Component

Scavenger receptor class B type 1 / SCARB1

Independent protein identity; organism and experimental state are specified on individual claims.

14 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.

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 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 evidence
  2. SR-BI inhibitor BLT1 and an SR-BI antibody reduced all-E and 13Z astaxanthin uptake in human Caco-2 cells; neither reduced 9Z uptake in that experiment.

    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human Caco-2 inhibitor and antibody experiments.
    limitations
    Partial inhibition does not establish an exclusive route or clinical competition among carotenoids.
    nutrient_topic
    Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
    plain_language
    Different shapes of the same carotenoid used uptake machinery differently.
    primary_references
    Anti-Inflammatory Effects of Different Astaxanthin Isomers and the Roles of Lipid Transporters in the Cellular Transport of Astaxanthin Isomers in Caco-2 Cell Monolayers. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31117505/ · DOI 10.1021/acs.jafc.9b02102

    Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 54–60

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human Caco-2 inhibitor and antibody experiments. · source_derived_draft · unverified_draft

    ## astaxanthin-isomer-srbi Different shapes of the same carotenoid used uptake machinery differently. SR-BI inhibitor BLT1 and an SR-BI antibody reduced all-E and 13Z astaxanthin uptake in human Caco-2 cells; neither reduced 9Z uptake in that experiment. Model: Human Caco-2 inhibitor and antibody experiments. Limitations: Partial inhibition does not establish an exclusive route or clinical competition among carotenoids. Evidence access: Primary abstract Anti-Inflammatory Effects of Different Astaxanthin Isomers and the Roles of Lipid Transporters in the Cellular Transport of Astaxanthin Isomers in Caco-2 Cell Monolayers. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31117505/ · DOI 10.1021/acs.jafc.9b02102
    Complete structured claim and evidence
  3. SR-BI antibody or BLT1 inhibited all-E and 5Z lycopene uptake by up to 60% in Caco-2 monolayers.

    Scavenger receptor class B type 1 / SCARB1 → Lycopene 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
    One intestinal lipid transporter helps lycopene enter these cells.
    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 104–115

    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-srbi-uptake SR-BI antibody or BLT1 inhibited all-E and 5Z lycopene uptake by up to 60% in Caco-2 monolayers. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: One intestinal lipid transporter helps lycopene enter these cells. 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
  4. SR-BI expression increased lutein and zeaxanthin uptake preferentially over beta-carotene.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/lutein-research/36863431.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0", "start_char": 0, "end_char": 1551, "text_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0"}
    experimental_model
    SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays
    exposure
    Wild-type or C384Y SR-BI; HDL and hepatic lipase additions
    limitations
    Engineered-cell mechanisms, not a clinical HDL-raising recommendation; no selective direct binding to lutein demonstrated.
    nutrient_topic
    Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
    organism
    Human HEK293 cell system
    plain_language
    The receptor changed which pigments entered these cells.
    primary_references
    [lutein-p36863431] Mechanism for the selective uptake of macular carotenoids mediated by the HDL cholesterol receptor SR-BI. (2023). https://pubmed.ncbi.nlm.nih.gov/36863431/ DOI: 10.1016/j.exer.2023.109429
    tissue_or_cell_type
    Engineered cells without endogenous SR-BI

    Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 671–682

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays · source_derived_draft · unverified_draft

    ### lutein-srbi-cell-uptake SR-BI expression increased lutein and zeaxanthin uptake preferentially over beta-carotene. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor changed which pigments entered these cells. organism: Human HEK293 cell system tissue_or_cell_type: Engineered cells without endogenous SR-BI experimental_model: SR-BI expression, tunnel mutation, binding and lipoprotein-partner assays limitations: Engineered-cell mechanisms, not a clinical HDL-raising recommendation; no selective direct binding to lutein demonstrated. exposure: Wild-type or C384Y SR-BI; HDL and hepatic lipase additions evidence_span: {"source_cache": "artifacts/lutein-research/36863431.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0", "start_char": 0, "end_char": 1551, "text_sha256": "530dd42d442890be2e5cd11c18bf95c0bd850d8f67ad6682d12360dfc7f8aec0"} [lutein-p36863431] Mechanism for the selective uptake of macular carotenoids mediated by the HDL cholesterol receptor SR-BI. (2023). https://pubmed.ncbi.nlm.nih.gov/36863431/ DOI: 10.1016/j.exer.2023.109429
    Complete structured claim and evidence
  5. SR-BI antibody and BLT1 reduced lutein transport by approximately 30% and 57%, respectively.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/lutein-research/15554873.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0", "start_char": 0, "end_char": 2014, "text_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0"}
    experimental_model
    Mixed-micelle transport across Caco-2 TC-7 monolayers
    exposure
    Micellar lutein 1.5–15 micromolar; antibodies and BLT1
    limitations
    Partial inhibition supports a contribution, not an exclusive route; cell experiments do not set clinical supplement spacing.
    nutrient_topic
    Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
    organism
    Human intestinal cell model
    plain_language
    Part of intestinal uptake used the SR-BI pathway.
    primary_references
    [lutein-p15554873] Lutein transport by Caco-2 TC-7 cells occurs partly by a facilitated process involving the scavenger receptor class B type I (SR-BI). (2005). https://pubmed.ncbi.nlm.nih.gov/15554873/ DOI: 10.1042/bj20040554
    tissue_or_cell_type
    Apical intestinal epithelial transport

    Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 476–487

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mixed-micelle transport across Caco-2 TC-7 monolayers · source_derived_draft · unverified_draft

    ### lutein-srbi-intestine SR-BI antibody and BLT1 reduced lutein transport by approximately 30% and 57%, respectively. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Part of intestinal uptake used the SR-BI pathway. organism: Human intestinal cell model tissue_or_cell_type: Apical intestinal epithelial transport experimental_model: Mixed-micelle transport across Caco-2 TC-7 monolayers limitations: Partial inhibition supports a contribution, not an exclusive route; cell experiments do not set clinical supplement spacing. exposure: Micellar lutein 1.5–15 micromolar; antibodies and BLT1 evidence_span: {"source_cache": "artifacts/lutein-research/15554873.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0", "start_char": 0, "end_char": 2014, "text_sha256": "3dfbef37e3c73db4732f66083063e548a1654cb759ff46392c981c50f338d8a0"} [lutein-p15554873] Lutein transport by Caco-2 TC-7 cells occurs partly by a facilitated process involving the scavenger receptor class B type I (SR-BI). (2005). https://pubmed.ncbi.nlm.nih.gov/15554873/ DOI: 10.1042/bj20040554
    Complete structured claim and evidence
  6. BLT-1-sensitive uptake supported SR-BI involvement after dipalmitate exposure.

    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
    Esterification did not remove this transporter contribution.
    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 730–741

    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-srbi-ester BLT-1-sensitive uptake supported SR-BI involvement after dipalmitate exposure. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Esterification did not remove this transporter contribution. 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
  7. BLT-1-sensitive uptake supported SR-BI involvement in free-zeaxanthin uptake.

    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 shared carotenoid transporter contributed here too.
    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 652–663

    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-srbi-intestinal BLT-1-sensitive uptake supported SR-BI 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 shared carotenoid transporter contributed here too. 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
  8. SR-BI supported zeaxanthin uptake in the transfected-cell experiment.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/zeaxanthin-research/28947101.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2", "start_char": 0, "end_char": 1330, "text_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2"}
    experimental_model
    SPR and transporter overexpression
    exposure
    SR-BI, SCARB2/LIMP-II and CD36; HDL or LDL carriers
    limitations
    The study used SCARB2/LIMP-II (methods reagent AF1966), not the similarly named SCARB1 splice variant SR-BII. Reagent identity: https://www.rndsystems.com/products/human-limpii-sr-b2-antibody_af1966 . Transporter overexpression is not an oral absorption trial.
    nutrient_topic
    Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. · Dietary (3R,3-prime-R)-zeaxanthin
    organism
    Human proteins in HEK-293T cells and donor eye tissue
    plain_language
    A shared lipid receptor can deliver zeaxanthin.
    primary_references
    [zeaxanthin-p28947101] All three human scavenger receptor class B proteins can bind and transport all three macular xanthophyll carotenoids. (2017). https://pubmed.ncbi.nlm.nih.gov/28947101/ DOI: 10.1016/j.abb.2017.09.013
    tissue_or_cell_type
    Recombinant receptors and HEK-293T cells

    Zeaxanthin: metabolism, signaling and nutrient connections (2026-09-17) · lines 587–598

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

    ### zeaxanthin-srbi-uptake SR-BI supported zeaxanthin uptake in the transfected-cell experiment. Condition category: normal nutrient_topic: Zeaxanthin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A shared lipid receptor can deliver zeaxanthin. organism: Human proteins in HEK-293T cells and donor eye tissue tissue_or_cell_type: Recombinant receptors and HEK-293T cells experimental_model: SPR and transporter overexpression limitations: The study used SCARB2/LIMP-II (methods reagent AF1966), not the similarly named SCARB1 splice variant SR-BII. Reagent identity: https://www.rndsystems.com/products/human-limpii-sr-b2-antibody_af1966 . Transporter overexpression is not an oral absorption trial. exposure: SR-BI, SCARB2/LIMP-II and CD36; HDL or LDL carriers evidence_span: {"source_cache": "artifacts/zeaxanthin-research/28947101.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2", "start_char": 0, "end_char": 1330, "text_sha256": "8899547af674d9bc7acc413d58c440726a1469ca705aa82bc5dafd5c89aadcc2"} [zeaxanthin-p28947101] All three human scavenger receptor class B proteins can bind and transport all three macular xanthophyll carotenoids. (2017). https://pubmed.ncbi.nlm.nih.gov/28947101/ DOI: 10.1016/j.abb.2017.09.013
    Complete structured claim and evidence
  9. SCARB1 supported intestinal beta-carotene absorption in mice on a high-fat diet.

    Experimental context and source evidence
    evidence_location
    Abstract
    experimental_model
    Scarb1-knockout mice, intestinal brush-border vesicles and transfected COS-7 cells.
    exposure
    Wild-type versus Scarb1-knockout mice; high-fat feeding.
    limitations
    Dependence was diet/model specific; this does not establish exclusive human transport.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    outcome
    SCARB1 supported intestinal beta-carotene absorption in mice on a high-fat diet.
    plain_language
    The intestinal receptor helps beta-carotene enter the body.
    primary_references
    [va-vanbennekum-2005] Class B scavenger receptor-mediated intestinal absorption of dietary beta-carotene and cholesterol (2005). https://pubmed.ncbi.nlm.nih.gov/15766282/ DOI: 10.1021/bi0484320
    tissue_or_cell_type
    Small-intestinal brush border
    transport_direction
    intestinal lumen to enterocyte

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 116–129

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Scarb1-knockout mice, intestinal brush-border vesicles and transfected COS-7 cells. · source_derived_draft · unverified_draft

    ### va-scarb1-beta-carotene-uptake SCARB1 supported intestinal beta-carotene absorption in mice on a high-fat diet. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The intestinal receptor helps beta-carotene enter the body. organism: Mus musculus tissue_or_cell_type: Small-intestinal brush border experimental_model: Scarb1-knockout mice, intestinal brush-border vesicles and transfected COS-7 cells. limitations: Dependence was diet/model specific; this does not establish exclusive human transport. exposure: Wild-type versus Scarb1-knockout mice; high-fat feeding. outcome: SCARB1 supported intestinal beta-carotene absorption in mice on a high-fat diet. evidence_location: Abstract transport_direction: intestinal lumen to enterocyte [va-vanbennekum-2005] Class B scavenger receptor-mediated intestinal absorption of dietary beta-carotene and cholesterol (2005). https://pubmed.ncbi.nlm.nih.gov/15766282/ DOI: 10.1021/bi0484320
    Complete structured claim and evidence
  10. SR-BI antibody or BLT1 reduced RRR-alpha-tocopherol efflux from loaded Caco-2 TC7 cells into apical vitamin-free mixed micelles.

    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Preloaded Caco-2 TC7 monolayers
    exposure
    Tocopherol-preloaded cells; apical acceptor micelles; time-course Figure 4.
    limitations
    Apical return is distinct from basolateral secretion; acceptor availability affects the result.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    The same receptor also helped vitamin E leave toward the gut-facing side.
    primary_references
    [reboul2006] Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. (2006). https://pubmed.ncbi.nlm.nih.gov/16380385/ DOI: 10.1074/jbc.m509042200
    tissue_or_cell_type
    Intestinal epithelial cell model

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 194–205

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Preloaded Caco-2 TC7 monolayers · source_derived_draft · unverified_draft

    ### ve-transport-scarb1-apical-efflux SR-BI antibody or BLT1 reduced RRR-alpha-tocopherol efflux from loaded Caco-2 TC7 cells into apical vitamin-free mixed micelles. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: The same receptor also helped vitamin E leave toward the gut-facing side. organism: Homo sapiens tissue_or_cell_type: Intestinal epithelial cell model experimental_model: Preloaded Caco-2 TC7 monolayers limitations: Apical return is distinct from basolateral secretion; acceptor availability affects the result. exposure: Tocopherol-preloaded cells; apical acceptor micelles; time-course Figure 4. cross_nutrient: false [reboul2006] Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. (2006). https://pubmed.ncbi.nlm.nih.gov/16380385/ DOI: 10.1074/jbc.m509042200
    Complete structured claim and evidence
  11. Blocking SR-BI with an extracellular antibody or BLT1 reduced RRR-alpha-tocopherol uptake by human Caco-2 TC7 cells.

    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Differentiated Caco-2 TC7 monolayers
    exposure
    60-min pretreatment: antibody 3.75 µg/mL or BLT1 10 µM; 40 µM micellar RRR-alpha-tocopherol for 60 min.
    limitations
    Inhibitor/antibody evidence; contribution under these conditions is not the sole absorption route.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    SR-BI helped these intestinal cells take up vitamin E.
    primary_references
    [reboul2006] Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. (2006). https://pubmed.ncbi.nlm.nih.gov/16380385/ DOI: 10.1074/jbc.m509042200
    tissue_or_cell_type
    Intestinal epithelial cell model

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 181–192

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Differentiated Caco-2 TC7 monolayers · source_derived_draft · unverified_draft

    ### ve-transport-scarb1-uptake Blocking SR-BI with an extracellular antibody or BLT1 reduced RRR-alpha-tocopherol uptake by human Caco-2 TC7 cells. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: SR-BI helped these intestinal cells take up vitamin E. organism: Homo sapiens tissue_or_cell_type: Intestinal epithelial cell model experimental_model: Differentiated Caco-2 TC7 monolayers limitations: Inhibitor/antibody evidence; contribution under these conditions is not the sole absorption route. exposure: 60-min pretreatment: antibody 3.75 µg/mL or BLT1 10 µM; 40 µM micellar RRR-alpha-tocopherol for 60 min. cross_nutrient: false [reboul2006] Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. (2006). https://pubmed.ncbi.nlm.nih.gov/16380385/ DOI: 10.1074/jbc.m509042200
    Complete structured claim and evidence

What acts on it

  1. ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression.

    Experimental context and source evidence
    evidence_location
    Abstract
    experimental_model
    Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets.
    exposure
    Isx genotypes and promoter-binding experiments.
    limitations
    Tissue-specific regulation, not suppression in every organ.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus and promoter-binding preparations
    outcome
    ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression.
    plain_language
    The feedback factor lowers the uptake receptor.
    primary_references
    [va-widjajaadhi-2015] A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4424956/ DOI: 10.1093/hmg/ddv072
    tissue_or_cell_type
    Jejunum and DNA-binding assays

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 274–286

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets. · source_derived_draft · unverified_draft

    ### va-isx-scarb1-repression ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The feedback factor lowers the uptake receptor. organism: Mus musculus and promoter-binding preparations tissue_or_cell_type: Jejunum and DNA-binding assays experimental_model: Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets. limitations: Tissue-specific regulation, not suppression in every organ. exposure: Isx genotypes and promoter-binding experiments. outcome: ISX bound upstream SCARB1 regulatory motifs and repressed intestinal SCARB1 expression. evidence_location: Abstract [va-widjajaadhi-2015] A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4424956/ DOI: 10.1093/hmg/ddv072
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Co-incubated lutein reduced alpha-tocopherol uptake in Caco-2 TC-7 cells.

    Lutein → Intestinal alpha-tocopherol uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/lutein-research/16380385.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "410a6cc6c3325e6d2f459b06ddaf9c7b7806f9b82a918f1df02b1626f5f84074", "start_char": 0, "end_char": 1960, "text_sha256": "410a6cc6c3325e6d2f459b06ddaf9c7b7806f9b82a918f1df02b1626f5f84074"}
    experimental_model
    Mixed-micelle uptake in Caco-2 TC-7 cells
    exposure
    Alpha-tocopherol with co-incubated lutein
    limitations
    In vitro competition is not demonstrated vitamin E deficiency or a clinical dose-spacing rule.
    nutrient_topic
    Lutein research collection; topical membership is not evidence of a direct dietary effect. · Lutein
    organism
    Human cell model
    plain_language
    Lutein and vitamin E can interact during intestinal uptake.
    primary_references
    [lutein-p16380385] Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. (2006). https://pubmed.ncbi.nlm.nih.gov/16380385/ DOI: 10.1074/jbc.m509042200
    tissue_or_cell_type
    Intestinal epithelium

    Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 541–552

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mixed-micelle uptake in Caco-2 TC-7 cells · source_derived_draft · unverified_draft

    ### lutein-vitamin-e-competition Co-incubated lutein reduced alpha-tocopherol uptake in Caco-2 TC-7 cells. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: Lutein and vitamin E can interact during intestinal uptake. organism: Human cell model tissue_or_cell_type: Intestinal epithelium experimental_model: Mixed-micelle uptake in Caco-2 TC-7 cells limitations: In vitro competition is not demonstrated vitamin E deficiency or a clinical dose-spacing rule. exposure: Alpha-tocopherol with co-incubated lutein evidence_span: {"source_cache": "artifacts/lutein-research/16380385.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "410a6cc6c3325e6d2f459b06ddaf9c7b7806f9b82a918f1df02b1626f5f84074", "start_char": 0, "end_char": 1960, "text_sha256": "410a6cc6c3325e6d2f459b06ddaf9c7b7806f9b82a918f1df02b1626f5f84074"} [lutein-p16380385] Scavenger receptor class B type I (SR-BI) is involved in vitamin E transport across the enterocyte. (2006). https://pubmed.ncbi.nlm.nih.gov/16380385/ DOI: 10.1074/jbc.m509042200
    Complete structured claim and evidence
  2. Isx-deficient mice had higher hepatic alpha-tocopherol; the Isx/Bco2 double mutant showed about twice wild-type levels.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Retinoid/ISX control of a shared intestinal transporter affects vitamin E status.
    evidence_location
    Figure 7
    experimental_model
    Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets.
    exposure
    Females; ten weeks of AIN93G with 75 IU vitamin E/kg, with or without 50 mg zeaxanthin/kg.
    limitations
    Accumulation is not a clinical benefit; compound mutants had a larger effect than Isx single mutants.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    outcome
    Isx-deficient mice had higher hepatic alpha-tocopherol; the Isx/Bco2 double mutant showed about twice wild-type levels.
    plain_language
    Disrupting vitamin A feedback also changed vitamin E accumulation.
    primary_references
    [va-widjajaadhi-2015] A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4424956/ DOI: 10.1093/hmg/ddv072
    tissue_or_cell_type
    Jejunum and liver
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 302–315

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets. · source_derived_draft · unverified_draft

    ### va-isx-loss-tocopherol Isx-deficient mice had higher hepatic alpha-tocopherol; the Isx/Bco2 double mutant showed about twice wild-type levels. Condition category: machinery_impairment nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Disrupting vitamin A feedback also changed vitamin E accumulation. organism: Mus musculus tissue_or_cell_type: Jejunum and liver experimental_model: Isx, Bco1, Bco2 and Scarb1 mouse mutants; promoter binding and controlled diets. limitations: Accumulation is not a clinical benefit; compound mutants had a larger effect than Isx single mutants. exposure: Females; ten weeks of AIN93G with 75 IU vitamin E/kg, with or without 50 mg zeaxanthin/kg. outcome: Isx-deficient mice had higher hepatic alpha-tocopherol; the Isx/Bco2 double mutant showed about twice wild-type levels. evidence_location: Figure 7 cross_nutrient: Retinoid/ISX control of a shared intestinal transporter affects vitamin E status. [va-widjajaadhi-2015] A genetic dissection of intestinal fat-soluble vitamin and carotenoid absorption (2015). https://pmc.ncbi.nlm.nih.gov/articles/PMC4424956/ DOI: 10.1093/hmg/ddv072
    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