Component

Small-intestinal tissue metformin accumulation

Small-intestinal tissue metformin accumulation. Species, exposure and limitations are retained in each linked claim.

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

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. The greatest accumulation of metformin occurred in small-intestinal tissue, exceeding 1000 micromol/kg wet weight at 0.5-2 hours, and intravenous metformin was also selectively accumulated there.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/8165821.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "60471d633165552bd5a5c4e9e5ff05686d069ceedfd367ca892828c66d116bbd", "start_char": 0, "end_char": 1265, "text_sha256": "60471d633165552bd5a5c4e9e5ff05686d069ceedfd367ca892828c66d116bbd"}
    experimental_model
    Radiolabelled metformin tissue distribution in normal and streptozotocin-diabetic mice
    exposure
    Oral metformin 50 mg/kg with 14C-metformin, and a separate intravenous study
    limitations
    Mouse tissue concentrations at a single dose level. Metformin is not metabolised, so these are distribution rather than metabolic findings.
    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
    The gut wall holds far more of the drug than blood does, even when the dose is given by vein.
    primary_references
    [metformin-p8165821] Accumulation of metformin by tissues of the normal and diabetic mouse. (1994). https://pubmed.ncbi.nlm.nih.gov/8165821/ DOI: 10.3109/00498259409043220
    tissue_or_cell_type
    Small intestine, stomach, colon, salivary gland, kidney, liver, heart and skeletal muscle

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 294–305

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Radiolabelled metformin tissue distribution in normal and streptozotocin-diabetic mice · source_derived_draft · unverified_draft

    ### metformin-intestinal-depot The greatest accumulation of metformin occurred in small-intestinal tissue, exceeding 1000 micromol/kg wet weight at 0.5-2 hours, and intravenous metformin was also selectively accumulated there. 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 gut wall holds far more of the drug than blood does, even when the dose is given by vein. organism: Mouse tissue_or_cell_type: Small intestine, stomach, colon, salivary gland, kidney, liver, heart and skeletal muscle experimental_model: Radiolabelled metformin tissue distribution in normal and streptozotocin-diabetic mice limitations: Mouse tissue concentrations at a single dose level. Metformin is not metabolised, so these are distribution rather than metabolic findings. exposure: Oral metformin 50 mg/kg with 14C-metformin, and a separate intravenous study evidence_span: {"source_cache": "artifacts/metformin-research/8165821.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "60471d633165552bd5a5c4e9e5ff05686d069ceedfd367ca892828c66d116bbd", "start_char": 0, "end_char": 1265, "text_sha256": "60471d633165552bd5a5c4e9e5ff05686d069ceedfd367ca892828c66d116bbd"} [metformin-p8165821] Accumulation of metformin by tissues of the normal and diabetic mouse. (1994). https://pubmed.ncbi.nlm.nih.gov/8165821/ DOI: 10.3109/00498259409043220
    Complete structured claim and evidence
  2. Distribution of metformin to the small intestine was also decreased in Oct1(-/-) mice, whereas renal distribution and urinary excretion differed only minimally.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/metformin-research/12130709.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2bd4b1f58d2b0b30807a1a521298f4713a86049a53f62cfc5d6463927644d82b", "start_char": 0, "end_char": 1411, "text_sha256": "2bd4b1f58d2b0b30807a1a521298f4713a86049a53f62cfc5d6463927644d82b"}
    experimental_model
    Rat Oct1-transfected CHO uptake kinetics and Oct1-knockout mouse tissue distribution
    exposure
    Intravenous metformin in Oct1(-/-) and Oct1(+/+) mice; buformin and phenformin compared in vitro
    limitations
    Transporter assignment in rodents. Affinities are assay values, not human tissue concentrations, and renal handling was governed by other transporters in this model.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Rat transporter in CHO cells; mouse in vivo
    plain_language
    The same carrier matters in the gut wall, while the kidney uses different routes.
    primary_references
    [metformin-p12130709] Involvement of organic cation transporter 1 in hepatic and intestinal distribution of metformin. (2002). https://pubmed.ncbi.nlm.nih.gov/12130709/ DOI: 10.1124/jpet.102.034140
    tissue_or_cell_type
    Liver, small intestine and kidney
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 112–123

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat Oct1-transfected CHO uptake kinetics and Oct1-knockout mouse tissue distribution · source_derived_draft · unverified_draft

    ### metformin-oct1-null-intestine Distribution of metformin to the small intestine was also decreased in Oct1(-/-) mice, whereas renal distribution and urinary excretion differed only minimally. 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: The same carrier matters in the gut wall, while the kidney uses different routes. organism: Rat transporter in CHO cells; mouse in vivo tissue_or_cell_type: Liver, small intestine and kidney experimental_model: Rat Oct1-transfected CHO uptake kinetics and Oct1-knockout mouse tissue distribution limitations: Transporter assignment in rodents. Affinities are assay values, not human tissue concentrations, and renal handling was governed by other transporters in this model. exposure: Intravenous metformin in Oct1(-/-) and Oct1(+/+) mice; buformin and phenformin compared in vitro evidence_span: {"source_cache": "artifacts/metformin-research/12130709.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "2bd4b1f58d2b0b30807a1a521298f4713a86049a53f62cfc5d6463927644d82b", "start_char": 0, "end_char": 1411, "text_sha256": "2bd4b1f58d2b0b30807a1a521298f4713a86049a53f62cfc5d6463927644d82b"} [metformin-p12130709] Involvement of organic cation transporter 1 in hepatic and intestinal distribution of metformin. (2002). https://pubmed.ncbi.nlm.nih.gov/12130709/ DOI: 10.1124/jpet.102.034140
    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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