Component

Mouse organic cation transporter 1 / Oct1

Mouse organic cation transporter 1 / Oct1. Species, exposure and limitations are retained in each linked claim.

8 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. Oct1 deletion reduced hepatic thiamine-dependent enzyme activity, including pyruvate dehydrogenase, in mice.

    Mouse organic cation transporter 1 / Oct1 → Mouse hepatic pyruvate dehydrogenase activity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/berberine-research/29659562.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "10efb675e4e0cf5cea9c8607b6b2a5e3ad77c383f8b0a55efff5ed6d163be558", "start_char": 0, "end_char": 1652, "text_sha256": "10efb675e4e0cf5cea9c8607b6b2a5e3ad77c383f8b0a55efff5ed6d163be558"}
    experimental_model
    Mouse gene deletion and dietary depletion, with human genetic associations
    exposure
    Oct1 deletion or a thiamine-deficient diet
    limitations
    Mouse Oct1 deletion is not pharmacological berberine inhibition; human genetic associations do not establish berberine-induced thiamine depletion.
    nutrient_topic
    Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
    organism
    Mice for causal thiamine and PDH experiments
    plain_language
    A transporter can affect how the liver uses a vitamin-dependent fuel pathway.
    primary_references
    [berberine-p29659562] Organic cation transporter 1 (OCT1) modulates multiple cardiometabolic traits through effects on hepatic thiamine content. (2018). https://pubmed.ncbi.nlm.nih.gov/29659562/ DOI: 10.1371/journal.pbio.2002907
    tissue_or_cell_type
    Hepatic thiamine-dependent metabolism
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 311–322

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse gene deletion and dietary depletion, with human genetic associations · source_derived_draft · unverified_draft

    ### berberine-oct1-pdh Oct1 deletion reduced hepatic thiamine-dependent enzyme activity, including pyruvate dehydrogenase, in mice. Condition category: machinery_impairment nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A transporter can affect how the liver uses a vitamin-dependent fuel pathway. organism: Mice for causal thiamine and PDH experiments tissue_or_cell_type: Hepatic thiamine-dependent metabolism experimental_model: Mouse gene deletion and dietary depletion, with human genetic associations limitations: Mouse Oct1 deletion is not pharmacological berberine inhibition; human genetic associations do not establish berberine-induced thiamine depletion. exposure: Oct1 deletion or a thiamine-deficient diet evidence_span: {"source_cache": "artifacts/berberine-research/29659562.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "10efb675e4e0cf5cea9c8607b6b2a5e3ad77c383f8b0a55efff5ed6d163be558", "start_char": 0, "end_char": 1652, "text_sha256": "10efb675e4e0cf5cea9c8607b6b2a5e3ad77c383f8b0a55efff5ed6d163be558"} [berberine-p29659562] Organic cation transporter 1 (OCT1) modulates multiple cardiometabolic traits through effects on hepatic thiamine content. (2018). https://pubmed.ncbi.nlm.nih.gov/29659562/ DOI: 10.1371/journal.pbio.2002907
    Complete structured claim and evidence

What acts on it

  1. The affinity for metformin was 4.9-fold lower in human than in mouse OCT1, giving a 6.5-fold lower intrinsic clearance and an estimated liver-to-blood partition coefficient of 3.34 in human compared with 14.4 in mouse.

    Human organic cation transporter 1 / OCT1 / SLC22A1 → Mouse organic cation transporter 1 / Oct1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/33037045.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "861e39b20a78d5d85a01c5de0febda8bf1c400de4fa8ef1e6944707521604c67", "start_char": 0, "end_char": 2296, "text_sha256": "861e39b20a78d5d85a01c5de0febda8bf1c400de4fa8ef1e6944707521604c67"}
    experimental_model
    Stably transfected HEK293 cells comparing human and mouse OCT1, with human-mouse chimeras and homology modelling
    exposure
    Metformin and thiamine uptake kinetics; transmembrane-helix substitutions
    limitations
    A species comparison of transport affinity. It limits how far mouse OCT1 results can be read as human ones; it is not itself a human tissue 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 and mouse orthologues side by side
    plain_language
    The mouse liver concentrates this drug far more than the human liver does.
    primary_references
    [metformin-p33037045] Differences in Metformin and Thiamine Uptake between Human and Mouse Organic Cation Transporter 1: Structural Determinants and Potential Consequences for Intrahepatic Concentrations. (2020). https://pubmed.ncbi.nlm.nih.gov/33037045/ DOI: 10.1124/dmd.120.000170
    tissue_or_cell_type
    Hepatic uptake

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 320–331

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Stably transfected HEK293 cells comparing human and mouse OCT1, with human-mouse chimeras and homology modelling · source_derived_draft · unverified_draft

    ### metformin-oct1-species-metformin The affinity for metformin was 4.9-fold lower in human than in mouse OCT1, giving a 6.5-fold lower intrinsic clearance and an estimated liver-to-blood partition coefficient of 3.34 in human compared with 14.4 in mouse. 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 mouse liver concentrates this drug far more than the human liver does. organism: Human and mouse orthologues side by side tissue_or_cell_type: Hepatic uptake experimental_model: Stably transfected HEK293 cells comparing human and mouse OCT1, with human-mouse chimeras and homology modelling limitations: A species comparison of transport affinity. It limits how far mouse OCT1 results can be read as human ones; it is not itself a human tissue measurement. exposure: Metformin and thiamine uptake kinetics; transmembrane-helix substitutions evidence_span: {"source_cache": "artifacts/metformin-research/33037045.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "861e39b20a78d5d85a01c5de0febda8bf1c400de4fa8ef1e6944707521604c67", "start_char": 0, "end_char": 2296, "text_sha256": "861e39b20a78d5d85a01c5de0febda8bf1c400de4fa8ef1e6944707521604c67"} [metformin-p33037045] Differences in Metformin and Thiamine Uptake between Human and Mouse Organic Cation Transporter 1: Structural Determinants and Potential Consequences for Intrahepatic Concentrations. (2020). https://pubmed.ncbi.nlm.nih.gov/33037045/ DOI: 10.1124/dmd.120.000170
    Complete structured claim and evidence

  2. The affinity for thiamine was 9.5-fold lower in human than in mouse OCT1.

    Human organic cation transporter 1 / OCT1 / SLC22A1 → Mouse organic cation transporter 1 / Oct1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/33037045.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "861e39b20a78d5d85a01c5de0febda8bf1c400de4fa8ef1e6944707521604c67", "start_char": 0, "end_char": 2296, "text_sha256": "861e39b20a78d5d85a01c5de0febda8bf1c400de4fa8ef1e6944707521604c67"}
    experimental_model
    Stably transfected HEK293 cells comparing human and mouse OCT1, with human-mouse chimeras and homology modelling
    exposure
    Metformin and thiamine uptake kinetics; transmembrane-helix substitutions
    limitations
    A species comparison of transport affinity. It limits how far mouse OCT1 results can be read as human ones; it is not itself a human tissue 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 and mouse orthologues side by side
    plain_language
    The same species gap applies to the vitamin the transporter carries.
    primary_references
    [metformin-p33037045] Differences in Metformin and Thiamine Uptake between Human and Mouse Organic Cation Transporter 1: Structural Determinants and Potential Consequences for Intrahepatic Concentrations. (2020). https://pubmed.ncbi.nlm.nih.gov/33037045/ DOI: 10.1124/dmd.120.000170
    tissue_or_cell_type
    Hepatic uptake

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 333–344

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Stably transfected HEK293 cells comparing human and mouse OCT1, with human-mouse chimeras and homology modelling · source_derived_draft · unverified_draft

    ### metformin-oct1-species-thiamine The affinity for thiamine was 9.5-fold lower in human than in mouse OCT1. 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 same species gap applies to the vitamin the transporter carries. organism: Human and mouse orthologues side by side tissue_or_cell_type: Hepatic uptake experimental_model: Stably transfected HEK293 cells comparing human and mouse OCT1, with human-mouse chimeras and homology modelling limitations: A species comparison of transport affinity. It limits how far mouse OCT1 results can be read as human ones; it is not itself a human tissue measurement. exposure: Metformin and thiamine uptake kinetics; transmembrane-helix substitutions evidence_span: {"source_cache": "artifacts/metformin-research/33037045.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "861e39b20a78d5d85a01c5de0febda8bf1c400de4fa8ef1e6944707521604c67", "start_char": 0, "end_char": 2296, "text_sha256": "861e39b20a78d5d85a01c5de0febda8bf1c400de4fa8ef1e6944707521604c67"} [metformin-p33037045] Differences in Metformin and Thiamine Uptake between Human and Mouse Organic Cation Transporter 1: Structural Determinants and Potential Consequences for Intrahepatic Concentrations. (2020). https://pubmed.ncbi.nlm.nih.gov/33037045/ DOI: 10.1124/dmd.120.000170
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Wild-type mice fed thiamine-deficient diet for 10 days had higher plasma glucose, hepatic glucose and hepatic glycogen.

    Thiamine (vitamin B1) → Plasma glucose concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    curation_topic
    thiamine · Thiamine (vitamin B1)
    experimental_condition
    5 mg/kg control diet 0 mg/kg added thiamine diet · Thiamine (vitamin B1) Condition belongs to the full experimental contrast; do not separate a joint intervention.
    experimental_contrast
    {"intervention": "0 mg/kg added thiamine diet", "comparator": "5 mg/kg control diet", "endpoint": "Plasma glucose", "effect_direction": "increase", "combination": "single", "conditions": [{"entity_slug": "thiamine", "state": "0 mg/kg added thiamine diet"}]} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Mouse dietary experiment, figure 5; 16-hour fast before sampling; n=4 per genotype/treatment
    limitations
    A separate dietary arm of the OCT1 paper; not a berberine exposure experiment or direct proof of human diabetes causation.
    primary_references
    OCT1 cardiometabolic study 2018; DOI:10.1371/journal.pbio.2002907; PMID:29659562; https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2002907
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Diabetes cascade: targeted primary-source supplement · lines 36–36

    See claim-local references; curated paraphrases reviewed 2026-09-20. · supports · Mouse dietary experiment, figure 5; 16-hour fast before sampling; n=4 per genotype/treatment · source_derived_draft · unverified_draft

    Wild-type mice fed thiamine-deficient diet for 10 days had higher plasma glucose, hepatic glucose and hepatic glycogen. Model: Mouse dietary experiment, figure 5; 16-hour fast before sampling; n=4 per genotype/treatment. Limits: A separate dietary arm of the OCT1 paper; not a berberine exposure experiment or direct proof of human diabetes causation. Primary reference: OCT1 cardiometabolic study 2018; DOI:10.1371/journal.pbio.2002907; PMID:29659562; https://journals.plos.org/plosbiology/article?id=10.1371/journal.pbio.2002907
    Complete structured claim and evidence

  2. Human OCT1 transported thiamine with approximately 9.5-fold lower affinity than mouse Oct1.

    Human organic cation transporter 1 / OCT1 / SLC22A1 → Thiamine (vitamin B1) source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/berberine-research/33037045.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "61d53435dfc952ba419da91767e79c07d75e2a432d9d4a2afd0d8d2560d570fd", "start_char": 0, "end_char": 2298, "text_sha256": "61d53435dfc952ba419da91767e79c07d75e2a432d9d4a2afd0d8d2560d570fd"}
    experimental_model
    Human versus mouse transporter kinetics in transfected HEK293 cells
    exposure
    Thiamine and metformin transport; transporter chimeras
    limitations
    Human OCT1 affinity for thiamine was substantially lower than mouse Oct1. This is a shared-transporter connection, not proof berberine causes B1 deficiency.
    nutrient_topic
    Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
    organism
    Human OCT1 and mouse Oct1
    plain_language
    Vitamin B1 shares this transporter, but the mouse and human versions behave differently.
    primary_references
    [berberine-p33037045] Differences in Metformin and Thiamine Uptake between Human and Mouse Organic Cation Transporter 1: Structural Determinants and Potential Consequences for Intrahepatic Concentrations. (2020). https://pubmed.ncbi.nlm.nih.gov/33037045/ DOI: 10.1124/dmd.120.000170
    tissue_or_cell_type
    Cellular thiamine uptake
    transport_effect
    raises A species-affinity comparison, but the measurement is thiamine carried into the expressing cell, which stands for the hepatocyte.
    transport_pool
    the hepatocyte interior A species-affinity comparison, but the measurement is thiamine carried into the expressing cell, which stands for the hepatocyte.

    Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 298–309

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human versus mouse transporter kinetics in transfected HEK293 cells · source_derived_draft · unverified_draft

    ### berberine-human-thiamine-transport Human OCT1 transported thiamine with approximately 9.5-fold lower affinity than mouse Oct1. Condition category: normal nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin B1 shares this transporter, but the mouse and human versions behave differently. organism: Human OCT1 and mouse Oct1 tissue_or_cell_type: Cellular thiamine uptake experimental_model: Human versus mouse transporter kinetics in transfected HEK293 cells limitations: Human OCT1 affinity for thiamine was substantially lower than mouse Oct1. This is a shared-transporter connection, not proof berberine causes B1 deficiency. exposure: Thiamine and metformin transport; transporter chimeras evidence_span: {"source_cache": "artifacts/berberine-research/33037045.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "61d53435dfc952ba419da91767e79c07d75e2a432d9d4a2afd0d8d2560d570fd", "start_char": 0, "end_char": 2298, "text_sha256": "61d53435dfc952ba419da91767e79c07d75e2a432d9d4a2afd0d8d2560d570fd"} [berberine-p33037045] Differences in Metformin and Thiamine Uptake between Human and Mouse Organic Cation Transporter 1: Structural Determinants and Potential Consequences for Intrahepatic Concentrations. (2020). https://pubmed.ncbi.nlm.nih.gov/33037045/ DOI: 10.1124/dmd.120.000170
    Complete structured claim and evidence

  3. 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

  4. 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

  5. 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

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