Component

Mouse glucose transporter 9 / Slc2a9

Mouse glucose transporter 9 / Slc2a9. Species, exposure and limitations are retained in each linked claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Intestinal GLUT9 protein decreased in the hyperuricemic mice.

    Mangiferin → Mouse glucose transporter 9 / Slc2a9 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mangiferin-research/32827538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958", "start_char": 0, "end_char": 1796, "text_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958"}
    experimental_model
    Rodent intestinal-loop secretion/absorption experiments
    exposure
    Mangiferin in normal and hyperuricemic loop experiments
    limitations
    Expression association does not establish direct binding; intestinal effects need not mirror kidney effects.
    nutrient_topic
    Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
    organism
    Mice for secretion/proteins; rats for absorption
    plain_language
    Another intestinal urate route changed in the opposite direction.
    primary_references
    [mangiferin-p32827538] Mangiferin promotes intestinal elimination of uric acid by modulating intestinal transporters. (2020). https://pubmed.ncbi.nlm.nih.gov/32827538/ DOI: 10.1016/j.ejphar.2020.173490
    tissue_or_cell_type
    Intestine

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1121–1132

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rodent intestinal-loop secretion/absorption experiments · source_derived_draft · unverified_draft

    ### mangiferin-intestinal-glut9 Intestinal GLUT9 protein decreased in the hyperuricemic mice. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Another intestinal urate route changed in the opposite direction. organism: Mice for secretion/proteins; rats for absorption tissue_or_cell_type: Intestine experimental_model: Rodent intestinal-loop secretion/absorption experiments limitations: Expression association does not establish direct binding; intestinal effects need not mirror kidney effects. exposure: Mangiferin in normal and hyperuricemic loop experiments evidence_span: {"source_cache": "artifacts/mangiferin-research/32827538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958", "start_char": 0, "end_char": 1796, "text_sha256": "96aea91b79bcbc9d1f63f83c0bda025138e3b97f3f7657b56149c9cc3e0e5958"} [mangiferin-p32827538] Mangiferin promotes intestinal elimination of uric acid by modulating intestinal transporters. (2020). https://pubmed.ncbi.nlm.nih.gov/32827538/ DOI: 10.1016/j.ejphar.2020.173490
    Complete structured claim and evidence

  2. Mangiferin reduced renal Mouse glucose transporter 9 / Slc2a9 expression in the hyperuricemic mice.

    Mangiferin → Mouse glucose transporter 9 / Slc2a9 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mangiferin-research/21348301.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58", "start_char": 0, "end_char": 1981, "text_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58"}
    experimental_model
    Seven-day potassium-oxonate hyperuricemia model
    exposure
    Mangiferin 50, 100 or 200 mg/kg orally
    limitations
    Animal expression findings; no human carnitine-retention or gout-treatment conclusion.
    nutrient_topic
    Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
    organism
    Mus musculus
    plain_language
    Another urate transporter responded.
    primary_references
    [mangiferin-p21348301] [Mangiferin promotes uric acid excretion and kidney function improvement and modulates related renal transporters in hyperuricemic mice]. (2010). https://pubmed.ncbi.nlm.nih.gov/21348301/
    tissue_or_cell_type
    Kidney

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 978–989

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Seven-day potassium-oxonate hyperuricemia model · source_derived_draft · unverified_draft

    ### mangiferin-mouse-slc2a9 Mangiferin reduced renal Mouse glucose transporter 9 / Slc2a9 expression in the hyperuricemic mice. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Another urate transporter responded. organism: Mus musculus tissue_or_cell_type: Kidney experimental_model: Seven-day potassium-oxonate hyperuricemia model limitations: Animal expression findings; no human carnitine-retention or gout-treatment conclusion. exposure: Mangiferin 50, 100 or 200 mg/kg orally evidence_span: {"source_cache": "artifacts/mangiferin-research/21348301.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58", "start_char": 0, "end_char": 1981, "text_sha256": "7c27a677db4a27cc088cfd83ce3506ffdfd866ef91250732b1dd2287d4cf4b58"} [mangiferin-p21348301] [Mangiferin promotes uric acid excretion and kidney function improvement and modulates related renal transporters in hyperuricemic mice]. (2010). https://pubmed.ncbi.nlm.nih.gov/21348301/
    Complete structured claim and evidence

  3. No change in renal Mouse glucose transporter 9 / Slc2a9 expression was detected in the nephropathy model.

    Mangiferin → Mouse glucose transporter 9 / Slc2a9 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mangiferin-research/32116724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5", "start_char": 0, "end_char": 1810, "text_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5"}
    experimental_model
    Mouse hyperuricemic nephropathy experiment
    exposure
    Mangiferin in the study-specific nephropathy model
    limitations
    Different model from earlier oxonate experiments; associations do not prove AQP2 mediation. Null expression results do not rule out changes in activity.
    nutrient_topic
    Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
    organism
    Mus musculus
    plain_language
    This transport-protein response differed from the earlier hyperuricemia model.
    primary_references
    [mangiferin-p32116724] Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion. (2020). https://pubmed.ncbi.nlm.nih.gov/32116724/ DOI: 10.3389/fphar.2020.00049
    tissue_or_cell_type
    Kidney and metabolic-cage urine

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 1056–1067

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse hyperuricemic nephropathy experiment · source_derived_draft · unverified_draft

    ### mangiferin-mouse-slc2a9-null No change in renal Mouse glucose transporter 9 / Slc2a9 expression was detected in the nephropathy model. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This transport-protein response differed from the earlier hyperuricemia model. organism: Mus musculus tissue_or_cell_type: Kidney and metabolic-cage urine experimental_model: Mouse hyperuricemic nephropathy experiment limitations: Different model from earlier oxonate experiments; associations do not prove AQP2 mediation. Null expression results do not rule out changes in activity. exposure: Mangiferin in the study-specific nephropathy model evidence_span: {"source_cache": "artifacts/mangiferin-research/32116724.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5", "start_char": 0, "end_char": 1810, "text_sha256": "f18a5e0ea5cd0f421555870fbfcaede81ecb40cd62a7de27f356d6addf076ee5"} [mangiferin-p32116724] Mangiferin Ameliorates Hyperuricemic Nephropathy Which Is Associated With Downregulation of AQP2 and Increased Urinary Uric Acid Excretion. (2020). https://pubmed.ncbi.nlm.nih.gov/32116724/ DOI: 10.3389/fphar.2020.00049
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards