Component

Norepinephrine-stimulated lipolysis in mouse brown adipocytes

Context-specific entity; species, compartment and exposure are stated on each claim.

4 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. Aralar1 silencing in primary mouse brown adipocytes impaired norepinephrine-induced lipid mobilization and increased small lipid-droplet accumulation.

    Mouse aralar / Slc25a12 → Norepinephrine-stimulated lipolysis in mouse brown adipocytes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse primary brown adipocytes; approximately 80% knockdown in the reported experiment.
    limitations
    This does not establish human weight-loss effects or a nutrient-intake threshold.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    Disrupting the carrier changed fat handling in the cell.
    primary_references
    The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41704162/ · DOI 10.1111/febs.70461
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 330–336

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse primary brown adipocytes; approximately 80% knockdown in the reported experiment. · source_derived_draft · unverified_draft

    ## l-aspartate-brown-aralar-lipids Disrupting the carrier changed fat handling in the cell. Aralar1 silencing in primary mouse brown adipocytes impaired norepinephrine-induced lipid mobilization and increased small lipid-droplet accumulation. Model: Mouse primary brown adipocytes; approximately 80% knockdown in the reported experiment. Limitations: This does not establish human weight-loss effects or a nutrient-intake threshold. Evidence access: Primary full text The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41704162/ · DOI 10.1111/febs.70461
    Complete structured claim and evidence

  2. Oxoglutarate-carrier silencing similarly increased small lipid droplets and impaired norepinephrine-induced lipolysis in mouse brown adipocytes.

    Mouse mitochondrial oxoglutarate carrier / Slc25a11 → Norepinephrine-stimulated lipolysis in mouse brown adipocytes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse primary brown adipocytes; adenoviral shRNA with metabolic assays.
    limitations
    Shared pathway dependence does not make the two carriers interchangeable.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    A second carrier in the same shuttle also affected lipid mobilization.
    primary_references
    The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41704162/ · DOI 10.1111/febs.70461
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 338–344

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse primary brown adipocytes; adenoviral shRNA with metabolic assays. · source_derived_draft · unverified_draft

    ## l-aspartate-brown-ogc-lipids A second carrier in the same shuttle also affected lipid mobilization. Oxoglutarate-carrier silencing similarly increased small lipid droplets and impaired norepinephrine-induced lipolysis in mouse brown adipocytes. Model: Mouse primary brown adipocytes; adenoviral shRNA with metabolic assays. Limitations: Shared pathway dependence does not make the two carriers interchangeable. Evidence access: Primary full text The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41704162/ · DOI 10.1111/febs.70461
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. In Dio2-null brown adipocytes the acute norepinephrine-, CL316,243- or forskolin-induced increases in lipolysis, UCP1 mRNA and oxygen consumption were all reduced because of impaired cAMP generation, and all were completely reversed by a single T3 injection 14 hours earlier.

    Experimental Dio2-disrupted mouse genotype → Cyclic adenosine monophosphate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/cold-research/11696583.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "adbd82ff8c43d8a2718cfa752c9a0607c367648d6573b968eb885c883376dc68", "start_char": 0, "end_char": 1332, "text_sha256": "adbd82ff8c43d8a2718cfa752c9a0607c367648d6573b968eb885c883376dc68"}
    experimental_model
    Mice with targeted disruption of the Dio2 gene, with brown adipocyte assays and T3 rescue
    exposure
    Cold stress, with norepinephrine, CL316,243 or forskolin stimulation, and a single T3 injection
    limitations
    The selenoenzyme is the link between thyroid hormone and sympathetic signalling. Plasma T3 was normal in the knockouts, so the defect is local hormone generation, not circulating hormone.
    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
    Without locally made hormone the cell cannot even hear the nerve signal properly.
    primary_references
    [cold-p11696583] The type 2 iodothyronine deiodinase is essential for adaptive thermogenesis in brown adipose tissue. (2001). https://pubmed.ncbi.nlm.nih.gov/11696583/ DOI: 10.1172/jci13803
    tissue_or_cell_type
    Brown adipose tissue
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Cold water immersion: cold sensing, heat production, the catecholamine axis and what repeated exposure changes (2026-09-19) · lines 403–414

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mice with targeted disruption of the Dio2 gene, with brown adipocyte assays and T3 rescue · source_derived_draft · unverified_draft

    ### cold-dio2-camp-defect In Dio2-null brown adipocytes the acute norepinephrine-, CL316,243- or forskolin-induced increases in lipolysis, UCP1 mRNA and oxygen consumption were all reduced because of impaired cAMP generation, and all were completely reversed by a single T3 injection 14 hours earlier. Condition category: nutrient_deficiency 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: Without locally made hormone the cell cannot even hear the nerve signal properly. organism: Mouse tissue_or_cell_type: Brown adipose tissue experimental_model: Mice with targeted disruption of the Dio2 gene, with brown adipocyte assays and T3 rescue limitations: The selenoenzyme is the link between thyroid hormone and sympathetic signalling. Plasma T3 was normal in the knockouts, so the defect is local hormone generation, not circulating hormone. exposure: Cold stress, with norepinephrine, CL316,243 or forskolin stimulation, and a single T3 injection evidence_span: {"source_cache": "artifacts/cold-research/11696583.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "adbd82ff8c43d8a2718cfa752c9a0607c367648d6573b968eb885c883376dc68", "start_char": 0, "end_char": 1332, "text_sha256": "adbd82ff8c43d8a2718cfa752c9a0607c367648d6573b968eb885c883376dc68"} [cold-p11696583] The type 2 iodothyronine deiodinase is essential for adaptive thermogenesis in brown adipose tissue. (2001). https://pubmed.ncbi.nlm.nih.gov/11696583/ DOI: 10.1172/jci13803
    Complete structured claim and evidence

  2. Silencing either carrier had no apparent effect on the measured respiratory rates despite changes in lipid handling.

    Aralar1 or OGC silencing in mouse brown adipocytes → Respiratory rate in mouse brown adipocyte carrier-knockdown experiments source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Same mouse primary-cell experiments; respiration measurements.
    limitations
    The null result is limited to the tested conditions and does not establish that the shuttle never contributes to respiration.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    A lipid-storage phenotype did not imply that mitochondrial oxygen consumption had collapsed.
    primary_references
    The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41704162/ · DOI 10.1111/febs.70461
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 346–352

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same mouse primary-cell experiments; respiration measurements. · source_derived_draft · unverified_draft

    ## l-aspartate-brown-respiration-limit A lipid-storage phenotype did not imply that mitochondrial oxygen consumption had collapsed. Silencing either carrier had no apparent effect on the measured respiratory rates despite changes in lipid handling. Model: Same mouse primary-cell experiments; respiration measurements. Limitations: The null result is limited to the tested conditions and does not establish that the shuttle never contributes to respiration. Evidence access: Primary full text The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41704162/ · DOI 10.1111/febs.70461
    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.

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