{"id":"1a4e0806-9fd3-51f1-8880-76d91a0c6115","stable_key":"research:selenot-beta-cell-insulin","predicate":"supports_in_tested_model","statement":"Pancreatic beta-cell Selenot deletion in mice produced an insulin production/secretion deficit and impaired glucose tolerance.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"literature_reviewed:supported_interpretation","direction":"positive","is_public":true,"mechanism_event_id":"4df022db-c7f6-5ea4-b233-687fbc4a7be0","mechanism_event_label":"In the studied mice, pancreatic cells needed SELENOT for normal insulin output.","subject":{"id":"3fa46a05-7b68-5595-bf0a-1844c4b081e5","slug":"selenot","display_name":"SELENOT","entity_type_key":"protein"},"object":{"id":"7c50efe8-650e-5145-81ef-1c430510a538","slug":"insulin-secretion","display_name":"Insulin secretion","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"4df022db-c7f6-5ea4-b233-687fbc4a7be0","stable_key":"research:selenot-beta-cell-insulin","event_type":"experimentally_scoped_interaction","label":"In the studied mice, pancreatic cells needed SELENOT for normal insulin output.","description":"Pancreatic beta-cell Selenot deletion in mice produced an insulin production/secretion deficit and impaired glucose tolerance.","status":"active","compartment":null,"participants":[{"entity":{"id":"3fa46a05-7b68-5595-bf0a-1844c4b081e5","slug":"selenot","display_name":"SELENOT","entity_type_key":"protein"},"role":"regulator","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"7c50efe8-650e-5145-81ef-1c430510a538","slug":"insulin-secretion","display_name":"Insulin secretion","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""}]},"contexts":[{"dimension":"experimental_model","value_text":"Human/mouse pancreatic expression and beta-cell-specific Selenot-knockout mice.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Production versus secretion and the direct enzymatic substrate are not fully separated here; the knockout is not a human supplementation trial.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"organism","value_text":"Mouse knockout; human and mouse expression","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"32e309d2-ea81-5973-91ff-0d9527c40462","evidence_kind":"curated_literature_summary","locator":"lines 1097-1106","start_line":1097,"end_line":1106,"excerpt":"## selenot-beta-cell-insulin\n\nIn the studied mice, pancreatic cells needed SELENOT for normal insulin output.\n\nPancreatic beta-cell Selenot deletion in mice produced an insulin production/secretion deficit and impaired glucose tolerance.\n\nExperimental model: Human/mouse pancreatic expression and beta-cell-specific Selenot-knockout mice.\nOrganism: Mouse knockout; human and mouse expression\nLimitations: Production versus secretion and the direct enzymatic substrate are not fully separated here; the knockout is not a human supplementation trial.\nPrimary reference: [The PACAP-regulated gene selenoprotein T is abundantly expressed in mouse and human beta-cells and its targeted inactivation impairs glucose tolerance](https://pubmed.ncbi.nlm.nih.gov/23913443/)","model_system":"Human/mouse pancreatic expression and beta-cell-specific Selenot-knockout mice.","directness":"author_interpretation","verification_status":"secondary_verified","notes":"Curated summary; inspect the linked primary papers for original methods and results.","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"4f892f13-06ea-5199-a33c-a703f35c80ae","stable_key":"selenium-research-2026-09-17","title":"Selenium: literature corrections and mechanism additions","document_type":"curated_literature_review","citation_label":"Metabolic Ledger literature curation, 17 September 2026; primary papers linked individually","file_path":"","sha256":"0b818b10c1c7120e5caf7f4d4019d7bd025d745692e424f515d3ef903c9ab7f3","revision_id":"80984e03-5f0f-5877-8094-afef7637444e","review_status":"secondary_verified","notes":"Secondary curated summaries of primary experiments, with explicit models and limitations. Not archived primary full text."}}],"relations":[],"conflicts":[],"corrections":[],"research":{"topic":"Endocrine signaling","plain_language":"In the studied mice, pancreatic cells needed SELENOT for normal insulin output.","evidence_scope":"supported_interpretation","papers":[{"key":"catalog-selenot-2013","title":"The PACAP-regulated gene selenoprotein T is abundantly expressed in mouse and human beta-cells and its targeted inactivation impairs glucose tolerance","url":"https://pubmed.ncbi.nlm.nih.gov/23913443/","doi":null,"year":2013,"model":"Human/mouse pancreatic expression and beta-cell-specific Selenot-knockout mice.","summary":"Beta-cell Selenot loss impaired glucose regulation with evidence of deficient insulin production/secretion; a direct catalytic substrate was not isolated."}]}}