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(2026). https://pubmed.ncbi.nlm.nih.gov/41641916/ DOI: 10.1111/liv.70539","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"Hepatic lipid droplets","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"trigger_kind","value_text":"machinery_impairment","comparator":null,"unit":null,"notes":"Imported condition classification; unverified.","entity":null}],"evidence":[{"id":"54f227ce-21ff-5a74-a4cd-986b235080ad","evidence_kind":"source_excerpt","locator":"Lines 1561-1572","start_line":1561,"end_line":1572,"excerpt":"### mo-marc-lipid-enzymes\nMtarc1 loss post-transcriptionally increased CEPT1 and PEMT, altering lipid-droplet phospholipids; knocking down these enzymes reversed protection.\nCondition category: machinery_impairment\nnutrient_topic: Molybdenum research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: Changing the droplet surface helped connect the enzyme loss to fat handling.\norganism: Mus musculus; supporting cell studies\ntissue_or_cell_type: Hepatic lipid droplets\nexperimental_model: Global/liver Mtarc1 knockout with Pnpla2, Lipa, Pemt and Cept1 interventions\nlimitations: Preclinical mechanism; no evidence that dietary molybdenum restriction selectively reproduces MTARC1 targeting.\nexposure: Diet-induced liver disease with gene knockouts/knockdowns and multi-omics\nevidence_span: {\"source_cache\": \"artifacts/molybdenum-research/41641916.abstract.txt\", \"locator\": \"Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64\", \"start_char\": 0, \"end_char\": 1681, \"text_sha256\": \"52b4d4d00867faaa1bb51ff6055f887a72c4c0d266bf7a1665b3780ce03aee64\"}\n[mo-p41641916] MTARC1 Inactivation Remodels Lipid Droplets to Protect Against Metabolic Fatty Liver Disease. 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