Component

Whole-body energy expenditure

Whole-body energy expenditure. Species, exposure and limitations are retained in each linked claim.

2 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.

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. Pharmacological reduction of creatine decreased whole-body energy expenditure after beta-3 agonist administration and reduced beige and brown adipose metabolic rate, and creatine metabolism genes were compensatorily induced when UCP1-dependent thermogenesis was ablated, with creatine reduction in Ucp1-deficient mice lowering core body temperature.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/cold-research/26496606.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f2d52dfe935e633b9d69280d707a124080d6f6c4d650f94bc8cf6a00f26e43e7", "start_char": 0, "end_char": 1097, "text_sha256": "f2d52dfe935e633b9d69280d707a124080d6f6c4d650f94bc8cf6a00f26e43e7"}
    experimental_model
    Quantitative mitochondrial proteomics of brown and beige fat with pharmacological creatine reduction
    exposure
    Cold exposure, beta-3 agonist administration, and creatine depletion
    limitations
    Identifies a UCP1-independent route. Pharmacological creatine reduction is a blunt tool, and the compensatory induction in UCP1-deficient mice is an expression finding.
    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
    Take creatine away and the burn falls, most visibly when the usual heat protein is already gone.
    primary_references
    [cold-p26496606] A creatine-driven substrate cycle enhances energy expenditure and thermogenesis in beige fat. (2015). https://pubmed.ncbi.nlm.nih.gov/26496606/ DOI: 10.1016/j.cell.2015.09.035
    tissue_or_cell_type
    Beige and brown 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 455–466

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Quantitative mitochondrial proteomics of brown and beige fat with pharmacological creatine reduction · source_derived_draft · unverified_draft

    ### cold-creatine-depletion-energy Pharmacological reduction of creatine decreased whole-body energy expenditure after beta-3 agonist administration and reduced beige and brown adipose metabolic rate, and creatine metabolism genes were compensatorily induced when UCP1-dependent thermogenesis was ablated, with creatine reduction in Ucp1-deficient mice lowering core body temperature. 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: Take creatine away and the burn falls, most visibly when the usual heat protein is already gone. organism: Mouse tissue_or_cell_type: Beige and brown adipose tissue experimental_model: Quantitative mitochondrial proteomics of brown and beige fat with pharmacological creatine reduction limitations: Identifies a UCP1-independent route. Pharmacological creatine reduction is a blunt tool, and the compensatory induction in UCP1-deficient mice is an expression finding. exposure: Cold exposure, beta-3 agonist administration, and creatine depletion evidence_span: {"source_cache": "artifacts/cold-research/26496606.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f2d52dfe935e633b9d69280d707a124080d6f6c4d650f94bc8cf6a00f26e43e7", "start_char": 0, "end_char": 1097, "text_sha256": "f2d52dfe935e633b9d69280d707a124080d6f6c4d650f94bc8cf6a00f26e43e7"} [cold-p26496606] A creatine-driven substrate cycle enhances energy expenditure and thermogenesis in beige fat. (2015). https://pubmed.ncbi.nlm.nih.gov/26496606/ DOI: 10.1016/j.cell.2015.09.035
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Cold exposure activated oxidative metabolism in brown adipose tissue but not in adjoining skeletal muscle or subcutaneous adipose tissue, with substantial non-esterified fatty acid and glucose uptake, and this was associated with an increase in total energy expenditure.

    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/cold-research/22269323.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "74713401a7fdc40f7921b595ecc554999d10e2406589f231fc68bf0ae460812f", "start_char": 0, "end_char": 1306, "text_sha256": "74713401a7fdc40f7921b595ecc554999d10e2406589f231fc68bf0ae460812f"}
    experimental_model
    Six healthy men studied with 11C-acetate, 18FDG and a fatty acid tracer under controlled cold
    exposure
    Controlled cold exposure with quantified oxidative metabolism and substrate turnover
    limitations
    The acetate tracer measures oxidative metabolism rather than glucose uptake alone, which is what makes the thermogenic claim interpretable. Six subjects is a small sample.
    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
    Human
    plain_language
    The tissue really does burn fuel in the cold, and its neighbours do not.
    primary_references
    [cold-p22269323] Brown adipose tissue oxidative metabolism contributes to energy expenditure during acute cold exposure in humans. (2012). https://pubmed.ncbi.nlm.nih.gov/22269323/ DOI: 10.1172/jci60433
    tissue_or_cell_type
    Brown adipose tissue, skeletal muscle and subcutaneous fat

    Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 273–284

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six healthy men studied with 11C-acetate, 18FDG and a fatty acid tracer under controlled cold · source_derived_draft · unverified_draft

    ### cold-bat-oxidative-activation Cold exposure activated oxidative metabolism in brown adipose tissue but not in adjoining skeletal muscle or subcutaneous adipose tissue, with substantial non-esterified fatty acid and glucose uptake, and this was associated with an increase in total energy expenditure. Condition category: normal 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: The tissue really does burn fuel in the cold, and its neighbours do not. organism: Human tissue_or_cell_type: Brown adipose tissue, skeletal muscle and subcutaneous fat experimental_model: Six healthy men studied with 11C-acetate, 18FDG and a fatty acid tracer under controlled cold limitations: The acetate tracer measures oxidative metabolism rather than glucose uptake alone, which is what makes the thermogenic claim interpretable. Six subjects is a small sample. exposure: Controlled cold exposure with quantified oxidative metabolism and substrate turnover evidence_span: {"source_cache": "artifacts/cold-research/22269323.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "74713401a7fdc40f7921b595ecc554999d10e2406589f231fc68bf0ae460812f", "start_char": 0, "end_char": 1306, "text_sha256": "74713401a7fdc40f7921b595ecc554999d10e2406589f231fc68bf0ae460812f"} [cold-p22269323] Brown adipose tissue oxidative metabolism contributes to energy expenditure during acute cold exposure in humans. (2012). https://pubmed.ncbi.nlm.nih.gov/22269323/ DOI: 10.1172/jci60433
    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