Component
Mouse tissue-nonspecific alkaline phosphatase / Alpl
Mouse tissue-nonspecific alkaline phosphatase / Alpl. 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
Adipocyte Alpl deletion reduced energy expenditure and increased obesity susceptibility without altered feeding or movement.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/creatine-research/33981039.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "915403423e16b5e0e5db70e99ebc6518e612bc9ef69ceb1e25da3074a8410dca", "start_char": 0, "end_char": 1400, "text_sha256": "915403423e16b5e0e5db70e99ebc6518e612bc9ef69ceb1e25da3074a8410dca"}
- experimental_model
- Phosphatase biochemistry, mitochondrial inhibition and adipocyte gene deletion
- exposure
- TNAP inhibition and adipocyte Alpl deletion
- limitations
- Mouse mechanism; it does not establish that creatine supplements cause weight loss in humans.
- nutrient_topic
- Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
- organism
- Mouse thermogenic adipocytes and mice
- plain_language
- The lower energy use was not explained by eating more or moving less in these mice.
- primary_references
- [creatine-p33981039] Mitochondrial TNAP controls thermogenesis by hydrolysis of phosphocreatine. (2021). https://pubmed.ncbi.nlm.nih.gov/33981039/ DOI: 10.1038/s41586-021-03533-z
- tissue_or_cell_type
- Adipocyte mitochondria
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 529–540
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phosphatase biochemistry, mitochondrial inhibition and adipocyte gene deletion · source_derived_draft · unverified_draft
### creatine-tnap-fat-loss Adipocyte Alpl deletion reduced energy expenditure and increased obesity susceptibility without altered feeding or movement. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The lower energy use was not explained by eating more or moving less in these mice. organism: Mouse thermogenic adipocytes and mice tissue_or_cell_type: Adipocyte mitochondria experimental_model: Phosphatase biochemistry, mitochondrial inhibition and adipocyte gene deletion limitations: Mouse mechanism; it does not establish that creatine supplements cause weight loss in humans. exposure: TNAP inhibition and adipocyte Alpl deletion evidence_span: {"source_cache": "artifacts/creatine-research/33981039.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "915403423e16b5e0e5db70e99ebc6518e612bc9ef69ceb1e25da3074a8410dca", "start_char": 0, "end_char": 1400, "text_sha256": "915403423e16b5e0e5db70e99ebc6518e612bc9ef69ceb1e25da3074a8410dca"} [creatine-p33981039] Mitochondrial TNAP controls thermogenesis by hydrolysis of phosphocreatine. (2021). https://pubmed.ncbi.nlm.nih.gov/33981039/ DOI: 10.1038/s41586-021-03533-z
Complete structured claim and evidenceTNAP inhibition abolished the measured futile creatine cycle in isolated thermogenic-fat mitochondria.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/creatine-research/33981039.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "915403423e16b5e0e5db70e99ebc6518e612bc9ef69ceb1e25da3074a8410dca", "start_char": 0, "end_char": 1400, "text_sha256": "915403423e16b5e0e5db70e99ebc6518e612bc9ef69ceb1e25da3074a8410dca"}
- experimental_model
- Phosphatase biochemistry, mitochondrial inhibition and adipocyte gene deletion
- exposure
- TNAP inhibition and adipocyte Alpl deletion
- limitations
- Mouse mechanism; it does not establish that creatine supplements cause weight loss in humans.
- nutrient_topic
- Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
- organism
- Mouse thermogenic adipocytes and mice
- plain_language
- Blocking phosphate release stopped the measured cycle.
- primary_references
- [creatine-p33981039] Mitochondrial TNAP controls thermogenesis by hydrolysis of phosphocreatine. (2021). https://pubmed.ncbi.nlm.nih.gov/33981039/ DOI: 10.1038/s41586-021-03533-z
- tissue_or_cell_type
- Adipocyte mitochondria
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 516–527
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phosphatase biochemistry, mitochondrial inhibition and adipocyte gene deletion · source_derived_draft · unverified_draft
### creatine-tnap-inhibits-cycle TNAP inhibition abolished the measured futile creatine cycle in isolated thermogenic-fat mitochondria. Condition category: machinery_impairment nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking phosphate release stopped the measured cycle. organism: Mouse thermogenic adipocytes and mice tissue_or_cell_type: Adipocyte mitochondria experimental_model: Phosphatase biochemistry, mitochondrial inhibition and adipocyte gene deletion limitations: Mouse mechanism; it does not establish that creatine supplements cause weight loss in humans. exposure: TNAP inhibition and adipocyte Alpl deletion evidence_span: {"source_cache": "artifacts/creatine-research/33981039.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "915403423e16b5e0e5db70e99ebc6518e612bc9ef69ceb1e25da3074a8410dca", "start_char": 0, "end_char": 1400, "text_sha256": "915403423e16b5e0e5db70e99ebc6518e612bc9ef69ceb1e25da3074a8410dca"} [creatine-p33981039] Mitochondrial TNAP controls thermogenesis by hydrolysis of phosphocreatine. (2021). https://pubmed.ncbi.nlm.nih.gov/33981039/ DOI: 10.1038/s41586-021-03533-z
Complete structured claim and evidenceTNAP localized to thermogenic adipocyte mitochondria and hydrolyzed phosphocreatine to support the futile creatine cycle.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/creatine-research/33981039.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "915403423e16b5e0e5db70e99ebc6518e612bc9ef69ceb1e25da3074a8410dca", "start_char": 0, "end_char": 1400, "text_sha256": "915403423e16b5e0e5db70e99ebc6518e612bc9ef69ceb1e25da3074a8410dca"}
- experimental_model
- Phosphatase biochemistry, mitochondrial inhibition and adipocyte gene deletion
- exposure
- TNAP inhibition and adipocyte Alpl deletion
- limitations
- Mouse mechanism; it does not establish that creatine supplements cause weight loss in humans.
- nutrient_topic
- Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
- organism
- Mouse thermogenic adipocytes and mice
- plain_language
- This phosphatase releases the stored phosphate without making ATP, allowing continued fuel use and heat production.
- primary_references
- [creatine-p33981039] Mitochondrial TNAP controls thermogenesis by hydrolysis of phosphocreatine. (2021). https://pubmed.ncbi.nlm.nih.gov/33981039/ DOI: 10.1038/s41586-021-03533-z
- tissue_or_cell_type
- Adipocyte mitochondria
Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 503–514
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Phosphatase biochemistry, mitochondrial inhibition and adipocyte gene deletion · source_derived_draft · unverified_draft
### creatine-tnap-pcr-hydrolysis TNAP localized to thermogenic adipocyte mitochondria and hydrolyzed phosphocreatine to support the futile creatine cycle. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: This phosphatase releases the stored phosphate without making ATP, allowing continued fuel use and heat production. organism: Mouse thermogenic adipocytes and mice tissue_or_cell_type: Adipocyte mitochondria experimental_model: Phosphatase biochemistry, mitochondrial inhibition and adipocyte gene deletion limitations: Mouse mechanism; it does not establish that creatine supplements cause weight loss in humans. exposure: TNAP inhibition and adipocyte Alpl deletion evidence_span: {"source_cache": "artifacts/creatine-research/33981039.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "915403423e16b5e0e5db70e99ebc6518e612bc9ef69ceb1e25da3074a8410dca", "start_char": 0, "end_char": 1400, "text_sha256": "915403423e16b5e0e5db70e99ebc6518e612bc9ef69ceb1e25da3074a8410dca"} [creatine-p33981039] Mitochondrial TNAP controls thermogenesis by hydrolysis of phosphocreatine. (2021). https://pubmed.ncbi.nlm.nih.gov/33981039/ DOI: 10.1038/s41586-021-03533-z
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.