Component

Lutein uptake by engineered human HEK293 cells

Lutein uptake by engineered human HEK293 cells. Species, exposure and limitations are retained in each linked claim.

4 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 acts on it

  1. Adding HDL reduced cellular lutein in the HEK293 assay despite preferential retention relative to beta-carotene.

    High-density lipoprotein particles; preparation specified → Lutein uptake by engineered human HEK293 cells source_derived_draftungraded
    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
    More carrier did not simply mean more uptake in this assay.
    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 697–708

    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-hdl-cell-context Adding HDL reduced cellular lutein in the HEK293 assay despite preferential retention relative to beta-carotene. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: More carrier did not simply mean more uptake in this assay. 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

  2. Hepatic lipase increased carotenoid uptake in HDL-treated SR-BI-expressing cells, favoring lutein/zeaxanthin over beta-carotene.

    Human hepatic lipase / LIPC → Lutein uptake by engineered human HEK293 cells source_derived_draftungraded
    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
    A lipoprotein-processing partner changed pigment delivery.
    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 684–695

    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-lipc-cell-uptake Hepatic lipase increased carotenoid uptake in HDL-treated SR-BI-expressing cells, favoring lutein/zeaxanthin over beta-carotene. Condition category: normal nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: A lipoprotein-processing partner changed pigment delivery. 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

  3. SR-BI expression increased lutein and zeaxanthin uptake preferentially over beta-carotene.

    Scavenger receptor class B type 1 / SCARB1 → Lutein uptake by engineered human HEK293 cells source_derived_draftungraded
    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

  4. SR-BI C384Y abolished the preferential lutein/zeaxanthin uptake effect observed with wild-type receptor.

    Human SR-BI C384Y tunnel-blocking variant → Lutein uptake by engineered human HEK293 cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    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
    An altered transport tunnel disrupted the effect.
    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
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Lutein: metabolism, signaling and nutrient connections (2026-09-17) · lines 710–721

    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-mutant SR-BI C384Y abolished the preferential lutein/zeaxanthin uptake effect observed with wild-type receptor. Condition category: machinery_impairment nutrient_topic: Lutein research collection; topical membership is not evidence of a direct dietary effect. plain_language: An altered transport tunnel disrupted the effect. 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

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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