Component

Human Caco-2 permeability during aspartame exposure

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

6 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. Aspartame at 0.1 mM for 24 hours increased Caco-2 monolayer permeability.

    Aspartame → Human Caco-2 permeability during aspartame exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text; methods and results
    experimental_model
    Human colon-cancer-derived cell line; dextran flux and electrical resistance assays.
    limitations
    Not a living human gut exposure or clinical disease endpoint.
    nutrient_topic
    Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
    plain_language
    Intact sweetener altered a cultured epithelial barrier.
    primary_references
    Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32580504/ · DOI 10.3390/nu12061862

    Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 194–200

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human colon-cancer-derived cell line; dextran flux and electrical resistance assays. · source_derived_draft · unverified_draft

    ## aspartame-barrier-permeability Intact sweetener altered a cultured epithelial barrier. Aspartame at 0.1 mM for 24 hours increased Caco-2 monolayer permeability. Model: Human colon-cancer-derived cell line; dextran flux and electrical resistance assays. Limitations: Not a living human gut exposure or clinical disease endpoint. Evidence access: Primary full text; methods and results Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32580504/ · DOI 10.3390/nu12061862
    Complete structured claim and evidence

  2. Claudin-3 overexpression attenuated aspartame-associated permeability and ROS changes in Caco-2 cells.

    Human claudin 3 / CLDN3 → Human Caco-2 permeability during aspartame exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Human cell-line expression rescue.
    limitations
    Does not establish that the same rescue is clinically achievable.
    nutrient_topic
    Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
    plain_language
    Restoring a barrier component altered downstream readouts.
    primary_references
    Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32580504/ · DOI 10.3390/nu12061862

    Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 234–240

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cell-line expression rescue. · source_derived_draft · unverified_draft

    ## aspartame-claudin-rescue Restoring a barrier component altered downstream readouts. Claudin-3 overexpression attenuated aspartame-associated permeability and ROS changes in Caco-2 cells. Model: Human cell-line expression rescue. Limitations: Does not establish that the same rescue is clinically achievable. Evidence access: Primary full text Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32580504/ · DOI 10.3390/nu12061862
    Complete structured claim and evidence

  3. N-acetylcysteine at 1 mM attenuated aspartame-associated oxidative and barrier changes.

    N-Acetyl-L-cysteine → Human Caco-2 permeability during aspartame exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text; Figure 5
    experimental_model
    Caco-2 co-exposure experiments.
    limitations
    Not evidence that NAC supplements prevent effects of dietary aspartame.
    nutrient_topic
    Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
    plain_language
    An antioxidant-related perturbation changed the pathway response.
    primary_references
    Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32580504/ · DOI 10.3390/nu12061862

    Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 226–232

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Caco-2 co-exposure experiments. · source_derived_draft · unverified_draft

    ## aspartame-nac-rescue An antioxidant-related perturbation changed the pathway response. N-acetylcysteine at 1 mM attenuated aspartame-associated oxidative and barrier changes. Model: Caco-2 co-exposure experiments. Limitations: Not evidence that NAC supplements prevent effects of dietary aspartame. Evidence access: Primary full text; Figure 5 Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32580504/ · DOI 10.3390/nu12061862
    Complete structured claim and evidence

  4. T1R3 siRNA attenuated aspartame-associated barrier and claudin-3 changes in Caco-2 cells.

    Human taste receptor TAS1R3 → Human Caco-2 permeability during aspartame exposure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Human cell-line siRNA perturbation.
    limitations
    Supports functional involvement, not proof of direct binding to T1R3 alone.
    nutrient_topic
    Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
    plain_language
    Removing a signaling component reduced the response.
    primary_references
    Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32580504/ · DOI 10.3390/nu12061862
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 210–216

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human cell-line siRNA perturbation. · source_derived_draft · unverified_draft

    ## aspartame-t1r3-knockdown Removing a signaling component reduced the response. T1R3 siRNA attenuated aspartame-associated barrier and claudin-3 changes in Caco-2 cells. Model: Human cell-line siRNA perturbation. Limitations: Supports functional involvement, not proof of direct binding to T1R3 alone. Evidence access: Primary full text Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32580504/ · DOI 10.3390/nu12061862
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The Caco-2 study found reduced cell-surface claudin 3 after 0.1 mM aspartame exposure.

    Aspartame → Human claudin 3 / CLDN3 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text; Figure 4
    experimental_model
    24-hour exposure and surface ELISA.
    limitations
    Does not establish direct aspartame–claudin binding.
    nutrient_topic
    Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
    plain_language
    Junction location matters as well as protein presence.
    primary_references
    Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32580504/ · DOI 10.3390/nu12061862

    Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 202–208

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 24-hour exposure and surface ELISA. · source_derived_draft · unverified_draft

    ## aspartame-claudin-surface Junction location matters as well as protein presence. The Caco-2 study found reduced cell-surface claudin 3 after 0.1 mM aspartame exposure. Model: 24-hour exposure and surface ELISA. Limitations: Does not establish direct aspartame–claudin binding. Evidence access: Primary full text; Figure 4 Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32580504/ · DOI 10.3390/nu12061862
    Complete structured claim and evidence

  2. Aspartame increased the ROS-sensitive fluorescence signal in exposed Caco-2 cells.

    Aspartame → Human Caco-2 ROS signal during aspartame exposure source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text; Figure 5
    experimental_model
    0.1 mM, 24 hours; DCFDA assay.
    limitations
    Probe fluorescence does not identify a single radical species.
    nutrient_topic
    Aspartame collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Aspartame
    plain_language
    Oxidative signaling is an experimentally measured intermediate.
    primary_references
    Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32580504/ · DOI 10.3390/nu12061862

    Aspartame: digestion, taste, metabolite dependencies and experimental signaling (2026-09-20) · lines 218–224

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · 0.1 mM, 24 hours; DCFDA assay. · source_derived_draft · unverified_draft

    ## aspartame-ros-induction Oxidative signaling is an experimentally measured intermediate. Aspartame increased the ROS-sensitive fluorescence signal in exposed Caco-2 cells. Model: 0.1 mM, 24 hours; DCFDA assay. Limitations: Probe fluorescence does not identify a single radical species. Evidence access: Primary full text; Figure 5 Artificial Sweeteners Disrupt Tight Junctions and Barrier Function in the Intestinal Epithelium through Activation of the Sweet Taste Receptor, T1R3. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32580504/ · DOI 10.3390/nu12061862
    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