Component

Body fat mass

Body fat mass. 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. Cold-activated brown adipose tissue activity was significantly lower in overweight or obese subjects than in lean subjects, with body-mass index and percentage body fat both negatively correlated and resting metabolic rate positively correlated.

    Brown adipose tissue glucose uptake → Body fat mass source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/cold-research/19357405.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fc69ba9ec6aa4e295cde530497a3ef435ad5fa436888932b81565c05eb4ecf67", "start_char": 0, "end_char": 2035, "text_sha256": "fc69ba9ec6aa4e295cde530497a3ef435ad5fa436888932b81565c05eb4ecf67"}
    experimental_model
    Twenty-four lean and overweight healthy men studied by integrated FDG PET and CT
    exposure
    Thermoneutral 22 degrees C versus mild cold exposure at 16 degrees C
    limitations
    A systematic human survey establishing that the tissue is present and cold-activated. Glucose uptake on PET is an activity surrogate, not a heat measurement.
    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 people with more fat had less of the tissue that burns it.
    primary_references
    [cold-p19357405] Cold-activated brown adipose tissue in healthy men. (2009). https://pubmed.ncbi.nlm.nih.gov/19357405/ DOI: 10.1056/nejmoa0808718
    tissue_or_cell_type
    Supraclavicular and paravertebral brown adipose tissue

    Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 260–271

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Twenty-four lean and overweight healthy men studied by integrated FDG PET and CT · source_derived_draft · unverified_draft

    ### cold-bat-inverse-adiposity Cold-activated brown adipose tissue activity was significantly lower in overweight or obese subjects than in lean subjects, with body-mass index and percentage body fat both negatively correlated and resting metabolic rate positively correlated. 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 people with more fat had less of the tissue that burns it. organism: Human tissue_or_cell_type: Supraclavicular and paravertebral brown adipose tissue experimental_model: Twenty-four lean and overweight healthy men studied by integrated FDG PET and CT limitations: A systematic human survey establishing that the tissue is present and cold-activated. Glucose uptake on PET is an activity surrogate, not a heat measurement. exposure: Thermoneutral 22 degrees C versus mild cold exposure at 16 degrees C evidence_span: {"source_cache": "artifacts/cold-research/19357405.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fc69ba9ec6aa4e295cde530497a3ef435ad5fa436888932b81565c05eb4ecf67", "start_char": 0, "end_char": 2035, "text_sha256": "fc69ba9ec6aa4e295cde530497a3ef435ad5fa436888932b81565c05eb4ecf67"} [cold-p19357405] Cold-activated brown adipose tissue in healthy men. (2009). https://pubmed.ncbi.nlm.nih.gov/19357405/ DOI: 10.1056/nejmoa0808718
    Complete structured claim and evidence

  2. 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. 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.

    Adipocyte-selective Gatm knockout mouse genotype → Diet-induced thermogenesis source_derived_draftungraded
    Experimental context and source evidence
    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
    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