{"id":"9f6f5402-996e-5fc2-b789-05ed353597ae","stable_key":"46d15d9e-d3b5-544d-ba01-b785aa3e4f42:thiamine-def-stimulated-glucose-oxidation","predicate":"antagonist-assisted-depletion-reduces","statement":"The potassium-induced increment in carbon-14 carbon dioxide production from labeled glucose was 50% lower in deficient rat brain slices; resting production was similar to controls.","claim_class":"mechanistic","status":"source_derived_draft","evidence_grade":"ungraded","direction":"negative","is_public":true,"mechanism_event_id":"6a4bf11f-ed60-5e3d-9dfb-6e464eaa20b8","mechanism_event_label":"The slices could maintain resting oxidation but had less capacity to increase it when stimulated.","subject":{"id":"36b7c3eb-068b-500f-af1c-078829df1ecc","slug":"thiamine","display_name":"Thiamine (vitamin B1)","entity_type_key":"small_molecule"},"object":{"id":"ef4f9254-15f0-5f11-8b0b-1208ce0a5b86","slug":"brain-glucose-oxidation","display_name":"Brain glucose oxidation","entity_type_key":"cellular_process"},"evidence_count":1,"mechanism_event":{"id":"6a4bf11f-ed60-5e3d-9dfb-6e464eaa20b8","stable_key":"46d15d9e-d3b5-544d-ba01-b785aa3e4f42:thiamine-def-stimulated-glucose-oxidation-event","event_type":"biochemical_relationship","label":"The slices could maintain resting oxidation but had less capacity to increase it when stimulated.","description":"The potassium-induced increment in carbon-14 carbon dioxide production from labeled glucose was 50% lower in deficient rat brain slices; resting production was similar to controls.","status":"provisional","compartment":null,"participants":[{"entity":{"id":"8ae7848b-f172-5e09-8acf-5ca914907b0b","slug":"glucose","display_name":"D-glucose","entity_type_key":"small_molecule"},"role":"labeled substrate","stoichiometry":null,"state_label":"","sequence_order":0,"notes":""},{"entity":{"id":"5dd31e52-f51e-51f3-880e-240abcc0ab1d","slug":"potassium-ion","display_name":"Potassium ion","entity_type_key":"ion"},"role":"experimental stimulation","stoichiometry":null,"state_label":"","sequence_order":1,"notes":""},{"entity":{"id":"36b7c3eb-068b-500f-af1c-078829df1ecc","slug":"thiamine","display_name":"Thiamine (vitamin B1)","entity_type_key":"small_molecule"},"role":"subject","stoichiometry":null,"state_label":"","sequence_order":2,"notes":""},{"entity":{"id":"ef4f9254-15f0-5f11-8b0b-1208ce0a5b86","slug":"brain-glucose-oxidation","display_name":"Brain glucose oxidation","entity_type_key":"cellular_process"},"role":"target","stoichiometry":null,"state_label":"","sequence_order":3,"notes":""}]},"contexts":[{"dimension":"availability_state","value_text":"nutrient_deficiency","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null},{"dimension":"evidence_location","value_text":"Abstract","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"evidence_span","value_text":"under resting conditions","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"experimental_model","value_text":"Symptomatic pyrithiamine-induced thiamine-deficient rats; brain slices assayed with uniformly carbon-14-labeled glucose at rest and during potassium stimulation; seven-day thiamine reversal arm.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"exposure","value_text":"Pyrithiamine-induced deficiency followed by potassium stimulation of rat brain slices","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"limitations","value_text":"Carbon dioxide labeling measures glucose oxidation under this stimulation protocol, not whole-brain ATP directly. Combined thiamine withdrawal and pyrithiamine exposure; not an estimate for mild dietary insufficiency or a human blood threshold.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"nutrient_topic","value_text":"Thiamine research collection; topical membership is not evidence of a direct dietary effect.","comparator":null,"unit":null,"notes":"","entity":{"slug":"thiamine","display_name":"Thiamine (vitamin B1)","entity_type_key":"small_molecule"}},{"dimension":"organism","value_text":"Rattus norvegicus","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"plain_language","value_text":"The slices could maintain resting oxidation but had less capacity to increase it when stimulated.","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"primary_references","value_text":"[gibson-1984-brain-flux] Correlation of enzymatic, metabolic, and behavioral deficits in thiamin deficiency and its reversal (1984). https://pubmed.ncbi.nlm.nih.gov/6149477/ DOI: 10.1007/BF00965667","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Brain slices","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"trigger_kind","value_text":"nutrient_deficiency","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null}],"evidence":[{"id":"4d12c16e-b433-59d5-96c0-47dc35d5f02c","evidence_kind":"source_excerpt","locator":"Lines 1098-1110","start_line":1098,"end_line":1110,"excerpt":"### thiamine-def-stimulated-glucose-oxidation\nThe potassium-induced increment in carbon-14 carbon dioxide production from labeled glucose was 50% lower in deficient rat brain slices; resting production was similar to controls.\nCondition category: nutrient_deficiency\nnutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: The slices could maintain resting oxidation but had less capacity to increase it when stimulated.\norganism: Rattus norvegicus\ntissue_or_cell_type: Brain slices\nexperimental_model: Symptomatic pyrithiamine-induced thiamine-deficient rats; brain slices assayed with uniformly carbon-14-labeled glucose at rest and during potassium stimulation; seven-day thiamine reversal arm.\nlimitations: Carbon dioxide labeling measures glucose oxidation under this stimulation protocol, not whole-brain ATP directly. Combined thiamine withdrawal and pyrithiamine exposure; not an estimate for mild dietary insufficiency or a human blood threshold.\nevidence_location: Abstract\nevidence_span: under resting conditions\nexposure: Pyrithiamine-induced deficiency followed by potassium stimulation of rat brain slices\n[gibson-1984-brain-flux] Correlation of enzymatic, metabolic, and behavioral deficits in thiamin deficiency and its reversal (1984). https://pubmed.ncbi.nlm.nih.gov/6149477/ DOI: 10.1007/BF00965667","model_system":"Symptomatic pyrithiamine-induced thiamine-deficient rats; brain slices assayed with uniformly carbon-14-labeled glucose at rest and during potassium stimulation; seven-day thiamine reversal arm.","directness":"author_interpretation","verification_status":"source_derived_draft","notes":"Exact curation-document quotation, not publisher quotation. Study references: [gibson-1984-brain-flux] Correlation of enzymatic, metabolic, and behavioral deficits in thiamin deficiency and its reversal (1984). https://pubmed.ncbi.nlm.nih.gov/6149477/ DOI: 10.1007/BF00965667","relationship":"supports","weight":1.0,"link_notes":"","source":{"id":"158d2c03-ac8c-589f-8270-c468165ae346","stable_key":"import-46d15d9e-d3b5-544d-ba01-b785aa3e4f42","title":"Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17)","document_type":"imported_text","citation_label":"AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text.","file_path":"","sha256":"f376512fb3310141315548015b387833e3af45146e73fb73cd02cee20e4ddb9c","revision_id":"53bc5eda-dec8-58cc-a56f-a9eb4ab036ef","review_status":"unverified_draft","notes":""}}],"relations":[],"conflicts":[],"corrections":[],"research":null}