Component

IRS1/PI3K/Akt insulin-signaling readouts in human endothelium

IRS1/PI3K/Akt insulin-signaling readouts in human endothelium. Interpret through the linked experimental species, preparation, compartment and exposure; no universal causal effect is implied.

2 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. C3G pretreatment improved IRS1/PI3K/Akt insulin signaling in palmitate-challenged human endothelial cells.

    Cyanidin 3-O-beta-D-glucopyranoside → IRS1/PI3K/Akt insulin-signaling readouts in human endothelium source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
    experimental_condition
    Palmitate challenge without C3G challenge · Palmitate / hexadecanoate Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Palmitate challenge without C3G present · Cyanidin 3-O-beta-D-glucopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    Palmitate challenge without C3G signaling stimulus · Insulin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "C3G pretreatment followed by palmitate challenge", "comparator": "Palmitate challenge without C3G", "endpoint": "C3G pretreatment improved IRS1/PI3K/Akt insulin signaling in palmitate-challenged human endothelial cells.", "effect_direction": "increase", "combination": "joint", "conditions": [{"entity_slug": "cyanidin-3-glucoside", "state": "present"}, {"entity_slug": "palmitate", "state": "challenge"}, {"entity_slug": "insulin", "state": "signaling stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Palmitate-challenged HUVECs; accessible primary abstract; exact C3G dose/timing not extracted.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Context-specific signaling rescue; no claim of direct KEAP1 binding or dietary circulating-metabolite effect.
    plain_language
    C3G pretreatment improved IRS1/PI3K/Akt insulin signaling in palmitate-challenged human endothelial cells.
    primary_references
    Cyanidin-3-O-glucoside ameliorates palmitate-induced insulin resistance by modulating IRS-1 phosphorylation and release of endothelial derived vasoactive factors. | 2017 | DOI 10.1016/j.bbalip.2016.12.008 | PMID 28011403 | https://pubmed.ncbi.nlm.nih.gov/28011403/ | https://doi.org/10.1016/j.bbalip.2016.12.008
    source_locator
    Reviewed reference lines 72-72; exact primary location described in quoted passage where extracted.

    Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 72–72

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · Palmitate-challenged HUVECs; accessible primary abstract; exact C3G dose/timing not extracted. · source_derived_draft · unverified_draft

    **Nrf2 dependence has been tested, but is context-specific.** C3G pretreatment in palmitate-challenged human endothelial cells improved IRS-1/PI3K/Akt-related insulin signaling and restored eNOS expression and NO release. Nrf2 silencing impaired the protective response. This is stronger than merely observing an antioxidant-gene increase, but neither direct KEAP1 binding nor the same action of circulating conjugates follows. The source's exact exposure protocol must accompany any quantitative reuse; only its accessible abstract was extracted here. [Fratantonio et al., 2017](https://pubmed.ncbi.nlm.nih.gov/28011403/).
    Complete structured claim and evidence

  2. Nrf2 silencing impaired C3G-associated protection in the palmitate-challenged endothelial model.

    Cyanidin 3-O-beta-D-glucopyranoside → IRS1/PI3K/Akt insulin-signaling readouts in human endothelium source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary indexed abstract reviewed; full methods, figures, exact doses or endpoint-specific species assignments may remain unextracted.
    experimental_condition
    C3G/palmitate experiment with Nrf2 retained challenge · Palmitate / hexadecanoate Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    C3G/palmitate experiment with Nrf2 retained present · Cyanidin 3-O-beta-D-glucopyranoside Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    C3G/palmitate experiment with Nrf2 retained signaling stimulus · Insulin Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_condition
    C3G/palmitate experiment with Nrf2 retained silenced · Human Nrf2 / NFE2L2 Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "C3G/palmitate experiment with Nrf2 silencing", "comparator": "C3G/palmitate experiment with Nrf2 retained", "endpoint": "Nrf2 silencing impaired C3G-associated protection in the palmitate-challenged endothelial model.", "effect_direction": "decrease", "combination": "joint", "conditions": [{"entity_slug": "cyanidin-3-glucoside", "state": "present"}, {"entity_slug": "nfe2l2", "state": "silenced"}, {"entity_slug": "palmitate", "state": "challenge"}, {"entity_slug": "insulin", "state": "signaling stimulus"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    HUVECs with Nrf2 transcript silencing and palmitate challenge.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    Exact experimental details remain abstract-level; no clinical cofactor-rescue claim.
    plain_language
    Nrf2 silencing impaired C3G-associated protection in the palmitate-challenged endothelial model.
    primary_references
    Cyanidin-3-O-glucoside ameliorates palmitate-induced insulin resistance by modulating IRS-1 phosphorylation and release of endothelial derived vasoactive factors. | 2017 | DOI 10.1016/j.bbalip.2016.12.008 | PMID 28011403 | https://pubmed.ncbi.nlm.nih.gov/28011403/ | https://doi.org/10.1016/j.bbalip.2016.12.008
    source_locator
    Reviewed reference lines 72-72; exact primary location described in quoted passage where extracted.
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Anthocyanins: detailed mechanisms of action (reviewed 4 October 2026) · lines 72–72

    Original AI-assisted review of primary studies and, where relevant, official regulatory records. Access level is retained per claim. Corrections, null results and unresolved questions remain explicit. Not publisher full text or independent replication. · supports · HUVECs with Nrf2 transcript silencing and palmitate challenge. · source_derived_draft · unverified_draft

    **Nrf2 dependence has been tested, but is context-specific.** C3G pretreatment in palmitate-challenged human endothelial cells improved IRS-1/PI3K/Akt-related insulin signaling and restored eNOS expression and NO release. Nrf2 silencing impaired the protective response. This is stronger than merely observing an antioxidant-gene increase, but neither direct KEAP1 binding nor the same action of circulating conjugates follows. The source's exact exposure protocol must accompany any quantitative reuse; only its accessible abstract was extracted here. [Fratantonio et al., 2017](https://pubmed.ncbi.nlm.nih.gov/28011403/).
    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.