Component

ApoE-null mouse atherosclerosis during aspartame exposure

Context-specific entity; species, compartment and exposure are stated on each claim.

3 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. Monocyte/macrophage Cx3cr1 deletion abolished aspartame-exacerbated atherosclerosis in the model.

    Mouse fractalkine receptor / Cx3cr1 → ApoE-null mouse atherosclerosis during aspartame exposure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Conditional mouse genetic perturbation.
    limitations
    One preclinical study, not independently replicated clinical causality.
    nutrient_topic
    Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
    plain_language
    A separate immune receptor was required for the added plaque effect.
    primary_references
    Sweetener aspartame aggravates atherosclerosis through insulin-triggered inflammation. · 2025 · https://pubmed.ncbi.nlm.nih.gov/39978336/ · DOI 10.1016/j.cmet.2025.01.006
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 282–288

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Conditional mouse genetic perturbation. · source_derived_draft · unverified_draft

    ## aspartame-cx3cr1-loss A separate immune receptor was required for the added plaque effect. Monocyte/macrophage Cx3cr1 deletion abolished aspartame-exacerbated atherosclerosis in the model. Model: Conditional mouse genetic perturbation. Limitations: One preclinical study, not independently replicated clinical causality. Evidence access: Primary abstract Sweetener aspartame aggravates atherosclerosis through insulin-triggered inflammation. · 2025 · https://pubmed.ncbi.nlm.nih.gov/39978336/ · DOI 10.1016/j.cmet.2025.01.006
    Complete structured claim and evidence

  2. Slow-release insulin pumps worsened atherosclerosis in ApoE-null mice.

    Insulin → ApoE-null mouse atherosclerosis during aspartame exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse insulin-pump experiment.
    limitations
    Does not prove every aspartame effect is insulin-mediated.
    nutrient_topic
    Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
    plain_language
    A mediator intervention supported the proposed chain.
    primary_references
    Sweetener aspartame aggravates atherosclerosis through insulin-triggered inflammation. · 2025 · https://pubmed.ncbi.nlm.nih.gov/39978336/ · DOI 10.1016/j.cmet.2025.01.006

    Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 266–272

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse insulin-pump experiment. · source_derived_draft · unverified_draft

    ## aspartame-insulin-pump A mediator intervention supported the proposed chain. Slow-release insulin pumps worsened atherosclerosis in ApoE-null mice. Model: Mouse insulin-pump experiment. Limitations: Does not prove every aspartame effect is insulin-mediated. Evidence access: Primary abstract Sweetener aspartame aggravates atherosclerosis through insulin-triggered inflammation. · 2025 · https://pubmed.ncbi.nlm.nih.gov/39978336/ · DOI 10.1016/j.cmet.2025.01.006
    Complete structured claim and evidence

  3. Sustained aspartame feeding aggravated plaque formation in ApoE-null mice.

    Aspartame → ApoE-null mouse atherosclerosis during aspartame exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    ApoE-deficient mouse feeding study.
    limitations
    Not a human cardiovascular risk estimate.
    nutrient_topic
    Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
    plain_language
    A susceptible vascular model produced a disease endpoint.
    primary_references
    Sweetener aspartame aggravates atherosclerosis through insulin-triggered inflammation. · 2025 · https://pubmed.ncbi.nlm.nih.gov/39978336/ · DOI 10.1016/j.cmet.2025.01.006

    Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 258–264

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · ApoE-deficient mouse feeding study. · source_derived_draft · unverified_draft

    ## aspartame-plaque-feeding A susceptible vascular model produced a disease endpoint. Sustained aspartame feeding aggravated plaque formation in ApoE-null mice. Model: ApoE-deficient mouse feeding study. Limitations: Not a human cardiovascular risk estimate. Evidence access: Primary abstract Sweetener aspartame aggravates atherosclerosis through insulin-triggered inflammation. · 2025 · https://pubmed.ncbi.nlm.nih.gov/39978336/ · DOI 10.1016/j.cmet.2025.01.006
    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