Component

Human Niemann-Pick C1-like protein 1 / NPC1L1

Intestinal sterol transport protein tested in vitamin D3 uptake assays.

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 it acts on

  1. Expression of NPC1L1 in HEK cells increased cholecalciferol uptake, and its corresponding inhibitor reduced this uptake.

    Human Niemann-Pick C1-like protein 1 / NPC1L1 → Intestinal cholecalciferol uptake source_derived_draftungraded
    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 evidence

  2. NPC1L1 antibody and ezetimibe did not significantly reduce all-E or 5Z lycopene uptake in Caco-2 cells.

    Human Niemann-Pick C1-like protein 1 / NPC1L1 → Intestinal epithelial lycopene uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/lycopene-research/18641187.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d", "start_char": 0, "end_char": 1557, "text_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d"}
    experimental_model
    Transporter inhibition in Caco-2 cells; intestinal SR-BI transgenic mice
    exposure
    All-E and 5Z lycopene; mice received 0.25 g/kg diet for one month
    limitations
    Partial uptake inhibition is not proof of a sole transporter. Ezetimibe result is a cell assay, not a clinical drug-interaction trial.
    nutrient_topic
    Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene
    organism
    Human Caco-2 cells
    plain_language
    A transporter used by other lipids was not necessary in this particular assay.
    primary_references
    [lycopene-p18641187] Lycopene absorption in human intestinal cells and in mice involves scavenger receptor class B type I but not Niemann-Pick C1-like 1. (2008). https://pubmed.ncbi.nlm.nih.gov/18641187/ DOI: 10.1093/jn/138.8.1432
    tissue_or_cell_type
    Intestinal epithelium and plasma

    Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 117–128

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter inhibition in Caco-2 cells; intestinal SR-BI transgenic mice · source_derived_draft · unverified_draft

    ### lycopene-npc1l1-null NPC1L1 antibody and ezetimibe did not significantly reduce all-E or 5Z lycopene uptake in Caco-2 cells. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transporter used by other lipids was not necessary in this particular assay. organism: Human Caco-2 cells tissue_or_cell_type: Intestinal epithelium and plasma experimental_model: Transporter inhibition in Caco-2 cells; intestinal SR-BI transgenic mice limitations: Partial uptake inhibition is not proof of a sole transporter. Ezetimibe result is a cell assay, not a clinical drug-interaction trial. exposure: All-E and 5Z lycopene; mice received 0.25 g/kg diet for one month evidence_span: {"source_cache": "artifacts/lycopene-research/18641187.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d", "start_char": 0, "end_char": 1557, "text_sha256": "7c71fd4fd3be9d14176bceb3c2104143269a788587feec232350a6f1c5913e3d"} [lycopene-p18641187] Lycopene absorption in human intestinal cells and in mice involves scavenger receptor class B type I but not Niemann-Pick C1-like 1. (2008). https://pubmed.ncbi.nlm.nih.gov/18641187/ DOI: 10.1093/jn/138.8.1432
    Complete structured claim and evidence

  3. Ezetimibe-sensitive lutein uptake supported a contribution from NPC1L1 in Caco-2 cells.

    Human Niemann-Pick C1-like protein 1 / NPC1L1 → Intestinal epithelial lutein uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/lutein-research/22579005.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1dd51af5fd10e865810b3fa2fdab5ed4f6613212a3cd418a009554ae601c076b", "start_char": 0, "end_char": 1895, "text_sha256": "1dd51af5fd10e865810b3fa2fdab5ed4f6613212a3cd418a009554ae601c076b"}
    experimental_model
    Transporter-inhibitor uptake/permeability experiment
    exposure
    Ezetimibe, BLT1 and ATP-depletion reagents
    limitations
    Pharmacological evidence supports involvement, not an exclusive transporter or proven human clinical interaction.
    nutrient_topic
    Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
    organism
    Human Caco-2 cells
    plain_language
    A cholesterol-uptake pathway also contributed to lutein entry.
    primary_references
    [lutein-p22579005] Involvement of cholesterol membrane transporter Niemann-Pick C1-like 1 in the intestinal absorption of lutein. (2012). https://pubmed.ncbi.nlm.nih.gov/22579005/ DOI: 10.18433/j38k56
    tissue_or_cell_type
    Intestinal epithelial model

    Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 515–526

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter-inhibitor uptake/permeability experiment · source_derived_draft · unverified_draft

    ### lutein-npc1l1-intestine Ezetimibe-sensitive lutein uptake supported a contribution from NPC1L1 in Caco-2 cells. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A cholesterol-uptake pathway also contributed to lutein entry. organism: Human Caco-2 cells tissue_or_cell_type: Intestinal epithelial model experimental_model: Transporter-inhibitor uptake/permeability experiment limitations: Pharmacological evidence supports involvement, not an exclusive transporter or proven human clinical interaction. exposure: Ezetimibe, BLT1 and ATP-depletion reagents evidence_span: {"source_cache": "artifacts/lutein-research/22579005.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1dd51af5fd10e865810b3fa2fdab5ed4f6613212a3cd418a009554ae601c076b", "start_char": 0, "end_char": 1895, "text_sha256": "1dd51af5fd10e865810b3fa2fdab5ed4f6613212a3cd418a009554ae601c076b"} [lutein-p22579005] Involvement of cholesterol membrane transporter Niemann-Pick C1-like 1 in the intestinal absorption of lutein. (2012). https://pubmed.ncbi.nlm.nih.gov/22579005/ DOI: 10.18433/j38k56
    Complete structured claim and evidence

  4. Ezetimibe-sensitive uptake also supported NPC1L1 involvement after dipalmitate exposure.

    Human Niemann-Pick C1-like protein 1 / NPC1L1 → Zeaxanthin dipalmitate-associated uptake in intestinal epithelial models source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"}
    experimental_model
    Micelle uptake, transporter inhibition and protein-expression assays
    exposure
    Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe
    limitations
    Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing.
    nutrient_topic
    Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
    organism
    Human Caco-2 monolayers
    plain_language
    The ester formulation also used the tested pathway.
    primary_references
    [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
    tissue_or_cell_type
    Intestinal epithelial model

    Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 717–728

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Micelle uptake, transporter inhibition and protein-expression assays · source_derived_draft · unverified_draft

    ### zeaxanthin-npc1l1-ester Ezetimibe-sensitive uptake also supported NPC1L1 involvement after dipalmitate exposure. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The ester formulation also used the tested pathway. organism: Human Caco-2 monolayers tissue_or_cell_type: Intestinal epithelial model experimental_model: Micelle uptake, transporter inhibition and protein-expression assays limitations: Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing. exposure: Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe evidence_span: {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"} [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
    Complete structured claim and evidence

  5. Ezetimibe-sensitive uptake supported NPC1L1 involvement in free-zeaxanthin uptake.

    Human Niemann-Pick C1-like protein 1 / NPC1L1 → Zeaxanthin uptake in intestinal epithelial models source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"}
    experimental_model
    Micelle uptake, transporter inhibition and protein-expression assays
    exposure
    Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe
    limitations
    Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing.
    nutrient_topic
    Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
    organism
    Human Caco-2 monolayers
    plain_language
    The cholesterol-uptake pathway contributed in intestinal cells.
    primary_references
    [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
    tissue_or_cell_type
    Intestinal epithelial model

    Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 639–650

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Micelle uptake, transporter inhibition and protein-expression assays · source_derived_draft · unverified_draft

    ### zeaxanthin-npc1l1-uptake Ezetimibe-sensitive uptake supported NPC1L1 involvement in free-zeaxanthin uptake. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cholesterol-uptake pathway contributed in intestinal cells. organism: Human Caco-2 monolayers tissue_or_cell_type: Intestinal epithelial model experimental_model: Micelle uptake, transporter inhibition and protein-expression assays limitations: Inhibitors support pathway involvement rather than exclusivity. Protein-expression changes do not prove efflux; a cell model cannot establish clinical drug spacing. exposure: Free and dipalmitate xanthophyll micelles; BLT-1 and ezetimibe evidence_span: {"source_cache": "artifacts/zeaxanthin-research/42123990.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4", "start_char": 0, "end_char": 1803, "text_sha256": "c0b42011e7f16c3fe60d599d489d01e4b3098db9ad04856d26aca10008e995f4"} [zeaxanthin-p42123990] Mechanisms of Cell Uptake and Transport of Xanthophylls in the Caco-2 Cell Model. (2026). https://pubmed.ncbi.nlm.nih.gov/42123990/ DOI: 10.3390/nu18091389
    Complete structured claim and evidence

  6. Human NPC1L1 overexpression increased alpha-tocopherol uptake, which was inhibited by ezetimibe.

    Human Niemann-Pick C1-like protein 1 / NPC1L1 → Intestinal alpha-tocopherol uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Human NPC1L1 overexpression uptake assay
    exposure
    NPC1L1 expression with alpha-tocopherol and ezetimibe; dose/time not reported in abstract.
    limitations
    Cell experiment does not establish a clinical vitamin E deficiency from ezetimibe.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Human protein in cultured cells
    plain_language
    The cholesterol transporter NPC1L1 can also take up vitamin E.
    primary_references
    [narushima2008] Niemann-pick C1-like 1 mediates alpha-tocopherol transport. (2008). https://pubmed.ncbi.nlm.nih.gov/18403720/ DOI: 10.1124/mol.107.043034
    tissue_or_cell_type
    Cellular uptake model

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 207–218

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human NPC1L1 overexpression uptake assay · source_derived_draft · unverified_draft

    ### ve-transport-npc1l1-uptake Human NPC1L1 overexpression increased alpha-tocopherol uptake, which was inhibited by ezetimibe. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cholesterol transporter NPC1L1 can also take up vitamin E. organism: Human protein in cultured cells tissue_or_cell_type: Cellular uptake model experimental_model: Human NPC1L1 overexpression uptake assay limitations: Cell experiment does not establish a clinical vitamin E deficiency from ezetimibe. exposure: NPC1L1 expression with alpha-tocopherol and ezetimibe; dose/time not reported in abstract. cross_nutrient: false [narushima2008] Niemann-pick C1-like 1 mediates alpha-tocopherol transport. (2008). https://pubmed.ncbi.nlm.nih.gov/18403720/ DOI: 10.1124/mol.107.043034
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Cholesterol inhibited human NPC1L1-mediated alpha-tocopherol uptake in mutual substrate-interaction experiments.

    Cholesterol → Intestinal alpha-tocopherol uptake source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    true
    experimental_model
    Human NPC1L1 overexpression co-substrate assay
    exposure
    Cholesterol and alpha-tocopherol co-incubation; concentrations unavailable in abstract.
    limitations
    No dietary cholesterol threshold or universal supplement-spacing rule follows.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Human protein in cultured cells
    plain_language
    Cholesterol changed vitamin E uptake through their shared transporter.
    primary_references
    [narushima2008] Niemann-pick C1-like 1 mediates alpha-tocopherol transport. (2008). https://pubmed.ncbi.nlm.nih.gov/18403720/ DOI: 10.1124/mol.107.043034
    tissue_or_cell_type
    Cellular uptake model

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 220–231

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human NPC1L1 overexpression co-substrate assay · source_derived_draft · unverified_draft

    ### ve-transport-npc1l1-cholesterol-competition Cholesterol inhibited human NPC1L1-mediated alpha-tocopherol uptake in mutual substrate-interaction experiments. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cholesterol changed vitamin E uptake through their shared transporter. organism: Human protein in cultured cells tissue_or_cell_type: Cellular uptake model experimental_model: Human NPC1L1 overexpression co-substrate assay limitations: No dietary cholesterol threshold or universal supplement-spacing rule follows. exposure: Cholesterol and alpha-tocopherol co-incubation; concentrations unavailable in abstract. cross_nutrient: true [narushima2008] Niemann-pick C1-like 1 mediates alpha-tocopherol transport. (2008). https://pubmed.ncbi.nlm.nih.gov/18403720/ DOI: 10.1124/mol.107.043034
    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.

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