Human glycine amidinotransferase AGAT / GATM

evidence_access

Primary full text; Figure 4B

experimental_model

Recombinant human enzyme assay.

limitations

No competition magnitude with glycine or taurine in a living person was established.

nutrient_topic

Agmatine Sulfate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Agmatine Sulfate

plain_language

Beta-alanine connects to the guanidino-acid network through a distinct reaction.

primary_references

Guanidino acid hydrolysis by the human enzyme annotated as agmatinase. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36543883/ · DOI 10.1038/s41598-022-26655-4

Agmatine Sulfate: transport, guanidino metabolism, ion channels and cross-nutrient mechanisms (2026-09-20) · lines 204–210

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human enzyme assay. · source_derived_draft · unverified_draft

## agmatine-sulfate-gatm-beta-alanine Beta-alanine connects to the guanidino-acid network through a distinct reaction. Human GATM transferred the amidino group of arginine to beta-alanine, producing guanidinopropionate. Model: Recombinant human enzyme assay. Limitations: No competition magnitude with glycine or taurine in a living person was established. Evidence access: Primary full text; Figure 4B Guanidino acid hydrolysis by the human enzyme annotated as agmatinase. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36543883/ · DOI 10.1038/s41598-022-26655-4

evidence_access

Primary full text; Figure 4B

experimental_model

Purified human GATM.

limitations

Presence of this route does not prove a change in brain inhibitory neurotransmission after agmatine supplementation.

nutrient_topic

Agmatine Sulfate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Agmatine Sulfate

plain_language

The same guanidino metabolite has another possible source besides agmatine oxidation.

primary_references

Guanidino acid hydrolysis by the human enzyme annotated as agmatinase. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36543883/ · DOI 10.1038/s41598-022-26655-4

Agmatine Sulfate: transport, guanidino metabolism, ion channels and cross-nutrient mechanisms (2026-09-20) · lines 196–202

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Purified human GATM. · source_derived_draft · unverified_draft

## agmatine-sulfate-gatm-gaba The same guanidino metabolite has another possible source besides agmatine oxidation. Human GATM used GABA as an amidino acceptor to form guanidinobutyrate in vitro. Model: Purified human GATM. Limitations: Presence of this route does not prove a change in brain inhibitory neurotransmission after agmatine supplementation. Evidence access: Primary full text; Figure 4B Guanidino acid hydrolysis by the human enzyme annotated as agmatinase. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36543883/ · DOI 10.1038/s41598-022-26655-4

evidence_access

Primary full text; Figure 4B

experimental_model

Recombinant human GATM substrate comparison.

limitations

Taurine is a secondary substrate in this assay; tissue flux and clinically important depletion were not established.

nutrient_topic

Agmatine Sulfate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Agmatine Sulfate

plain_language

Creatine-synthesis machinery also accepts a taurine-related side reaction.

primary_references

Guanidino acid hydrolysis by the human enzyme annotated as agmatinase. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36543883/ · DOI 10.1038/s41598-022-26655-4

Agmatine Sulfate: transport, guanidino metabolism, ion channels and cross-nutrient mechanisms (2026-09-20) · lines 188–194

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Recombinant human GATM substrate comparison. · source_derived_draft · unverified_draft

## agmatine-sulfate-gatm-taurine Creatine-synthesis machinery also accepts a taurine-related side reaction. Purified human GATM transferred an amidino group from arginine to taurine, producing taurocyamine in vitro. Model: Recombinant human GATM substrate comparison. Limitations: Taurine is a secondary substrate in this assay; tissue flux and clinically important depletion were not established. Evidence access: Primary full text; Figure 4B Guanidino acid hydrolysis by the human enzyme annotated as agmatinase. · 2022 · https://pubmed.ncbi.nlm.nih.gov/36543883/ · DOI 10.1038/s41598-022-26655-4

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

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experimental_model

Biochemical and genetic investigation with oral replacement observations

exposure

Inherited AGAT deficiency and oral creatine substitution

limitations

Rare synthesis disorder; treatment response is not equivalent to a diagnosis of dietary creatine deficiency.

nutrient_topic

Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine

organism

Two human sisters

plain_language

A broken first synthesis step can leave both precursor and brain creatine low.

primary_references

[creatine-p11555793] Arginine:glycine amidinotransferase deficiency: the third inborn error of creatine metabolism in humans. (2001). https://pubmed.ncbi.nlm.nih.gov/11555793/ DOI: 10.1086/323765

tissue_or_cell_type

Urine, brain magnetic-resonance spectroscopy and AGAT assays

trigger_kind

machinery_impairment Imported condition classification; unverified.

Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 841–852

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical and genetic investigation with oral replacement observations · source_derived_draft · unverified_draft

### creatine-agat-brain-deficiency The AGAT-deficient sisters had low urinary guanidinoacetate, absent AGAT activity and brain creatine depletion. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A broken first synthesis step can leave both precursor and brain creatine low. organism: Two human sisters tissue_or_cell_type: Urine, brain magnetic-resonance spectroscopy and AGAT assays experimental_model: Biochemical and genetic investigation with oral replacement observations limitations: Rare synthesis disorder; treatment response is not equivalent to a diagnosis of dietary creatine deficiency. exposure: Inherited AGAT deficiency and oral creatine substitution evidence_span: {"source_cache": "artifacts/creatine-research/11555793.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "89ef028281e917c6af5ac6975c05f6ff421852645e695550b737ca4eff6d78f3", "start_char": 0, "end_char": 1044, "text_sha256": "89ef028281e917c6af5ac6975c05f6ff421852645e695550b737ca4eff6d78f3"} [creatine-p11555793] Arginine:glycine amidinotransferase deficiency: the third inborn error of creatine metabolism in humans. (2001). https://pubmed.ncbi.nlm.nih.gov/11555793/ DOI: 10.1086/323765

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

evidence_span

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experimental_model

Human AGAT crystal structures and inactive-mutant substrate complex

exposure

Native, ornithine-bound and inactive mutant structures

limitations

Structures support an amidino-transfer mechanism; substrate availability in a person and effects of amino-acid supplementation were not measured.

nutrient_topic

Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine

organism

Recombinant human enzyme

plain_language

The first synthesis step joins material from arginine and glycine to make the precursor of creatine.

primary_references

[creatine-p9218780] Crystal structure and mechanism of human L-arginine:glycine amidinotransferase: a mitochondrial enzyme involved in creatine biosynthesis. (1997). https://pubmed.ncbi.nlm.nih.gov/9218780/ DOI: 10.1093/emboj/16.12.3373

tissue_or_cell_type

Purified protein

Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 177–188

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human AGAT crystal structures and inactive-mutant substrate complex · source_derived_draft · unverified_draft

### creatine-agat-reaction AGAT catalyzes transfer of an amidino group from arginine to glycine, forming guanidinoacetate and ornithine. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The first synthesis step joins material from arginine and glycine to make the precursor of creatine. organism: Recombinant human enzyme tissue_or_cell_type: Purified protein experimental_model: Human AGAT crystal structures and inactive-mutant substrate complex limitations: Structures support an amidino-transfer mechanism; substrate availability in a person and effects of amino-acid supplementation were not measured. exposure: Native, ornithine-bound and inactive mutant structures evidence_span: {"source_cache": "artifacts/creatine-research/9218780.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "407baedc2f982a5abb9d14a01e8ac9dc331d60115acc716604c1e6003aa12c1b", "start_char": 0, "end_char": 1112, "text_sha256": "407baedc2f982a5abb9d14a01e8ac9dc331d60115acc716604c1e6003aa12c1b"} [creatine-p9218780] Crystal structure and mechanism of human L-arginine:glycine amidinotransferase: a mitochondrial enzyme involved in creatine biosynthesis. (1997). https://pubmed.ncbi.nlm.nih.gov/9218780/ DOI: 10.1093/emboj/16.12.3373

evidence_span

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experimental_model

Human AGAT crystal structures and inactive-mutant substrate complex

exposure

Native, ornithine-bound and inactive mutant structures

limitations

Structures support an amidino-transfer mechanism; substrate availability in a person and effects of amino-acid supplementation were not measured.

nutrient_topic

Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine

organism

Recombinant human enzyme

plain_language

A product of the first step can bind back to the enzyme and change its working shape.

primary_references

[creatine-p9218780] Crystal structure and mechanism of human L-arginine:glycine amidinotransferase: a mitochondrial enzyme involved in creatine biosynthesis. (1997). https://pubmed.ncbi.nlm.nih.gov/9218780/ DOI: 10.1093/emboj/16.12.3373

tissue_or_cell_type

Purified protein

Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 190–201

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human AGAT crystal structures and inactive-mutant substrate complex · source_derived_draft · unverified_draft

### creatine-ornithine-agat Ornithine binding to human AGAT induced movement of a flexible loop and neighboring helix at the active-site region. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A product of the first step can bind back to the enzyme and change its working shape. organism: Recombinant human enzyme tissue_or_cell_type: Purified protein experimental_model: Human AGAT crystal structures and inactive-mutant substrate complex limitations: Structures support an amidino-transfer mechanism; substrate availability in a person and effects of amino-acid supplementation were not measured. exposure: Native, ornithine-bound and inactive mutant structures evidence_span: {"source_cache": "artifacts/creatine-research/9218780.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "407baedc2f982a5abb9d14a01e8ac9dc331d60115acc716604c1e6003aa12c1b", "start_char": 0, "end_char": 1112, "text_sha256": "407baedc2f982a5abb9d14a01e8ac9dc331d60115acc716604c1e6003aa12c1b"} [creatine-p9218780] Crystal structure and mechanism of human L-arginine:glycine amidinotransferase: a mitochondrial enzyme involved in creatine biosynthesis. (1997). https://pubmed.ncbi.nlm.nih.gov/9218780/ DOI: 10.1093/emboj/16.12.3373

evidence_span

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experimental_model

CRISPR AGAT reporter, transporter knockout and rescue

exposure

Manipulated extracellular and intracellular creatine with intact or deleted SLC6A8

limitations

Cell-line reporter regulation; the intracellular sensor was inferred rather than molecularly identified.

nutrient_topic

Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine

organism

Human HAP1 cells

plain_language

The usual transporter shaped feedback, but the engineered cells also showed a separate low-affinity route.

primary_references

[creatine-p38104212] Evidence of an intracellular creatine-sensing mechanism that modulates creatine biosynthesis via AGAT expression in human HAP1 cells. (2023). https://pubmed.ncbi.nlm.nih.gov/38104212/ DOI: 10.1038/s41598-023-49860-1

tissue_or_cell_type

Cultured cells

Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 321–332

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CRISPR AGAT reporter, transporter knockout and rescue · source_derived_draft · unverified_draft

### creatine-feedback-transporter-component The high-affinity component of creatine accumulation and AGAT regulation depended on SLC6A8, whereas a nonsaturable component remained without the transporter. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The usual transporter shaped feedback, but the engineered cells also showed a separate low-affinity route. organism: Human HAP1 cells tissue_or_cell_type: Cultured cells experimental_model: CRISPR AGAT reporter, transporter knockout and rescue limitations: Cell-line reporter regulation; the intracellular sensor was inferred rather than molecularly identified. exposure: Manipulated extracellular and intracellular creatine with intact or deleted SLC6A8 evidence_span: {"source_cache": "artifacts/creatine-research/38104212.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936", "start_char": 0, "end_char": 1889, "text_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936"} [creatine-p38104212] Evidence of an intracellular creatine-sensing mechanism that modulates creatine biosynthesis via AGAT expression in human HAP1 cells. (2023). https://pubmed.ncbi.nlm.nih.gov/38104212/ DOI: 10.1038/s41598-023-49860-1

evidence_span

{"source_cache": "artifacts/creatine-research/38104212.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936", "start_char": 0, "end_char": 1889, "text_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936"}

experimental_model

CRISPR AGAT reporter, transporter knockout and rescue

exposure

Manipulated extracellular and intracellular creatine with intact or deleted SLC6A8

limitations

Cell-line reporter regulation; the intracellular sensor was inferred rather than molecularly identified.

nutrient_topic

Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine

organism

Human HAP1 cells

plain_language

Cells responded to the creatine inside them when regulating the first synthesis enzyme.

primary_references

[creatine-p38104212] Evidence of an intracellular creatine-sensing mechanism that modulates creatine biosynthesis via AGAT expression in human HAP1 cells. (2023). https://pubmed.ncbi.nlm.nih.gov/38104212/ DOI: 10.1038/s41598-023-49860-1

tissue_or_cell_type

Cultured cells

Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 308–319

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · CRISPR AGAT reporter, transporter knockout and rescue · source_derived_draft · unverified_draft

### creatine-intracellular-feedback AGAT reporter expression fell with intracellular creatine, with a reported intracellular IC50 of approximately 1–2 mM. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cells responded to the creatine inside them when regulating the first synthesis enzyme. organism: Human HAP1 cells tissue_or_cell_type: Cultured cells experimental_model: CRISPR AGAT reporter, transporter knockout and rescue limitations: Cell-line reporter regulation; the intracellular sensor was inferred rather than molecularly identified. exposure: Manipulated extracellular and intracellular creatine with intact or deleted SLC6A8 evidence_span: {"source_cache": "artifacts/creatine-research/38104212.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936", "start_char": 0, "end_char": 1889, "text_sha256": "28686c279fa726cb1596357628d69b5d5606fbe38e0177fe7b27b1931f249936"} [creatine-p38104212] Evidence of an intracellular creatine-sensing mechanism that modulates creatine biosynthesis via AGAT expression in human HAP1 cells. (2023). https://pubmed.ncbi.nlm.nih.gov/38104212/ DOI: 10.1038/s41598-023-49860-1

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

{"source_cache": "artifacts/cold-research/28844881.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1341345f147cd7e59119d062b0523a4bf6087a6936b3434bb76a305033a724eb", "start_char": 0, "end_char": 1069, "text_sha256": "1341345f147cd7e59119d062b0523a4bf6087a6936b3434bb76a305033a724eb"}

experimental_model

Adipocyte-selective knockout of glycine amidinotransferase in mice

exposure

High-calorie feeding, beta-3 adrenergic activation, and dietary creatine supplementation

limitations

A genetic test of the same cycle with a dietary rescue. It concerns diet-induced thermogenesis rather than cold thermogenesis directly.

nutrient_topic

Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. · Cold water immersion

organism

Mouse

plain_language

Blocking the cell from making creatine caused obesity, and feeding creatine fixed it.

primary_references

[cold-p28844881] Genetic Depletion of Adipocyte Creatine Metabolism Inhibits Diet-Induced Thermogenesis and Drives Obesity. (2017). https://pubmed.ncbi.nlm.nih.gov/28844881/ DOI: 10.1016/j.cmet.2017.08.009

tissue_or_cell_type

Adipose tissue

trigger_kind

machinery_impairment Imported condition classification; unverified.

Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 468–479

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adipocyte-selective knockout of glycine amidinotransferase in mice · source_derived_draft · unverified_draft

### cold-gatm-knockout-obesity Mice lacking the first and rate-limiting enzyme of creatine biosynthesis selectively in fat were prone to diet-induced obesity through suppression of the elevated energy expenditure normally seen with high-calorie feeding, with a blunted capacity for beta-3 adrenergic activation of metabolic rate that was rescued by dietary creatine supplementation. Condition category: machinery_impairment nutrient_topic: Cold water immersion research collection; topical membership is not evidence of a direct clinical effect, and a therapeutic exposure is not a dietary intake. plain_language: Blocking the cell from making creatine caused obesity, and feeding creatine fixed it. organism: Mouse tissue_or_cell_type: Adipose tissue experimental_model: Adipocyte-selective knockout of glycine amidinotransferase in mice limitations: A genetic test of the same cycle with a dietary rescue. It concerns diet-induced thermogenesis rather than cold thermogenesis directly. exposure: High-calorie feeding, beta-3 adrenergic activation, and dietary creatine supplementation evidence_span: {"source_cache": "artifacts/cold-research/28844881.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1341345f147cd7e59119d062b0523a4bf6087a6936b3434bb76a305033a724eb", "start_char": 0, "end_char": 1069, "text_sha256": "1341345f147cd7e59119d062b0523a4bf6087a6936b3434bb76a305033a724eb"} [cold-p28844881] Genetic Depletion of Adipocyte Creatine Metabolism Inhibits Diet-Induced Thermogenesis and Drives Obesity. (2017). https://pubmed.ncbi.nlm.nih.gov/28844881/ DOI: 10.1016/j.cmet.2017.08.009