Component

Experimental UCP1-ablated mouse genotype

Experimental UCP1-ablated mouse genotype. 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 it acts on

  1. At thermoneutrality, UCP1 ablation induced obesity even on control diet and vastly augmented diet-induced obesity, and high-fat diet increased norepinephrine-induced thermogenesis in wild-type but not UCP1-ablated mice, showing diet-induced thermogenesis fully emanates from UCP1 activity.

    Experimental UCP1-ablated mouse genotype → Body fat mass source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/cold-research/19187776.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "007fc44fbc02ff64861f816e90139d469f59bbe7d95bd22c6e4daecd38070b30", "start_char": 0, "end_char": 1051, "text_sha256": "007fc44fbc02ff64861f816e90139d469f59bbe7d95bd22c6e4daecd38070b30"}
    experimental_model
    UCP1-ablated C57Bl6 mice housed at thermoneutrality on control or high-fat diet
    exposure
    Thermoneutral housing with control and high-fat diets
    limitations
    Housing temperature is the whole point: the obesogenic effect appears only when thermal stress is removed. Earlier studies missed it for that reason.
    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
    Remove the heat protein and take away the cold, and the animal gets fat.
    primary_references
    [cold-p19187776] UCP1 ablation induces obesity and abolishes diet-induced thermogenesis in mice exempt from thermal stress by living at thermoneutrality. (2009). https://pubmed.ncbi.nlm.nih.gov/19187776/ DOI: 10.1016/j.cmet.2008.12.014
    tissue_or_cell_type
    Brown adipose tissue and whole body
    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 325–336

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · UCP1-ablated C57Bl6 mice housed at thermoneutrality on control or high-fat diet · source_derived_draft · unverified_draft

    ### cold-ucp1-ablation-obesity At thermoneutrality, UCP1 ablation induced obesity even on control diet and vastly augmented diet-induced obesity, and high-fat diet increased norepinephrine-induced thermogenesis in wild-type but not UCP1-ablated mice, showing diet-induced thermogenesis fully emanates from UCP1 activity. 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: Remove the heat protein and take away the cold, and the animal gets fat. organism: Mouse tissue_or_cell_type: Brown adipose tissue and whole body experimental_model: UCP1-ablated C57Bl6 mice housed at thermoneutrality on control or high-fat diet limitations: Housing temperature is the whole point: the obesogenic effect appears only when thermal stress is removed. Earlier studies missed it for that reason. exposure: Thermoneutral housing with control and high-fat diets evidence_span: {"source_cache": "artifacts/cold-research/19187776.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "007fc44fbc02ff64861f816e90139d469f59bbe7d95bd22c6e4daecd38070b30", "start_char": 0, "end_char": 1051, "text_sha256": "007fc44fbc02ff64861f816e90139d469f59bbe7d95bd22c6e4daecd38070b30"} [cold-p19187776] UCP1 ablation induces obesity and abolishes diet-induced thermogenesis in mice exempt from thermal stress by living at thermoneutrality. (2009). https://pubmed.ncbi.nlm.nih.gov/19187776/ DOI: 10.1016/j.cmet.2008.12.014
    Complete structured claim and evidence

Where it participates (unsigned role)

  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.

    Pharmacological reduction of tissue creatine levels → Whole-body energy expenditure source_derived_draftungraded
    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

  2. UCP1-ablated mice acclimated to 4 degrees C sustained heat production at four times resting levels entirely by shivering, with no substitution by any adaptive non-shivering thermogenic process in muscle or any other organ, and neither UCP2 nor UCP3 could substitute.

    Human mitochondrial uncoupling protein 1 / UCP1 → Non-shivering thermogenesis source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/cold-research/11511509.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e49074478632e22aff36d236fa55e5afb956a4b335f7d95d2cae6f02c4f3d05", "start_char": 0, "end_char": 1527, "text_sha256": "6e49074478632e22aff36d236fa55e5afb956a4b335f7d95d2cae6f02c4f3d05"}
    experimental_model
    UCP1-ablated mice acclimated successively to 4 degrees C
    exposure
    Successive cold acclimation with heat production at four times resting level
    limitations
    A demanding negative result: no substitute for the protein was recruited even under extreme thermogenic demand. It is a mouse result about adaptive non-shivering thermogenesis specifically.
    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
    Only one protein can produce adaptive heat without shivering; nothing else stands in for it.
    primary_references
    [cold-p11511509] Only UCP1 can mediate adaptive nonshivering thermogenesis in the cold. (2001). https://pubmed.ncbi.nlm.nih.gov/11511509/ DOI: 10.1096/fj.00-0536fje
    tissue_or_cell_type
    Brown adipose tissue, muscle and whole body
    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 312–323

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · UCP1-ablated mice acclimated successively to 4 degrees C · source_derived_draft · unverified_draft

    ### cold-ucp1-only-mediator UCP1-ablated mice acclimated to 4 degrees C sustained heat production at four times resting levels entirely by shivering, with no substitution by any adaptive non-shivering thermogenic process in muscle or any other organ, and neither UCP2 nor UCP3 could substitute. 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: Only one protein can produce adaptive heat without shivering; nothing else stands in for it. organism: Mouse tissue_or_cell_type: Brown adipose tissue, muscle and whole body experimental_model: UCP1-ablated mice acclimated successively to 4 degrees C limitations: A demanding negative result: no substitute for the protein was recruited even under extreme thermogenic demand. It is a mouse result about adaptive non-shivering thermogenesis specifically. exposure: Successive cold acclimation with heat production at four times resting level evidence_span: {"source_cache": "artifacts/cold-research/11511509.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "6e49074478632e22aff36d236fa55e5afb956a4b335f7d95d2cae6f02c4f3d05", "start_char": 0, "end_char": 1527, "text_sha256": "6e49074478632e22aff36d236fa55e5afb956a4b335f7d95d2cae6f02c4f3d05"} [cold-p11511509] Only UCP1 can mediate adaptive nonshivering thermogenesis in the cold. (2001). https://pubmed.ncbi.nlm.nih.gov/11511509/ DOI: 10.1096/fj.00-0536fje
    Complete structured claim and evidence

In the sources

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

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