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(2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201","comparator":null,"unit":null,"notes":"","entity":null},{"dimension":"tissue_or_cell_type","value_text":"HepG2 cells","comparator":null,"unit":null,"notes":"","entity":null}],"evidence":[{"id":"3213ea7e-db9a-57d5-a56b-64851e8b3f96","evidence_kind":"source_excerpt","locator":"Lines 458-469","start_line":458,"end_line":469,"excerpt":"### mangiferin-lkb1-acetylation\nNorathyriol lowered measured LKB1 acetylation in HepG2 cells.\nCondition category: normal\nnutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect.\nplain_language: A chemical modification of an upstream kinase changed.\norganism: Homo sapiens for HepG2 experiments; mouse findings separately scoped\ntissue_or_cell_type: HepG2 cells\nexperimental_model: KK-Ay mouse liver experiments and mechanistic HepG2 studies\nlimitations: Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim.\nexposure: Norathyriol in sodium-oleate lipid-loading model; micromolar range\nevidence_span: {\"source_cache\": \"artifacts/mangiferin-research/29563875.fulltext.txt\", \"locator\": \"Primary full-text span; zero-based, end-exclusive Unicode character offsets\", \"file_sha256\": \"1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415\", \"start_char\": 35295, \"end_char\": 36269, \"text_sha256\": \"4b69cb6e7f09043eda3312b226bc03bbf8e0cbf25a4f6b51505c0aebed3b7d04\"}\n[mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. 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