Component

Experimental Oct1-null mouse genotype

Experimental Oct1-null mouse genotype. Species, exposure and limitations are retained in each linked claim.

4 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 it acts on

  1. In mouse hepatocytes, deletion of Oct1 reduced the effect of metformin on AMPK phosphorylation and on gluconeogenesis.

    Experimental Oct1-null mouse genotype → AMP-activated protein kinase complexes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/metformin-research/17476361.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e8d05affc6b49c7273e21804d2ad9092ca826c8d81431ee093c6215f18f0bce1", "start_char": 0, "end_char": 1361, "text_sha256": "e8d05affc6b49c7273e21804d2ad9092ca826c8d81431ee093c6215f18f0bce1"}
    experimental_model
    Oct1-knockout mouse hepatocytes and mice, human variant uptake assays, and human glucose-tolerance studies
    exposure
    Metformin in Oct1-deficient mice; seven non-synonymous human OCT1 variants; clinical glucose tolerance tests
    limitations
    Pharmacogenetic association with drug response, not proof that OCT1 genotype should guide prescribing.
    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 and human, stated per record
    plain_language
    If the drug cannot get in, the energy sensor inside is not switched on.
    primary_references
    [metformin-p17476361] Effect of genetic variation in the organic cation transporter 1 (OCT1) on metformin action. (2007). https://pubmed.ncbi.nlm.nih.gov/17476361/ DOI: 10.1172/jci30558
    tissue_or_cell_type
    Hepatocytes and whole body
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 138–149

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oct1-knockout mouse hepatocytes and mice, human variant uptake assays, and human glucose-tolerance studies · source_derived_draft · unverified_draft

    ### metformin-oct1-null-ampk In mouse hepatocytes, deletion of Oct1 reduced the effect of metformin on AMPK phosphorylation and on gluconeogenesis. 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: If the drug cannot get in, the energy sensor inside is not switched on. organism: Mouse and human, stated per record tissue_or_cell_type: Hepatocytes and whole body experimental_model: Oct1-knockout mouse hepatocytes and mice, human variant uptake assays, and human glucose-tolerance studies limitations: Pharmacogenetic association with drug response, not proof that OCT1 genotype should guide prescribing. exposure: Metformin in Oct1-deficient mice; seven non-synonymous human OCT1 variants; clinical glucose tolerance tests evidence_span: {"source_cache": "artifacts/metformin-research/17476361.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e8d05affc6b49c7273e21804d2ad9092ca826c8d81431ee093c6215f18f0bce1", "start_char": 0, "end_char": 1361, "text_sha256": "e8d05affc6b49c7273e21804d2ad9092ca826c8d81431ee093c6215f18f0bce1"} [metformin-p17476361] Effect of genetic variation in the organic cation transporter 1 (OCT1) on metformin action. (2007). https://pubmed.ncbi.nlm.nih.gov/17476361/ DOI: 10.1172/jci30558
    Complete structured claim and evidence

  2. In Oct1-deficient mice the glucose-lowering effects of metformin were completely abolished.

    Experimental Oct1-null mouse genotype → Serum glucose concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/metformin-research/17476361.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e8d05affc6b49c7273e21804d2ad9092ca826c8d81431ee093c6215f18f0bce1", "start_char": 0, "end_char": 1361, "text_sha256": "e8d05affc6b49c7273e21804d2ad9092ca826c8d81431ee093c6215f18f0bce1"}
    experimental_model
    Oct1-knockout mouse hepatocytes and mice, human variant uptake assays, and human glucose-tolerance studies
    exposure
    Metformin in Oct1-deficient mice; seven non-synonymous human OCT1 variants; clinical glucose tolerance tests
    limitations
    Pharmacogenetic association with drug response, not proof that OCT1 genotype should guide prescribing.
    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 and human, stated per record
    plain_language
    The whole glucose effect depended on the drug reaching the liver in this model.
    primary_references
    [metformin-p17476361] Effect of genetic variation in the organic cation transporter 1 (OCT1) on metformin action. (2007). https://pubmed.ncbi.nlm.nih.gov/17476361/ DOI: 10.1172/jci30558
    tissue_or_cell_type
    Hepatocytes and whole body
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 151–162

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oct1-knockout mouse hepatocytes and mice, human variant uptake assays, and human glucose-tolerance studies · source_derived_draft · unverified_draft

    ### metformin-oct1-null-glucose In Oct1-deficient mice the glucose-lowering effects of metformin were completely abolished. 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 whole glucose effect depended on the drug reaching the liver in this model. organism: Mouse and human, stated per record tissue_or_cell_type: Hepatocytes and whole body experimental_model: Oct1-knockout mouse hepatocytes and mice, human variant uptake assays, and human glucose-tolerance studies limitations: Pharmacogenetic association with drug response, not proof that OCT1 genotype should guide prescribing. exposure: Metformin in Oct1-deficient mice; seven non-synonymous human OCT1 variants; clinical glucose tolerance tests evidence_span: {"source_cache": "artifacts/metformin-research/17476361.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e8d05affc6b49c7273e21804d2ad9092ca826c8d81431ee093c6215f18f0bce1", "start_char": 0, "end_char": 1361, "text_sha256": "e8d05affc6b49c7273e21804d2ad9092ca826c8d81431ee093c6215f18f0bce1"} [metformin-p17476361] Effect of genetic variation in the organic cation transporter 1 (OCT1) on metformin action. (2007). https://pubmed.ncbi.nlm.nih.gov/17476361/ DOI: 10.1172/jci30558
    Complete structured claim and evidence

  3. Distribution of metformin to the small intestine was also decreased in Oct1(-/-) mice, whereas renal distribution and urinary excretion differed only minimally.

    Experimental Oct1-null mouse genotype → Small-intestinal tissue metformin accumulation source_derived_draftungraded
    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

  4. Liver distribution of metformin in Oct1(-/-) mice was more than 30-fold lower than in Oct1(+/+) mice and was accounted for by the extracellular space.

    Experimental Oct1-null mouse genotype → Hepatic metformin accumulation source_derived_draftungraded
    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
    Without the transporter the drug stays outside the liver cells rather than inside them.
    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 99–110

    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-liver Liver distribution of metformin in Oct1(-/-) mice was more than 30-fold lower than in Oct1(+/+) mice and was accounted for by the extracellular space. 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: Without the transporter the drug stays outside the liver cells rather than inside them. 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

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