Component
Homoarginine
Homoarginine. Species, exposure and limitations are retained in each linked claim.
3 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
Homoarginine supplementation rescued the aggravated stroke phenotype in AGAT-deficient mice in this study.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/creatine-research/24004504.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "301113d570a67df12332ca3574aa0714c6dc3c62297e72c2dd7863b146187d6a", "start_char": 0, "end_char": 1911, "text_sha256": "301113d570a67df12332ca3574aa0714c6dc3c62297e72c2dd7863b146187d6a"}
- experimental_model
- Human genetic/observational analyses, cell expression and mouse gene deletion
- exposure
- GATM variation, AGAT expression, AGAT or GAMT deletion and homoarginine rescue
- limitations
- Mouse stroke experiment; homoarginine rescue shows that AGAT deletion has a non-creatine consequence, not that homoarginine treats human stroke.
- nutrient_topic
- Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
- organism
- Humans, cultured cells and mice
- plain_language
- An AGAT-knockout effect cannot automatically be blamed entirely on creatine loss.
- primary_references
- [creatine-p24004504] Homoarginine levels are regulated by L-arginine:glycine amidinotransferase and affect stroke outcome: results from human and murine studies. (2013). https://pubmed.ncbi.nlm.nih.gov/24004504/ DOI: 10.1161/circulationaha.112.000580
- tissue_or_cell_type
- Plasma, expressing cells and experimental stroke models
Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 828–839
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human genetic/observational analyses, cell expression and mouse gene deletion · source_derived_draft · unverified_draft
### creatine-agat-knockout-confounding Homoarginine supplementation rescued the aggravated stroke phenotype in AGAT-deficient mice in this study. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: An AGAT-knockout effect cannot automatically be blamed entirely on creatine loss. organism: Humans, cultured cells and mice tissue_or_cell_type: Plasma, expressing cells and experimental stroke models experimental_model: Human genetic/observational analyses, cell expression and mouse gene deletion limitations: Mouse stroke experiment; homoarginine rescue shows that AGAT deletion has a non-creatine consequence, not that homoarginine treats human stroke. exposure: GATM variation, AGAT expression, AGAT or GAMT deletion and homoarginine rescue evidence_span: {"source_cache": "artifacts/creatine-research/24004504.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "301113d570a67df12332ca3574aa0714c6dc3c62297e72c2dd7863b146187d6a", "start_char": 0, "end_char": 1911, "text_sha256": "301113d570a67df12332ca3574aa0714c6dc3c62297e72c2dd7863b146187d6a"} [creatine-p24004504] Homoarginine levels are regulated by L-arginine:glycine amidinotransferase and affect stroke outcome: results from human and murine studies. (2013). https://pubmed.ncbi.nlm.nih.gov/24004504/ DOI: 10.1161/circulationaha.112.000580
Complete structured claim and evidenceHomoarginine produced a competitive inhibition pattern for CAT1-mediated arginine uptake.
Experimental context and source evidence
- evidence_access
- Full-text methods/results/discussion, Europe PMC PMC9217908.
- experimental_model
- HEK cells expressing human CAT1, compared with vector controls; radiolabeled substrate uptake.
- limitations
- No clinical benefit or harm follows from the assay alone.
- nutrient_topic
- L-Arginine collection; tissue, species, dose and formulation distinctions retained. · L-Arginine
- plain_language
- A related amino acid shares transport machinery.
- primary_references
- Screening of commonly prescribed drugs for effects on the CAT1-mediated transport of L-arginine and arginine derivatives. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35377022/ · DOI 10.1007/s00726-022-03156-2
L-Arginine: transport, metabolic branches, nutrient interactions, availability and discovery questions (2026-09-18) · lines 38–44
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · HEK cells expressing human CAT1, compared with vector controls; radiolabeled substrate uptake. · source_derived_draft · unverified_draft
## arg-homoarg-transport A related amino acid shares transport machinery. Homoarginine produced a competitive inhibition pattern for CAT1-mediated arginine uptake. Model: HEK cells expressing human CAT1, compared with vector controls; radiolabeled substrate uptake. Limitations: No clinical benefit or harm follows from the assay alone. Evidence access: Full-text methods/results/discussion, Europe PMC PMC9217908. Screening of commonly prescribed drugs for effects on the CAT1-mediated transport of L-arginine and arginine derivatives. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35377022/ · DOI 10.1007/s00726-022-03156-2
Complete structured claim and evidence
What acts on it
AGAT expression increased homoarginine in cells, and homoarginine was absent in AGAT-deficient mice.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/creatine-research/24004504.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "301113d570a67df12332ca3574aa0714c6dc3c62297e72c2dd7863b146187d6a", "start_char": 0, "end_char": 1911, "text_sha256": "301113d570a67df12332ca3574aa0714c6dc3c62297e72c2dd7863b146187d6a"}
- experimental_model
- Human genetic/observational analyses, cell expression and mouse gene deletion
- exposure
- GATM variation, AGAT expression, AGAT or GAMT deletion and homoarginine rescue
- limitations
- Human stroke associations are not supplementation causation. AGAT deletion disrupts more than creatine synthesis.
- nutrient_topic
- Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
- organism
- Humans, cultured cells and mice
- plain_language
- The first creatine-synthesis enzyme also helps make another metabolite, homoarginine.
- primary_references
- [creatine-p24004504] Homoarginine levels are regulated by L-arginine:glycine amidinotransferase and affect stroke outcome: results from human and murine studies. (2013). https://pubmed.ncbi.nlm.nih.gov/24004504/ DOI: 10.1161/circulationaha.112.000580
- tissue_or_cell_type
- Plasma, expressing cells and experimental stroke models
Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 815–826
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human genetic/observational analyses, cell expression and mouse gene deletion · source_derived_draft · unverified_draft
### creatine-agat-homoarginine AGAT expression increased homoarginine in cells, and homoarginine was absent in AGAT-deficient mice. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The first creatine-synthesis enzyme also helps make another metabolite, homoarginine. organism: Humans, cultured cells and mice tissue_or_cell_type: Plasma, expressing cells and experimental stroke models experimental_model: Human genetic/observational analyses, cell expression and mouse gene deletion limitations: Human stroke associations are not supplementation causation. AGAT deletion disrupts more than creatine synthesis. exposure: GATM variation, AGAT expression, AGAT or GAMT deletion and homoarginine rescue evidence_span: {"source_cache": "artifacts/creatine-research/24004504.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "301113d570a67df12332ca3574aa0714c6dc3c62297e72c2dd7863b146187d6a", "start_char": 0, "end_char": 1911, "text_sha256": "301113d570a67df12332ca3574aa0714c6dc3c62297e72c2dd7863b146187d6a"} [creatine-p24004504] Homoarginine levels are regulated by L-arginine:glycine amidinotransferase and affect stroke outcome: results from human and murine studies. (2013). https://pubmed.ncbi.nlm.nih.gov/24004504/ DOI: 10.1161/circulationaha.112.000580
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.