Component

GLP-1 secretion in mouse intestinal cultures

GLP-1 secretion in mouse intestinal cultures. Interpret through the linked study species, preparation, exposure and measured endpoint.

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. Capsaicin did not increase GLP-1 secretion in the tested mouse intestinal and GLUTag cultures.

    Capsaicin → GLP-1 secretion in mouse intestinal cultures Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
    experimental_contrast
    {"intervention": "Capsaicin", "comparator": "Matched basal culture", "endpoint": "Capsaicin did not increase GLP-1 secretion in the tested mouse intestinal and GLUTag cultures.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Capsaicin 100 nM, two-hour secretion assay.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    No generic TRPV1-to-GLP-1 effect inferred; no allicin exposure in this experiment.
    plain_language
    Capsaicin did not increase GLP-1 secretion in the tested mouse intestinal and GLUTag cultures.
    primary_references
    Stimulation of GLP-1 secretion downstream of the ligand-gated ion channel TRPA1. | 2015 | DOI 10.2337/db14-0737 | PMID 25325736 | https://pubmed.ncbi.nlm.nih.gov/25325736/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/ | https://doi.org/10.2337/db14-0737
    source_locator
    Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75

    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 · Capsaicin 100 nM, two-hour secretion assay. · Recorded from source · Recorded from source

    **The GLP-1 experiment did not test allicin.** Allyl isothiocyanate (AITC) and carvacrol increased calcium signaling and GLP-1 secretion in mouse intestinal cultures; antagonism or Trpa1 deletion limited those responses. Glucose-induced responses persisted during TRPA1 blockade. In vivo, oral AITC at 15 mg/kg raised GLP-1 even in Trpa1-null mice; lower doses did not significantly increase it. Capsaicin did not increase secretion in the tested cultures. These findings constrain a proposed allicin–TRPA1–GLP-1 connection, but they do not demonstrate it. AITC is not allicin. [Emery 2015](https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/)
    Complete structured claim and evidence

  2. The tested TRPA1 agonist allyl-isothiocyanate increased GLP-1 secretion in mouse intestinal cultures.

    Allyl isothiocyanate / AITC → GLP-1 secretion in mouse intestinal cultures Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
    experimental_contrast
    {"intervention": "allyl-isothiocyanate", "comparator": "Matched culture vehicle", "endpoint": "The tested TRPA1 agonist allyl-isothiocyanate increased GLP-1 secretion in mouse intestinal cultures.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Mouse intestinal cultures; 100 uM AITC or 50 uM carvacrol; two-hour secretion assay.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    This experiment did not test allicin. Shared receptor identity is a research connection, not transferred efficacy.
    plain_language
    The tested TRPA1 agonist allyl-isothiocyanate increased GLP-1 secretion in mouse intestinal cultures.
    primary_references
    Stimulation of GLP-1 secretion downstream of the ligand-gated ion channel TRPA1. | 2015 | DOI 10.2337/db14-0737 | PMID 25325736 | https://pubmed.ncbi.nlm.nih.gov/25325736/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/ | https://doi.org/10.2337/db14-0737
    source_locator
    Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75

    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 · Mouse intestinal cultures; 100 uM AITC or 50 uM carvacrol; two-hour secretion assay. · Recorded from source · Recorded from source

    **The GLP-1 experiment did not test allicin.** Allyl isothiocyanate (AITC) and carvacrol increased calcium signaling and GLP-1 secretion in mouse intestinal cultures; antagonism or Trpa1 deletion limited those responses. Glucose-induced responses persisted during TRPA1 blockade. In vivo, oral AITC at 15 mg/kg raised GLP-1 even in Trpa1-null mice; lower doses did not significantly increase it. Capsaicin did not increase secretion in the tested cultures. These findings constrain a proposed allicin–TRPA1–GLP-1 connection, but they do not demonstrate it. AITC is not allicin. [Emery 2015](https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/)
    Complete structured claim and evidence

  3. The tested TRPA1 agonist carvacrol increased GLP-1 secretion in mouse intestinal cultures.

    Carvacrol → GLP-1 secretion in mouse intestinal cultures Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.
    experimental_contrast
    {"intervention": "carvacrol", "comparator": "Matched culture vehicle", "endpoint": "The tested TRPA1 agonist carvacrol increased GLP-1 secretion in mouse intestinal cultures.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Mouse intestinal cultures; 100 uM AITC or 50 uM carvacrol; two-hour secretion assay.
    interpretation_status
    Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.
    limitations
    This experiment did not test allicin. Shared receptor identity is a research connection, not transferred efficacy.
    plain_language
    The tested TRPA1 agonist carvacrol increased GLP-1 secretion in mouse intestinal cultures.
    primary_references
    Stimulation of GLP-1 secretion downstream of the ligand-gated ion channel TRPA1. | 2015 | DOI 10.2337/db14-0737 | PMID 25325736 | https://pubmed.ncbi.nlm.nih.gov/25325736/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/ | https://doi.org/10.2337/db14-0737
    source_locator
    Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.

    Allicin: detailed mechanisms of action (reviewed 5 October 2026) · lines 75–75

    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 · Mouse intestinal cultures; 100 uM AITC or 50 uM carvacrol; two-hour secretion assay. · Recorded from source · Recorded from source

    **The GLP-1 experiment did not test allicin.** Allyl isothiocyanate (AITC) and carvacrol increased calcium signaling and GLP-1 secretion in mouse intestinal cultures; antagonism or Trpa1 deletion limited those responses. Glucose-induced responses persisted during TRPA1 blockade. In vivo, oral AITC at 15 mg/kg raised GLP-1 even in Trpa1-null mice; lower doses did not significantly increase it. Capsaicin did not increase secretion in the tested cultures. These findings constrain a proposed allicin–TRPA1–GLP-1 connection, but they do not demonstrate it. AITC is not allicin. [Emery 2015](https://pmc.ncbi.nlm.nih.gov/articles/PMC4375100/)
    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.