Component

Gamma-tocotrienol

Gamma member of the vitamin E tocotrienols with an unsaturated isoprenoid side chain.

5 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. In HepG2 cells, gamma-tocotrienol inhibited incorporation of [14C]acetate into cholesterol with approximately 50% inhibition at 2 µM and maximal approximately 80% inhibition within 6 h, while incorporation of [3H]mevalonate was not inhibited.

    Gamma-tocotrienol → Cholesterol biosynthesis source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Radiolabeled precursor incorporation in HepG2 cells
    exposure
    Gamma-tocotrienol approximately 2 µM for half-maximal inhibition; response developed within 6 h.
    limitations
    Primary abstract only; media and viability protocol unavailable. Tracer localization supports action upstream of mevalonate use, not a human cholesterol-lowering recommendation.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Gamma-tocotrienol reduced cholesterol production from an early precursor, while leaving production from the later precursor mevalonate intact in cultured liver cells.
    primary_references
    [parker1993] Tocotrienols regulate cholesterol production in mammalian cells by post-transcriptional suppression of 3-hydroxy-3-methylglutaryl-coenzyme A reductase. (1993). https://pubmed.ncbi.nlm.nih.gov/8388388/ DOI: 10.1016/s0021-9258(18)82115-9
    tissue_or_cell_type
    Hepatoma cell culture

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1102–1113

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiolabeled precursor incorporation in HepG2 cells · source_derived_draft · unverified_draft

    ### e-sig-gamma-te-cholesterol In HepG2 cells, gamma-tocotrienol inhibited incorporation of [14C]acetate into cholesterol with approximately 50% inhibition at 2 µM and maximal approximately 80% inhibition within 6 h, while incorporation of [3H]mevalonate was not inhibited. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Gamma-tocotrienol reduced cholesterol production from an early precursor, while leaving production from the later precursor mevalonate intact in cultured liver cells. organism: Homo sapiens tissue_or_cell_type: Hepatoma cell culture experimental_model: Radiolabeled precursor incorporation in HepG2 cells limitations: Primary abstract only; media and viability protocol unavailable. Tracer localization supports action upstream of mevalonate use, not a human cholesterol-lowering recommendation. exposure: Gamma-tocotrienol approximately 2 µM for half-maximal inhibition; response developed within 6 h. cross_nutrient: false [parker1993] Tocotrienols regulate cholesterol production in mammalian cells by post-transcriptional suppression of 3-hydroxy-3-methylglutaryl-coenzyme A reductase. (1993). https://pubmed.ncbi.nlm.nih.gov/8388388/ DOI: 10.1016/s0021-9258(18)82115-9
    Complete structured claim and evidence

  2. At 10 µM gamma-tocotrienol, HepG2 HMG-CoA reductase degradation increased 2.4-fold and its half-life fell from 3.73 to 1.59 h, measured by [35S]methionine pulse-chase and immunoprecipitation.

    Gamma-tocotrienol → HMG-CoA reductase protein degradation source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Radiolabeled protein pulse-chase and HMGCR immunoprecipitation
    exposure
    10 µM gamma-tocotrienol; reported HMGCR half-life 3.73 h control versus 1.59 h treated.
    limitations
    Primary abstract only; these data do not by themselves identify Insig proteins or prove direct binding to the reductase. Human supplementation effects cannot be inferred.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Gamma-tocotrienol made the cholesterol-synthesis enzyme turn over faster in cultured human liver tumor cells.
    primary_references
    [parker1993] Tocotrienols regulate cholesterol production in mammalian cells by post-transcriptional suppression of 3-hydroxy-3-methylglutaryl-coenzyme A reductase. (1993). https://pubmed.ncbi.nlm.nih.gov/8388388/ DOI: 10.1016/s0021-9258(18)82115-9
    tissue_or_cell_type
    Hepatoma cell culture

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1115–1126

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiolabeled protein pulse-chase and HMGCR immunoprecipitation · source_derived_draft · unverified_draft

    ### e-sig-gamma-te-hmgcr-turnover At 10 µM gamma-tocotrienol, HepG2 HMG-CoA reductase degradation increased 2.4-fold and its half-life fell from 3.73 to 1.59 h, measured by [35S]methionine pulse-chase and immunoprecipitation. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Gamma-tocotrienol made the cholesterol-synthesis enzyme turn over faster in cultured human liver tumor cells. organism: Homo sapiens tissue_or_cell_type: Hepatoma cell culture experimental_model: Radiolabeled protein pulse-chase and HMGCR immunoprecipitation limitations: Primary abstract only; these data do not by themselves identify Insig proteins or prove direct binding to the reductase. Human supplementation effects cannot be inferred. exposure: 10 µM gamma-tocotrienol; reported HMGCR half-life 3.73 h control versus 1.59 h treated. cross_nutrient: false [parker1993] Tocotrienols regulate cholesterol production in mammalian cells by post-transcriptional suppression of 3-hydroxy-3-methylglutaryl-coenzyme A reductase. (1993). https://pubmed.ncbi.nlm.nih.gov/8388388/ DOI: 10.1016/s0021-9258(18)82115-9
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Liposomes containing astaxanthin plus alpha- or gamma-tocotrienol showed radical-scavenging activity greater than the calculated additive activity in the reported singlet-oxygen/hydroxyl-radical assays.

    Astaxanthin → Singlet molecular oxygen source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Cell-free co-encapsulated liposomes; matched single-agent comparisons.
    limitations
    Measured assay synergy is not demonstrated oral or clinical synergy.
    nutrient_topic
    Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
    plain_language
    Some vitamin E forms worked together with astaxanthin in this test system.
    primary_references
    Synergistic antioxidative effect of astaxanthin and tocotrienol by co-encapsulated in liposomes. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27698536/ · DOI 10.3164/jcbn.15-153

    Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 190–196

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Cell-free co-encapsulated liposomes; matched single-agent comparisons. · source_derived_draft · unverified_draft

    ## astaxanthin-tocotrienol-synergy Some vitamin E forms worked together with astaxanthin in this test system. Liposomes containing astaxanthin plus alpha- or gamma-tocotrienol showed radical-scavenging activity greater than the calculated additive activity in the reported singlet-oxygen/hydroxyl-radical assays. Model: Cell-free co-encapsulated liposomes; matched single-agent comparisons. Limitations: Measured assay synergy is not demonstrated oral or clinical synergy. Evidence access: Primary abstract Synergistic antioxidative effect of astaxanthin and tocotrienol by co-encapsulated in liposomes. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27698536/ · DOI 10.3164/jcbn.15-153
    Complete structured claim and evidence

  2. Delta-tocotrienol stimulated HMG-CoA reductase ubiquitination in isolated SV-589 fibroblast membrane fractions supplemented with ubiquitin-activating enzyme; gamma-tocotrienol showed the same activity. The reconstituted result supported action without further tocotrienol metabolism.

    Delta-tocotrienol → HMG-CoA reductase ubiquitination source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    experimental_model
    Isolated membranes from sterol-depleted SV-589 human fibroblasts; FLAG-ubiquitin and purified E1 assay
    exposure
    Figure 5B: purified E1 5 µg/mL, FLAG-ubiquitin 0.1 mg/mL, ubiquitin-aldehyde 0.01 mg/mL and ATP-regenerating system; tocotrienol concentration not fully retrieved.
    limitations
    The assay does not prove direct molecular binding of tocotrienol to HMGCR or INSIG. No human cholesterol outcome follows from this reconstituted experiment.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    These tocotrienols promoted attachment of degradation tags to the cholesterol-synthesis enzyme in isolated cell membranes.
    primary_references
    [song2006] Insig-dependent ubiquitination and degradation of 3-hydroxy-3-methylglutaryl coenzyme a reductase stimulated by delta- and gamma-tocotrienols. (2006). https://pubmed.ncbi.nlm.nih.gov/16831864/ DOI: 10.1074/jbc.m605575200
    tissue_or_cell_type
    Fibroblast-derived membrane fractions

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1128–1139

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Isolated membranes from sterol-depleted SV-589 human fibroblasts; FLAG-ubiquitin and purified E1 assay · source_derived_draft · unverified_draft

    ### e-sig-delta-te-hmgcr-ubiquitination Delta-tocotrienol stimulated HMG-CoA reductase ubiquitination in isolated SV-589 fibroblast membrane fractions supplemented with ubiquitin-activating enzyme; gamma-tocotrienol showed the same activity. The reconstituted result supported action without further tocotrienol metabolism. Condition category: normal nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: These tocotrienols promoted attachment of degradation tags to the cholesterol-synthesis enzyme in isolated cell membranes. organism: Homo sapiens tissue_or_cell_type: Fibroblast-derived membrane fractions experimental_model: Isolated membranes from sterol-depleted SV-589 human fibroblasts; FLAG-ubiquitin and purified E1 assay limitations: The assay does not prove direct molecular binding of tocotrienol to HMGCR or INSIG. No human cholesterol outcome follows from this reconstituted experiment. exposure: Figure 5B: purified E1 5 µg/mL, FLAG-ubiquitin 0.1 mg/mL, ubiquitin-aldehyde 0.01 mg/mL and ATP-regenerating system; tocotrienol concentration not fully retrieved. cross_nutrient: false [song2006] Insig-dependent ubiquitination and degradation of 3-hydroxy-3-methylglutaryl coenzyme a reductase stimulated by delta- and gamma-tocotrienols. (2006). https://pubmed.ncbi.nlm.nih.gov/16831864/ DOI: 10.1074/jbc.m605575200
    Complete structured claim and evidence

  3. Combined RNAi against INSIG1 and INSIG2 abolished gamma- and delta-tocotrienol-stimulated degradation of endogenous HMG-CoA reductase in sterol-depleted SV-589 fibroblasts supplied with 10 mM mevalonate.

    Combined INSIG1 and INSIG2 depletion → HMG-CoA reductase protein degradation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Combined INSIG1/INSIG2 RNA interference in immortalized human SV-589 fibroblasts
    exposure
    Sterol depletion 16 h; gamma- or delta-tocotrienol plus 10 mM mevalonate for 5 h; tocotrienol concentration not retrieved from the accessible Figure 3 text.
    limitations
    Combined knockdown establishes a machinery requirement in this model, not the unique role of either INSIG isoform or nutritional deficiency. Does not quantify viability or predict supplement benefit.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Removing both INSIG regulators prevented these tocotrienols from accelerating loss of the reductase protein in this cell experiment.
    primary_references
    [song2006] Insig-dependent ubiquitination and degradation of 3-hydroxy-3-methylglutaryl coenzyme a reductase stimulated by delta- and gamma-tocotrienols. (2006). https://pubmed.ncbi.nlm.nih.gov/16831864/ DOI: 10.1074/jbc.m605575200
    tissue_or_cell_type
    Human fibroblast cell culture
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1141–1152

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Combined INSIG1/INSIG2 RNA interference in immortalized human SV-589 fibroblasts · source_derived_draft · unverified_draft

    ### e-sig-insig-depletion-hmgcr-turnover Combined RNAi against INSIG1 and INSIG2 abolished gamma- and delta-tocotrienol-stimulated degradation of endogenous HMG-CoA reductase in sterol-depleted SV-589 fibroblasts supplied with 10 mM mevalonate. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing both INSIG regulators prevented these tocotrienols from accelerating loss of the reductase protein in this cell experiment. organism: Homo sapiens tissue_or_cell_type: Human fibroblast cell culture experimental_model: Combined INSIG1/INSIG2 RNA interference in immortalized human SV-589 fibroblasts limitations: Combined knockdown establishes a machinery requirement in this model, not the unique role of either INSIG isoform or nutritional deficiency. Does not quantify viability or predict supplement benefit. exposure: Sterol depletion 16 h; gamma- or delta-tocotrienol plus 10 mM mevalonate for 5 h; tocotrienol concentration not retrieved from the accessible Figure 3 text. cross_nutrient: false [song2006] Insig-dependent ubiquitination and degradation of 3-hydroxy-3-methylglutaryl coenzyme a reductase stimulated by delta- and gamma-tocotrienols. (2006). https://pubmed.ncbi.nlm.nih.gov/16831864/ DOI: 10.1074/jbc.m605575200
    Complete structured claim and evidence

In the sources

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