{"id":"0bce386a-38f9-57cb-9937-3ac457088310","stable_key":"c836a883-ac18-5eb2-9971-2f0b542feba8:glucose-trpa1-block","predicate":"no_detected_change_in_recorded_experiment","statement":"Glucose-induced calcium signaling persisted during TRPA1 antagonist exposure in the tested mouse L cells.","claim_class":"observational","status":"source_recorded","evidence_grade":"ungraded","direction":"neutral","is_public":true,"mechanism_event_id":"e5d5a70d-18ab-5189-b1eb-acb13aec41ef","mechanism_event_label":"Glucose-induced calcium signaling persisted during TRPA1 antagonist exposure in the tested mouse L cells.","subject":{"id":"8ae7848b-f172-5e09-8acf-5ca914907b0b","slug":"glucose","display_name":"D-glucose","entity_type_key":"small_molecule"},"object":{"id":"6ac65933-f94f-5b08-a4df-71598a3294ad","slug":"mouse-intestinal-calcium-response","display_name":"Calcium signaling in mouse intestinal L cells","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"e5d5a70d-18ab-5189-b1eb-acb13aec41ef","stable_key":"c836a883-ac18-5eb2-9971-2f0b542feba8:glucose-trpa1-block-event","event_type":"experimental_observation","label":"Glucose-induced calcium signaling persisted during TRPA1 antagonist exposure in the tested mouse L cells.","description":"**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/)","status":"provisional","compartment":null,"participants":[{"entity":{"id":"8ae7848b-f172-5e09-8acf-5ca914907b0b","slug":"glucose","display_name":"D-glucose","entity_type_key":"small_molecule"},"role":"tested factor","stoichiometry":null,"state_label":"Glucose response with TRPA1 antagonist","sequence_order":0,"notes":""},{"entity":{"id":"6ac65933-f94f-5b08-a4df-71598a3294ad","slug":"mouse-intestinal-calcium-response","display_name":"Calcium signaling in mouse intestinal L cells","entity_type_key":"cellular_process"},"role":"measured outcome","stoichiometry":null,"state_label":"no_detected_change","sequence_order":1,"notes":""},{"entity":{"id":"05575212-6bc2-544a-8983-16b578525891","slug":"mouse-trpa1","display_name":"Mouse Trpa1 ion channel","entity_type_key":"protein"},"role":"blocked channel","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""}]},"contexts":[{"dimension":"evidence_access","value_text":"Primary full text available; selected claim-relevant methods, results, tables/figures and limitations reviewed. Supplemental proteome and all secondary findings are not exhaustively extracted.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_condition","value_text":"stimulus","comparator":"Glucose response without antagonist","unit":null,"notes":"Condition belongs to the full experimental contrast; do not separate a joint intervention.","entity":{"slug":"glucose","display_name":"D-glucose","entity_type_key":"small_molecule"}},{"dimension":"experimental_condition","value_text":"pharmacologically blocked","comparator":"Glucose response without antagonist","unit":null,"notes":"Condition belongs to the full experimental contrast; do not separate a joint intervention.","entity":{"slug":"mouse-trpa1","display_name":"Mouse Trpa1 ion channel","entity_type_key":"protein"}},{"dimension":"experimental_contrast","value_text":"{\"intervention\": \"Glucose response with TRPA1 antagonist\", \"comparator\": \"Glucose response without antagonist\", \"endpoint\": \"Glucose-induced calcium signaling persisted during TRPA1 antagonist exposure in the tested mouse L cells.\", \"effect_direction\": \"no_detected_change\", \"combination\": \"joint\", \"conditions\": [{\"entity_slug\": \"glucose\", \"state\": \"stimulus\"}, {\"entity_slug\": \"mouse-trpa1\", \"state\": \"pharmacologically blocked\"}]}","comparator":null,"unit":null,"notes":"Explicit extracted experimental comparison; source-derived draft.","entity":null},{"dimension":"experimental_model","value_text":"Mouse primary L cells; 10 mM glucose with or without A-967079.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"interpretation_status","value_text":"Source-derived extraction of a fact-checked reference; access is explicit, not independent raw-data verification.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"No loss of glucose response in this assay; not a general role for allicin in glycemic control.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"Glucose-induced calcium signaling persisted during TRPA1 antagonist exposure in the tested mouse L cells.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"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","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"source_locator","value_text":"Reviewed reference lines 75-75; exact primary location described in quoted passage where extracted.","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"e0ff348f-c102-57cb-be77-47674c3c5b2d","evidence_kind":"source_excerpt","locator":"Lines 75-75","start_line":75,"end_line":75,"excerpt":"**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/)","model_system":"Mouse primary L cells; 10 mM glucose with or without A-967079.","directness":"reported_statement","verification_status":"source_recorded","notes":"Exact excerpt of the retained AI-assisted reviewed reference; primary sources are cited in primary_references and access scope is retained. Not a verbatim quotation from a primary paper.","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"10820a6b-594a-547d-97f9-906ab4cc1d6e","stable_key":"import-c836a883-ac18-5eb2-9971-2f0b542feba8","title":"Allicin: detailed mechanisms of action (reviewed 5 October 2026)","document_type":"imported_text","citation_label":"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.","file_path":"","sha256":"2475d3eb681100a0a34577a47b7cba5b251df866fbd6ce795122ccabee360018","revision_id":"590df96d-2ed1-5763-b04c-bf0e096e603c","review_status":"source_recorded","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}