Component

Renal tubular secretion of metformin

Renal tubular secretion of metformin. 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. Renal clearance and renal secretory clearance of metformin in Mate1(-/-) mice were approximately 18% and 14% of those in wild-type mice.

    Experimental Mate1-null mouse genotype → Renal tubular secretion of metformin source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/metformin-research/19332510.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "79d5ec9a2d5c447e349d0e00742a2f2a05a3c9f9581199c4dde1f9b7910c029c", "start_char": 0, "end_char": 1536, "text_sha256": "79d5ec9a2d5c447e349d0e00742a2f2a05a3c9f9581199c4dde1f9b7910c029c"}
    experimental_model
    Targeted disruption of the murine Mate1 gene with metformin pharmacokinetics
    exposure
    Single intravenous metformin 5 mg/kg in Mate1(-/-) and Mate1(+/+) mice
    limitations
    Mouse pharmacokinetics; it does not establish a human exposure threshold or a clinical toxicity risk.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Mouse
    plain_language
    Removing the exit pump left most of the drug in the body.
    primary_references
    [metformin-p19332510] Targeted disruption of the multidrug and toxin extrusion 1 (mate1) gene in mice reduces renal secretion of metformin. (2009). https://pubmed.ncbi.nlm.nih.gov/19332510/ DOI: 10.1124/mol.109.056242
    tissue_or_cell_type
    Kidney and liver
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 268–279

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Targeted disruption of the murine Mate1 gene with metformin pharmacokinetics · source_derived_draft · unverified_draft

    ### metformin-mate1-null-clearance Renal clearance and renal secretory clearance of metformin in Mate1(-/-) mice were approximately 18% and 14% of those in wild-type mice. Condition category: machinery_impairment nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: Removing the exit pump left most of the drug in the body. organism: Mouse tissue_or_cell_type: Kidney and liver experimental_model: Targeted disruption of the murine Mate1 gene with metformin pharmacokinetics limitations: Mouse pharmacokinetics; it does not establish a human exposure threshold or a clinical toxicity risk. exposure: Single intravenous metformin 5 mg/kg in Mate1(-/-) and Mate1(+/+) mice evidence_span: {"source_cache": "artifacts/metformin-research/19332510.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "79d5ec9a2d5c447e349d0e00742a2f2a05a3c9f9581199c4dde1f9b7910c029c", "start_char": 0, "end_char": 1536, "text_sha256": "79d5ec9a2d5c447e349d0e00742a2f2a05a3c9f9581199c4dde1f9b7910c029c"} [metformin-p19332510] Targeted disruption of the multidrug and toxin extrusion 1 (mate1) gene in mice reduces renal secretion of metformin. (2009). https://pubmed.ncbi.nlm.nih.gov/19332510/ DOI: 10.1124/mol.109.056242
    Complete structured claim and evidence

  2. hMATE2-K is expressed predominantly in the kidney and localises to the brush-border membranes of proximal tubules, where it transports metformin with a Km of 1.05 mM.

    Human kidney-specific multidrug and toxin extrusion protein 2 / MATE2-K / SLC47A2 → Renal tubular secretion of metformin source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/16807400.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "681a4ea4ae958690a5a707397ee3a2b254ebeaab832292f14beea5716e58a9b2", "start_char": 0, "end_char": 1742, "text_sha256": "681a4ea4ae958690a5a707397ee3a2b254ebeaab832292f14beea5716e58a9b2"}
    experimental_model
    Cloning, expression and kinetic characterisation of hMATE2-K from human kidney
    exposure
    Proton-gradient-dependent antiport; ammonium-chloride-induced intracellular acidification
    limitations
    Kidney-specific expression and substrate list from a transfected system; thiamine appears in the same substrate list, which is an observation about the transporter, not a drug-nutrient competition measurement.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Human transporter
    plain_language
    The exit route sits on the urine-facing side of the kidney tubule.
    primary_references
    [metformin-p16807400] Identification and functional characterization of a new human kidney-specific H+/organic cation antiporter, kidney-specific multidrug and toxin extrusion 2. (2006). https://pubmed.ncbi.nlm.nih.gov/16807400/ DOI: 10.1681/asn.2006030205
    tissue_or_cell_type
    Renal proximal-tubule brush-border membrane

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 242–253

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cloning, expression and kinetic characterisation of hMATE2-K from human kidney · source_derived_draft · unverified_draft

    ### metformin-mate2k-kidney hMATE2-K is expressed predominantly in the kidney and localises to the brush-border membranes of proximal tubules, where it transports metformin with a Km of 1.05 mM. Condition category: normal nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: The exit route sits on the urine-facing side of the kidney tubule. organism: Human transporter tissue_or_cell_type: Renal proximal-tubule brush-border membrane experimental_model: Cloning, expression and kinetic characterisation of hMATE2-K from human kidney limitations: Kidney-specific expression and substrate list from a transfected system; thiamine appears in the same substrate list, which is an observation about the transporter, not a drug-nutrient competition measurement. exposure: Proton-gradient-dependent antiport; ammonium-chloride-induced intracellular acidification evidence_span: {"source_cache": "artifacts/metformin-research/16807400.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "681a4ea4ae958690a5a707397ee3a2b254ebeaab832292f14beea5716e58a9b2", "start_char": 0, "end_char": 1742, "text_sha256": "681a4ea4ae958690a5a707397ee3a2b254ebeaab832292f14beea5716e58a9b2"} [metformin-p16807400] Identification and functional characterization of a new human kidney-specific H+/organic cation antiporter, kidney-specific multidrug and toxin extrusion 2. (2006). https://pubmed.ncbi.nlm.nih.gov/16807400/ DOI: 10.1681/asn.2006030205
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Ten of fourteen patients with lactic acidosis during metformin treatment had significant metformin accumulation, generally because metformin was not withdrawn despite conditions affecting its renal elimination, and serum creatinine correlated positively with plasma metformin.

    Serum creatinine concentration → Plasma metformin exposure source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/metformin-research/7555503.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c960785146be30aa07921ceef25600c044dd421566e708cdc5c45bffccb0e301", "start_char": 0, "end_char": 2221, "text_sha256": "c960785146be30aa07921ceef25600c044dd421566e708cdc5c45bffccb0e301"}
    experimental_model
    Plasma metformin measurement by HPLC in 14 people with lactic acidosis during metformin treatment
    exposure
    Chronic metformin with intercurrent renal failure
    limitations
    A case series in an intensive-care setting. It argues against a simple dose-toxicity relationship; the numbers are small.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Human
    plain_language
    When the kidneys fail and the drug is not stopped, it builds up.
    primary_references
    [metformin-p7555503] Role of metformin accumulation in metformin-associated lactic acidosis. (1995). https://pubmed.ncbi.nlm.nih.gov/7555503/ DOI: 10.2337/diacare.18.6.779
    tissue_or_cell_type
    Whole body
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 1425–1436

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Plasma metformin measurement by HPLC in 14 people with lactic acidosis during metformin treatment · source_derived_draft · unverified_draft

    ### metformin-accumulation-lactic-acidosis Ten of fourteen patients with lactic acidosis during metformin treatment had significant metformin accumulation, generally because metformin was not withdrawn despite conditions affecting its renal elimination, and serum creatinine correlated positively with plasma metformin. Condition category: machinery_impairment nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: When the kidneys fail and the drug is not stopped, it builds up. organism: Human tissue_or_cell_type: Whole body experimental_model: Plasma metformin measurement by HPLC in 14 people with lactic acidosis during metformin treatment limitations: A case series in an intensive-care setting. It argues against a simple dose-toxicity relationship; the numbers are small. exposure: Chronic metformin with intercurrent renal failure evidence_span: {"source_cache": "artifacts/metformin-research/7555503.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c960785146be30aa07921ceef25600c044dd421566e708cdc5c45bffccb0e301", "start_char": 0, "end_char": 2221, "text_sha256": "c960785146be30aa07921ceef25600c044dd421566e708cdc5c45bffccb0e301"} [metformin-p7555503] Role of metformin accumulation in metformin-associated lactic acidosis. (1995). https://pubmed.ncbi.nlm.nih.gov/7555503/ DOI: 10.2337/diacare.18.6.779
    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.

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