Component
Diet-induced thermogenesis
Diet-induced thermogenesis. 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.
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 acts on it
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.
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
Where it participates (unsigned role)
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 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
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.