Component
Human guanidinoacetate methyltransferase / GAMT
Human guanidinoacetate methyltransferase / GAMT. Species, exposure and limitations are retained in each linked claim.
1 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
The GAMT-deficient children had high brain guanidinoacetate, low blood creatine and severely deficient liver GAMT activity.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/creatine-research/8651275.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d6999ce02dd6012eefd5981a91374d6c933af0924d5e82b1447fd322e8f211de", "start_char": 0, "end_char": 706, "text_sha256": "d6999ce02dd6012eefd5981a91374d6c933af0924d5e82b1447fd322e8f211de"}
- experimental_model
- Biochemical diagnosis and treatment observations
- exposure
- GAMT deficiency with oral creatine substitution
- limitations
- Small case series; biochemical and neurological responses are not a universal prognosis.
- nutrient_topic
- Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
- organism
- Two human children
- plain_language
- The blocked final step left precursor behind while reducing the finished product.
- primary_references
- [creatine-p8651275] Guanidinoacetate methyltransferase deficiency: the first inborn error of creatine metabolism in man. (1996). https://pubmed.ncbi.nlm.nih.gov/8651275/
- tissue_or_cell_type
- Brain spectroscopy, blood and liver enzyme assay
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 867–878
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical diagnosis and treatment observations · source_derived_draft · unverified_draft
### creatine-gamt-gaa-accumulation The GAMT-deficient children had high brain guanidinoacetate, low blood creatine and severely deficient liver GAMT activity. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The blocked final step left precursor behind while reducing the finished product. organism: Two human children tissue_or_cell_type: Brain spectroscopy, blood and liver enzyme assay experimental_model: Biochemical diagnosis and treatment observations limitations: Small case series; biochemical and neurological responses are not a universal prognosis. exposure: GAMT deficiency with oral creatine substitution evidence_span: {"source_cache": "artifacts/creatine-research/8651275.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "d6999ce02dd6012eefd5981a91374d6c933af0924d5e82b1447fd322e8f211de", "start_char": 0, "end_char": 706, "text_sha256": "d6999ce02dd6012eefd5981a91374d6c933af0924d5e82b1447fd322e8f211de"} [creatine-p8651275] Guanidinoacetate methyltransferase deficiency: the first inborn error of creatine metabolism in man. (1996). https://pubmed.ncbi.nlm.nih.gov/8651275/
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.