Component

Adipocyte futile creatine cycle

Adipocyte futile creatine cycle. Species, exposure and limitations are retained in each linked claim.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What acts on it

  1. CKB trafficked to adipocyte mitochondria through an internal mitochondrial targeting sequence and supported the futile creatine cycle.

    Mouse creatine kinase B / Ckb → Adipocyte futile creatine cycle source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/creatine-research/33597756.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b", "start_char": 0, "end_char": 942, "text_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b"}
    experimental_model
    Adipocyte biochemical experiments and conditional gene deletion
    exposure
    Thermogenic stimulation and adipocyte Ckb loss
    limitations
    Human cell induction and mouse causal phenotypes are separately scoped; no human weight-loss intervention was tested.
    nutrient_topic
    Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
    organism
    Mouse adipocyte mechanistic experiments
    plain_language
    In fat cells, CKB can move to mitochondria and help run an energy-consuming creatine cycle.
    primary_references
    [creatine-p33597756] Creatine kinase B controls futile creatine cycling in thermogenic fat. (2021). https://pubmed.ncbi.nlm.nih.gov/33597756/ DOI: 10.1038/s41586-021-03221-y
    tissue_or_cell_type
    Thermogenic adipose tissue

    Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 477–488

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adipocyte biochemical experiments and conditional gene deletion · source_derived_draft · unverified_draft

    ### creatine-ckb-mitochondrial-trafficking CKB trafficked to adipocyte mitochondria through an internal mitochondrial targeting sequence and supported the futile creatine cycle. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: In fat cells, CKB can move to mitochondria and help run an energy-consuming creatine cycle. organism: Mouse adipocyte mechanistic experiments tissue_or_cell_type: Thermogenic adipose tissue experimental_model: Adipocyte biochemical experiments and conditional gene deletion limitations: Human cell induction and mouse causal phenotypes are separately scoped; no human weight-loss intervention was tested. exposure: Thermogenic stimulation and adipocyte Ckb loss evidence_span: {"source_cache": "artifacts/creatine-research/33597756.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b", "start_char": 0, "end_char": 942, "text_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b"} [creatine-p33597756] Creatine kinase B controls futile creatine cycling in thermogenic fat. (2021). https://pubmed.ncbi.nlm.nih.gov/33597756/ DOI: 10.1038/s41586-021-03221-y
    Complete structured claim and evidence

  2. Thermogenic stimulation induced CKB expression in human and mouse adipocytes in the study.

    Human creatine kinase B / CKB → Adipocyte futile creatine cycle source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/creatine-research/33597756.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b", "start_char": 0, "end_char": 942, "text_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b"}
    experimental_model
    Adipocyte biochemical experiments and conditional gene deletion
    exposure
    Thermogenic stimulation and adipocyte Ckb loss
    limitations
    Human cell induction and mouse causal phenotypes are separately scoped; no human weight-loss intervention was tested.
    nutrient_topic
    Creatine research collection; topical membership is not evidence of a direct dietary effect. · Creatine
    organism
    Human and mouse adipocytes; mice for gene deletion
    plain_language
    The enzyme commonly called brain-type creatine kinase also participates in thermogenic fat.
    primary_references
    [creatine-p33597756] Creatine kinase B controls futile creatine cycling in thermogenic fat. (2021). https://pubmed.ncbi.nlm.nih.gov/33597756/ DOI: 10.1038/s41586-021-03221-y
    tissue_or_cell_type
    Thermogenic adipose tissue

    Creatine: synthesis, transport, phosphocreatine energetics and nutrient interactions (2026-09-17) · lines 464–475

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adipocyte biochemical experiments and conditional gene deletion · source_derived_draft · unverified_draft

    ### creatine-ckb-thermogenic-induction Thermogenic stimulation induced CKB expression in human and mouse adipocytes in the study. Condition category: normal nutrient_topic: Creatine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The enzyme commonly called brain-type creatine kinase also participates in thermogenic fat. organism: Human and mouse adipocytes; mice for gene deletion tissue_or_cell_type: Thermogenic adipose tissue experimental_model: Adipocyte biochemical experiments and conditional gene deletion limitations: Human cell induction and mouse causal phenotypes are separately scoped; no human weight-loss intervention was tested. exposure: Thermogenic stimulation and adipocyte Ckb loss evidence_span: {"source_cache": "artifacts/creatine-research/33597756.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b", "start_char": 0, "end_char": 942, "text_sha256": "90b9ec2286a126569876b65a77450dec9f600bf04cb6f3e8c4aeb43edcc34c4b"} [creatine-p33597756] Creatine kinase B controls futile creatine cycling in thermogenic fat. (2021). https://pubmed.ncbi.nlm.nih.gov/33597756/ DOI: 10.1038/s41586-021-03221-y
    Complete structured claim and evidence

  3. TNAP inhibition abolished the measured futile creatine cycle in isolated thermogenic-fat mitochondria.

    Mouse tissue-nonspecific alkaline phosphatase / Alpl → Adipocyte futile creatine cycle source_derived_draftungraded
    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 evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards