Component
Human organic cation transporter 2 / OCT2 / SLC22A2
Human organic cation transporter 2 / OCT2 / SLC22A2. Species, exposure and limitations are retained in each linked claim.
4 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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
Human OCT2 mediated pH- and concentration-dependent agmatine transport, with Km 1.84 ± 0.38 mM.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Matched human transporter expression systems.
- limitations
- Protein expression and assay conditions affect comparison with actual kidney clearance.
- nutrient_topic
- Agmatine Sulfate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Agmatine Sulfate
- plain_language
- Another organic-cation transporter handles agmatine more avidly in this assay.
- primary_references
- OCT2 and MATE1 provide bidirectional agmatine transport. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21128598/ · DOI 10.1021/mp100180a
- transport_effect
- raises pH- and concentration-dependent agmatine transport into the expressing cell.
- transport_pool
- the expressing cell pH- and concentration-dependent agmatine transport into the expressing cell.
Agmatine Sulfate: transport, guanidino metabolism, ion channels and cross-nutrient mechanisms (2026-09-20) · lines 28–34
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Matched human transporter expression systems. · source_derived_draft · unverified_draft
## agmatine-sulfate-oct2 Another organic-cation transporter handles agmatine more avidly in this assay. Human OCT2 mediated pH- and concentration-dependent agmatine transport, with Km 1.84 ± 0.38 mM. Model: Matched human transporter expression systems. Limitations: Protein expression and assay conditions affect comparison with actual kidney clearance. Evidence access: Primary abstract OCT2 and MATE1 provide bidirectional agmatine transport. · 2011 · https://pubmed.ncbi.nlm.nih.gov/21128598/ · DOI 10.1021/mp100180a
Complete structured claim and evidenceHuman OCT2 transported berberine in transfected cells, with reported Km 4.4 micromolar.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/berberine-research/18157518.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34651ed2e9ce3c38b6042e616b5c36d932fe6f1099c627d1b5403b338eae7b2b", "start_char": 0, "end_char": 1918, "text_sha256": "34651ed2e9ce3c38b6042e616b5c36d932fe6f1099c627d1b5403b338eae7b2b"}
- experimental_model
- Polarized transporter-transfected MDCKII cells
- exposure
- Berberine transport kinetics and transporter inhibition
- limitations
- Engineered system, not direct evidence for human oral bioavailability or a universal transport bottleneck.
- nutrient_topic
- Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
- organism
- Human OCT1, OCT2 and ABCB1 in engineered canine cells
- plain_language
- Berberine uses a separately identified organic-cation uptake transporter.
- primary_references
- [berberine-p18157518] Vectorial transport of the plant alkaloid berberine by double-transfected cells expressing the human organic cation transporter 1 (OCT1, SLC22A1) and the efflux pump MDR1 P-glycoprotein (ABCB1). (2008). https://pubmed.ncbi.nlm.nih.gov/18157518/ DOI: 10.1007/s00210-007-0219-x
- tissue_or_cell_type
- Basolateral uptake and apical export
- transport_effect
- raises Berberine uptake measured in transfected cells, which stand for the tubular cell, with a reported Km of 4.4 micromolar.
- transport_pool
- the renal tubular cell interior Berberine uptake measured in transfected cells, which stand for the tubular cell, with a reported Km of 4.4 micromolar.
Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 220–231
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Polarized transporter-transfected MDCKII cells · source_derived_draft · unverified_draft
### berberine-uptake-oct2 Human OCT2 transported berberine in transfected cells, with reported Km 4.4 micromolar. Condition category: normal nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Berberine uses a separately identified organic-cation uptake transporter. organism: Human OCT1, OCT2 and ABCB1 in engineered canine cells tissue_or_cell_type: Basolateral uptake and apical export experimental_model: Polarized transporter-transfected MDCKII cells limitations: Engineered system, not direct evidence for human oral bioavailability or a universal transport bottleneck. exposure: Berberine transport kinetics and transporter inhibition evidence_span: {"source_cache": "artifacts/berberine-research/18157518.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "34651ed2e9ce3c38b6042e616b5c36d932fe6f1099c627d1b5403b338eae7b2b", "start_char": 0, "end_char": 1918, "text_sha256": "34651ed2e9ce3c38b6042e616b5c36d932fe6f1099c627d1b5403b338eae7b2b"} [berberine-p18157518] Vectorial transport of the plant alkaloid berberine by double-transfected cells expressing the human organic cation transporter 1 (OCT1, SLC22A1) and the efflux pump MDR1 P-glycoprotein (ABCB1). (2008). https://pubmed.ncbi.nlm.nih.gov/18157518/ DOI: 10.1007/s00210-007-0219-x
Complete structured claim and evidenceHuman and rat OCT2 had roughly 10-fold and 100-fold greater capacity to transport metformin than OCT1 in the transfected-cell comparison.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/metformin-research/16272756.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9da4317752d37da62129139affd33016e879d367c4cf58cfefb9200c663fe4ed", "start_char": 0, "end_char": 1284, "text_sha256": "9da4317752d37da62129139affd33016e879d367c4cf58cfefb9200c663fe4ed"}
- experimental_model
- Human and rat transporter cDNA transfection into HEK293 cells with rat tissue distribution
- exposure
- Metformin uptake across five renal organic ion transporters and tissue accumulation in male rats
- limitations
- Relative capacities are transfection-dependent; the study itself notes that plasmid amount changes the apparent kinetics.
- 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 rat transporters; rat in vivo
- plain_language
- The kidney transporter moves far more of the drug than the liver one does.
- primary_references
- [metformin-p16272756] Metformin is a superior substrate for renal organic cation transporter OCT2 rather than hepatic OCT1. (2005). https://pubmed.ncbi.nlm.nih.gov/16272756/ DOI: 10.2133/dmpk.20.379
- tissue_or_cell_type
- Kidney and liver
- transport_effect
- raises A transfected-cell capacity comparison, measured as metformin carried into the cell.
- transport_pool
- the expressing cell A transfected-cell capacity comparison, measured as metformin carried into the cell.
Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 177–188
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and rat transporter cDNA transfection into HEK293 cells with rat tissue distribution · source_derived_draft · unverified_draft
### metformin-oct2-capacity Human and rat OCT2 had roughly 10-fold and 100-fold greater capacity to transport metformin than OCT1 in the transfected-cell comparison. 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 kidney transporter moves far more of the drug than the liver one does. organism: Human and rat transporters; rat in vivo tissue_or_cell_type: Kidney and liver experimental_model: Human and rat transporter cDNA transfection into HEK293 cells with rat tissue distribution limitations: Relative capacities are transfection-dependent; the study itself notes that plasmid amount changes the apparent kinetics. exposure: Metformin uptake across five renal organic ion transporters and tissue accumulation in male rats evidence_span: {"source_cache": "artifacts/metformin-research/16272756.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9da4317752d37da62129139affd33016e879d367c4cf58cfefb9200c663fe4ed", "start_char": 0, "end_char": 1284, "text_sha256": "9da4317752d37da62129139affd33016e879d367c4cf58cfefb9200c663fe4ed"} [metformin-p16272756] Metformin is a superior substrate for renal organic cation transporter OCT2 rather than hepatic OCT1. (2005). https://pubmed.ncbi.nlm.nih.gov/16272756/ DOI: 10.2133/dmpk.20.379
Complete structured claim and evidenceRenal OCT2 expression was the key factor controlling concentrative accumulation of metformin in the rat kidney.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/metformin-research/16272756.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9da4317752d37da62129139affd33016e879d367c4cf58cfefb9200c663fe4ed", "start_char": 0, "end_char": 1284, "text_sha256": "9da4317752d37da62129139affd33016e879d367c4cf58cfefb9200c663fe4ed"}
- experimental_model
- Human and rat transporter cDNA transfection into HEK293 cells with rat tissue distribution
- exposure
- Metformin uptake across five renal organic ion transporters and tissue accumulation in male rats
- limitations
- Relative capacities are transfection-dependent; the study itself notes that plasmid amount changes the apparent kinetics.
- 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
- plain_language
- Kidney tissue concentrates the drug because of this transporter.
- primary_references
- [metformin-p16272756] Metformin is a superior substrate for renal organic cation transporter OCT2 rather than hepatic OCT1. (2005). https://pubmed.ncbi.nlm.nih.gov/16272756/ DOI: 10.2133/dmpk.20.379
- tissue_or_cell_type
- Kidney and liver
Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 190–201
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and rat transporter cDNA transfection into HEK293 cells with rat tissue distribution · source_derived_draft · unverified_draft
### metformin-oct2-kidney-accumulation Renal OCT2 expression was the key factor controlling concentrative accumulation of metformin in the rat kidney. 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: Kidney tissue concentrates the drug because of this transporter. organism: Rat tissue_or_cell_type: Kidney and liver experimental_model: Human and rat transporter cDNA transfection into HEK293 cells with rat tissue distribution limitations: Relative capacities are transfection-dependent; the study itself notes that plasmid amount changes the apparent kinetics. exposure: Metformin uptake across five renal organic ion transporters and tissue accumulation in male rats evidence_span: {"source_cache": "artifacts/metformin-research/16272756.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9da4317752d37da62129139affd33016e879d367c4cf58cfefb9200c663fe4ed", "start_char": 0, "end_char": 1284, "text_sha256": "9da4317752d37da62129139affd33016e879d367c4cf58cfefb9200c663fe4ed"} [metformin-p16272756] Metformin is a superior substrate for renal organic cation transporter OCT2 rather than hepatic OCT1. (2005). https://pubmed.ncbi.nlm.nih.gov/16272756/ DOI: 10.2133/dmpk.20.379
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.