supplements or diagnosing D malabsorption.
- nutrient
- Vitamin D2 and D3 · Vitamin D2 and D3
- nutrient_topic
- Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
- organism
- Homo sapiens
- plain_language
- Vitamin E competed with D3 uptake in an intestinal cell model.
- primary_references
- [reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553 [goncalves2015] Fat-soluble vitamin intestinal absorption: absorption sites in the intestine and interactions for absorption. (2015). https://pubmed.ncbi.nlm.nih.gov/25442537/ DOI: 10.1016/j.foodchem.2014.09.021
- tissue_or_cell_type
- Caco-2 intestinal epithelial model
Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 211–225
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Caco-2 apical uptake assay · source_derived_draft · unverified_draft
### vd-act-tocopherol-uptake-competition Co-incubation with tocopherol significantly impaired cholecalciferol uptake in Caco-2 cells. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin E competed with D3 uptake in an intestinal cell model. organism: Homo sapiens tissue_or_cell_type: Caco-2 intestinal epithelial model experimental_model: Caco-2 apical uptake assay limitations: The primary abstract says tocopherol; the authors' subsequent primary paper identifies it as alpha-tocopherol. No evidence here warrants separating normal oral supplements or diagnosing D malabsorption. exposure: Tocopherol and cholecalciferol co-incubation; dose/time unavailable in primary abstract. cross_nutrient: true evidence_location: Primary abstract, Methods and results; exact incubation concentrations/durations unavailable in abstract. nutrient: Vitamin D2 and D3 [reboul2011] Vitamin D intestinal absorption is not a simple passive diffusion: evidences for involvement of cholesterol transporters. (2011). https://pubmed.ncbi.nlm.nih.gov/21280209/ DOI: 10.1002/mnfr.201000553 [goncalves2015] Fat-soluble vitamin intestinal absorption: absorption sites in the intestine and interactions for absorption. (2015). https://pubmed.ncbi.nlm.nih.gov/25442537/ DOI: 10.1016/j.foodchem.2014.09.021
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.