Component

Mouse fatty-acid translocase / Cd36

Mouse fatty-acid translocase / Cd36. Species, exposure and limitations are retained in each linked claim.

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. Cd36 knockout reduced astaxanthin uptake by 88.22% in the reported mouse experiment.

    Mouse fatty-acid translocase / Cd36 → Mouse intestinal astaxanthin uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse Cd36 knockout compared with controls.
    limitations
    A genetic transport defect is not ordinary low dietary intake and does not establish a human deficiency syndrome.
    nutrient_topic
    Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
    plain_language
    Removing a lipid transporter markedly reduced uptake.
    primary_references
    Cluster-determinant 36 (CD36) mediates intestinal absorption of dietary astaxanthin and affects its secretion. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37803639/ · DOI 10.1016/j.foodres.2023.113328
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 62–68

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse Cd36 knockout compared with controls. · source_derived_draft · unverified_draft

    ## astaxanthin-cd36-loss Removing a lipid transporter markedly reduced uptake. Cd36 knockout reduced astaxanthin uptake by 88.22% in the reported mouse experiment. Model: Mouse Cd36 knockout compared with controls. Limitations: A genetic transport defect is not ordinary low dietary intake and does not establish a human deficiency syndrome. Evidence access: Primary abstract Cluster-determinant 36 (CD36) mediates intestinal absorption of dietary astaxanthin and affects its secretion. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37803639/ · DOI 10.1016/j.foodres.2023.113328
    Complete structured claim and evidence

  2. CD36 inhibition or partial knockdown reduced lycopene uptake in 3T3-L1 adipocytes.

    Mouse fatty-acid translocase / Cd36 → Lycopene uptake by adipocytes source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/lycopene-research/21462325.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "de4990e5a9c520e6e528e181a4e81a469a4ebac313151bfa7828ad935b04a823", "start_char": 0, "end_char": 1048, "text_sha256": "de4990e5a9c520e6e528e181a4e81a469a4ebac313151bfa7828ad935b04a823"}
    experimental_model
    Transport inhibition, siRNA, overexpression and knockout explants
    exposure
    CD36 inhibitor, partial knockdown and Cd36-null tissue
    limitations
    Do not relabel adipose results as intestinal uptake or a clinical human transport-deficiency syndrome.
    nutrient_topic
    Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene
    organism
    Mouse 3T3-L1 adipocytes and mouse adipose explants; COS-1 expression experiment
    plain_language
    Fat cells have uptake machinery for lycopene too.
    primary_references
    [lycopene-p21462325] CD36 is involved in lycopene and lutein uptake by adipocytes and adipose tissue cultures. (2011). https://pubmed.ncbi.nlm.nih.gov/21462325/ DOI: 10.1002/mnfr.201000399
    tissue_or_cell_type
    Adipocytes and adipose tissue

    Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 260–271

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transport inhibition, siRNA, overexpression and knockout explants · source_derived_draft · unverified_draft

    ### lycopene-cd36-adipocyte CD36 inhibition or partial knockdown reduced lycopene uptake in 3T3-L1 adipocytes. Condition category: normal nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: Fat cells have uptake machinery for lycopene too. organism: Mouse 3T3-L1 adipocytes and mouse adipose explants; COS-1 expression experiment tissue_or_cell_type: Adipocytes and adipose tissue experimental_model: Transport inhibition, siRNA, overexpression and knockout explants limitations: Do not relabel adipose results as intestinal uptake or a clinical human transport-deficiency syndrome. exposure: CD36 inhibitor, partial knockdown and Cd36-null tissue evidence_span: {"source_cache": "artifacts/lycopene-research/21462325.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "de4990e5a9c520e6e528e181a4e81a469a4ebac313151bfa7828ad935b04a823", "start_char": 0, "end_char": 1048, "text_sha256": "de4990e5a9c520e6e528e181a4e81a469a4ebac313151bfa7828ad935b04a823"} [lycopene-p21462325] CD36 is involved in lycopene and lutein uptake by adipocytes and adipose tissue cultures. (2011). https://pubmed.ncbi.nlm.nih.gov/21462325/ DOI: 10.1002/mnfr.201000399
    Complete structured claim and evidence

  3. CD36 signaling activated PPARgamma in the reported pathway.

    Mouse fatty-acid translocase / Cd36 → Mouse peroxisome proliferator-activated receptor gamma / Pparg source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/41407214.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08", "start_char": 0, "end_char": 1949, "text_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08"}
    experimental_model
    Mouse transfer/ablation experiments, cell assays and virtual screening
    exposure
    Nasunin intervention reported; exact regimen and binding validation unavailable in the indexed abstract
    limitations
    New preclinical study: virtual screening nomination is not a measured binding affinity. The pathway findings and treatment outcomes are retained separately. No human efficacy or dose inference.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Type 2 diabetic and control mice; mouse primary-cell models
    plain_language
    The receptor response reaches a transcriptional regulator.
    primary_references
    [nasunin-p41407214] Neutrophil-derived thrombospondin-1 (THBS1) drives type 2 diabetes-induced osteoporosis via CD36-PPARγ-POU2F2 signaling. (2026). https://pubmed.ncbi.nlm.nih.gov/41407214/ DOI: 10.1016/j.bbadis.2025.168139
    tissue_or_cell_type
    Neutrophil-to-macrophage signaling and osteoclastogenesis

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 432–443

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse transfer/ablation experiments, cell assays and virtual screening · source_derived_draft · unverified_draft

    ### nasunin-cd36-pparg CD36 signaling activated PPARgamma in the reported pathway. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor response reaches a transcriptional regulator. organism: Type 2 diabetic and control mice; mouse primary-cell models tissue_or_cell_type: Neutrophil-to-macrophage signaling and osteoclastogenesis experimental_model: Mouse transfer/ablation experiments, cell assays and virtual screening limitations: New preclinical study: virtual screening nomination is not a measured binding affinity. The pathway findings and treatment outcomes are retained separately. No human efficacy or dose inference. exposure: Nasunin intervention reported; exact regimen and binding validation unavailable in the indexed abstract evidence_span: {"source_cache": "artifacts/nasunin-research/41407214.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08", "start_char": 0, "end_char": 1949, "text_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08"} [nasunin-p41407214] Neutrophil-derived thrombospondin-1 (THBS1) drives type 2 diabetes-induced osteoporosis via CD36-PPARγ-POU2F2 signaling. (2026). https://pubmed.ncbi.nlm.nih.gov/41407214/ DOI: 10.1016/j.bbadis.2025.168139
    Complete structured claim and evidence

What acts on it

  1. Astaxanthin increased Cd36 and Abca1 transcripts in elicited mouse peritoneal macrophages, despite different effects on the adipocyte program.

    Astaxanthin → Mouse fatty-acid translocase / Cd36 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse macrophage expression assays.
    limitations
    Expression does not measure net cholesterol clearance or prove clinical antiatherosclerotic efficacy.
    nutrient_topic
    Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
    plain_language
    The same treatment produced a different gene response in immune cells.
    primary_references
    Astaxanthin functions differently as a selective peroxisome proliferator-activated receptor γ modulator in adipocytes and macrophages. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22732454/ · DOI 10.1016/j.bcp.2012.05.021

    Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 286–292

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse macrophage expression assays. · source_derived_draft · unverified_draft

    ## astaxanthin-macrophage-cd36 The same treatment produced a different gene response in immune cells. Astaxanthin increased Cd36 and Abca1 transcripts in elicited mouse peritoneal macrophages, despite different effects on the adipocyte program. Model: Mouse macrophage expression assays. Limitations: Expression does not measure net cholesterol clearance or prove clinical antiatherosclerotic efficacy. Evidence access: Primary abstract Astaxanthin functions differently as a selective peroxisome proliferator-activated receptor γ modulator in adipocytes and macrophages. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22732454/ · DOI 10.1016/j.bcp.2012.05.021
    Complete structured claim and evidence

  2. Neutrophil-derived THBS1 engaged macrophage CD36 in the reported pathway.

    Mouse thrombospondin-1 / Thbs1 → Mouse fatty-acid translocase / Cd36 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/41407214.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08", "start_char": 0, "end_char": 1949, "text_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08"}
    experimental_model
    Mouse transfer/ablation experiments, cell assays and virtual screening
    exposure
    Nasunin intervention reported; exact regimen and binding validation unavailable in the indexed abstract
    limitations
    New preclinical study: virtual screening nomination is not a measured binding affinity. The pathway findings and treatment outcomes are retained separately. No human efficacy or dose inference.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Type 2 diabetic and control mice; mouse primary-cell models
    plain_language
    One cell type can influence another through a secreted protein.
    primary_references
    [nasunin-p41407214] Neutrophil-derived thrombospondin-1 (THBS1) drives type 2 diabetes-induced osteoporosis via CD36-PPARγ-POU2F2 signaling. (2026). https://pubmed.ncbi.nlm.nih.gov/41407214/ DOI: 10.1016/j.bbadis.2025.168139
    tissue_or_cell_type
    Neutrophil-to-macrophage signaling and osteoclastogenesis

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 419–430

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse transfer/ablation experiments, cell assays and virtual screening · source_derived_draft · unverified_draft

    ### nasunin-thbs1-cd36 Neutrophil-derived THBS1 engaged macrophage CD36 in the reported pathway. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: One cell type can influence another through a secreted protein. organism: Type 2 diabetic and control mice; mouse primary-cell models tissue_or_cell_type: Neutrophil-to-macrophage signaling and osteoclastogenesis experimental_model: Mouse transfer/ablation experiments, cell assays and virtual screening limitations: New preclinical study: virtual screening nomination is not a measured binding affinity. The pathway findings and treatment outcomes are retained separately. No human efficacy or dose inference. exposure: Nasunin intervention reported; exact regimen and binding validation unavailable in the indexed abstract evidence_span: {"source_cache": "artifacts/nasunin-research/41407214.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08", "start_char": 0, "end_char": 1949, "text_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08"} [nasunin-p41407214] Neutrophil-derived thrombospondin-1 (THBS1) drives type 2 diabetes-induced osteoporosis via CD36-PPARγ-POU2F2 signaling. (2026). https://pubmed.ncbi.nlm.nih.gov/41407214/ DOI: 10.1016/j.bbadis.2025.168139
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Chromium picolinate increased plasma-membrane CD36 localization in 3T3-L1 adipocytes; combining it with insulin did not produce additive CD36 translocation.

    Chromium(III) picolinate / CrPic → Mouse CD36 movement to the cell surface source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/chromium-research/20721637.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "550ce1e2898494fb6f385c11a446c6516812bffacefc4c78161fbee16adfc39f", "start_char": 0, "end_char": 1671, "text_sha256": "550ce1e2898494fb6f385c11a446c6516812bffacefc4c78161fbee16adfc39f"}
    experimental_model
    Transporter localization and substrate-uptake assays
    exposure
    Insulin, chromium picolinate and wortmannin comparisons
    limitations
    Membrane localization is not equivalent to transporter activity. CD36 trafficking responses to insulin and chromium were not additive; results do not show a general increase in beneficial fatty-acid disposal.
    nutrient_topic
    Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
    organism
    Mouse 3T3-L1 adipocytes
    plain_language
    Chromium affected a fatty-acid transporter as well as GLUT4, with a different response pattern.
    primary_references
    [chromium-p20721637] Insulin and chromium picolinate induce translocation of CD36 to the plasma membrane through different signaling pathways in 3T3-L1 adipocytes, and with a differential functionality of the CD36. (2011). https://pubmed.ncbi.nlm.nih.gov/20721637/ DOI: 10.1007/s12011-010-8809-8
    tissue_or_cell_type
    Plasma membrane

    Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 458–469

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transporter localization and substrate-uptake assays · source_derived_draft · unverified_draft

    ### chromium-cd36-trafficking Chromium picolinate increased plasma-membrane CD36 localization in 3T3-L1 adipocytes; combining it with insulin did not produce additive CD36 translocation. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Chromium affected a fatty-acid transporter as well as GLUT4, with a different response pattern. organism: Mouse 3T3-L1 adipocytes tissue_or_cell_type: Plasma membrane experimental_model: Transporter localization and substrate-uptake assays limitations: Membrane localization is not equivalent to transporter activity. CD36 trafficking responses to insulin and chromium were not additive; results do not show a general increase in beneficial fatty-acid disposal. exposure: Insulin, chromium picolinate and wortmannin comparisons evidence_span: {"source_cache": "artifacts/chromium-research/20721637.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "550ce1e2898494fb6f385c11a446c6516812bffacefc4c78161fbee16adfc39f", "start_char": 0, "end_char": 1671, "text_sha256": "550ce1e2898494fb6f385c11a446c6516812bffacefc4c78161fbee16adfc39f"} [chromium-p20721637] Insulin and chromium picolinate induce translocation of CD36 to the plasma membrane through different signaling pathways in 3T3-L1 adipocytes, and with a differential functionality of the CD36. (2011). https://pubmed.ncbi.nlm.nih.gov/20721637/ DOI: 10.1007/s12011-010-8809-8
    Complete structured claim and evidence

  2. Four weeks of astaxanthin feeding reduced exercise-associated oxidative modification of CPT I and increased FAT/CD36-CPT I colocalization in mice.

    Astaxanthin → Exercise-associated oxidative modification of mouse CPT I source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    ICR mice and treadmill exercise; protein modification and localization measurements.
    limitations
    CPT I isoform was not resolved in the accessed abstract; astaxanthin is not a demonstrated CPT cofactor.
    nutrient_topic
    Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
    plain_language
    A fat-transport pathway was less oxidatively modified during exercise.
    primary_references
    Astaxanthin improves muscle lipid metabolism in exercise via inhibitory effect of oxidative CPT I modification. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18082622/ · DOI 10.1016/j.bbrc.2007.12.019

    Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 342–348

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · ICR mice and treadmill exercise; protein modification and localization measurements. · source_derived_draft · unverified_draft

    ## astaxanthin-cpt1-oxidation A fat-transport pathway was less oxidatively modified during exercise. Four weeks of astaxanthin feeding reduced exercise-associated oxidative modification of CPT I and increased FAT/CD36-CPT I colocalization in mice. Model: ICR mice and treadmill exercise; protein modification and localization measurements. Limitations: CPT I isoform was not resolved in the accessed abstract; astaxanthin is not a demonstrated CPT cofactor. Evidence access: Primary abstract Astaxanthin improves muscle lipid metabolism in exercise via inhibitory effect of oxidative CPT I modification. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18082622/ · DOI 10.1016/j.bbrc.2007.12.019
    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