Component

Mouse adipocyte lipolysis

Mouse adipocyte lipolysis. 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. Copper-dependent PDE3B inhibition increased cAMP signaling and promoted lipolysis in 3T3-L1 adipocytes.

    Mouse cGMP-inhibited phosphodiesterase Pde3b → Mouse adipocyte lipolysis source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/copper-research/27272565.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8b7e13cc6ef608ddb589779fa85430ca530508013e710f380f4020c3f2632c7", "start_char": 0, "end_char": 1018, "text_sha256": "f8b7e13cc6ef608ddb589779fa85430ca530508013e710f380f4020c3f2632c7"}
    experimental_model
    Copper manipulation, purified Pde3b assays and adipocyte signaling
    exposure
    Copper perturbation and Pde3b cysteine mutations
    limitations
    This cellular signaling result is not a human weight-loss trial. Copper toxicity and systemic distribution are not captured by increasing one cell-culture signal.
    nutrient_topic
    Copper research collection; topical membership is not evidence of a direct dietary effect. · Copper
    organism
    Mouse proteins and 3T3-L1 adipocytes; Atp7b mutant mouse context
    plain_language
    The prolonged signal encouraged fat breakdown in these cells.
    primary_references
    [copper-p27272565] Copper regulates cyclic-AMP-dependent lipolysis. (2016). https://pubmed.ncbi.nlm.nih.gov/27272565/ DOI: 10.1038/nchembio.2098
    tissue_or_cell_type
    Adipocytes and purified enzyme

    Copper: transport, cuproenzymes, deficiency, excess and nutrient interactions (2026-09-17) · lines 1209–1220

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Copper manipulation, purified Pde3b assays and adipocyte signaling · source_derived_draft · unverified_draft

    ### copper-pde3b-camp-lipolysis Copper-dependent PDE3B inhibition increased cAMP signaling and promoted lipolysis in 3T3-L1 adipocytes. Condition category: normal nutrient_topic: Copper research collection; topical membership is not evidence of a direct dietary effect. plain_language: The prolonged signal encouraged fat breakdown in these cells. organism: Mouse proteins and 3T3-L1 adipocytes; Atp7b mutant mouse context tissue_or_cell_type: Adipocytes and purified enzyme experimental_model: Copper manipulation, purified Pde3b assays and adipocyte signaling limitations: This cellular signaling result is not a human weight-loss trial. Copper toxicity and systemic distribution are not captured by increasing one cell-culture signal. exposure: Copper perturbation and Pde3b cysteine mutations evidence_span: {"source_cache": "artifacts/copper-research/27272565.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f8b7e13cc6ef608ddb589779fa85430ca530508013e710f380f4020c3f2632c7", "start_char": 0, "end_char": 1018, "text_sha256": "f8b7e13cc6ef608ddb589779fa85430ca530508013e710f380f4020c3f2632c7"} [copper-p27272565] Copper regulates cyclic-AMP-dependent lipolysis. (2016). https://pubmed.ncbi.nlm.nih.gov/27272565/ DOI: 10.1038/nchembio.2098
    Complete structured claim and evidence

  2. D-beta-hydroxybutyrate inhibited mouse adipocyte lipolysis in an Hcar2-dependent manner.

    D-(R)-beta-hydroxybutyrate → Mouse adipocyte lipolysis source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse adipocyte experiments.
    limitations
    Whole-body ketone feedback was proposed; magnitude in human fasting was not established.
    nutrient_topic
    Fasting physiological-state collection; human protocols, cellular deprivation and refeeding are distinguished. · Fasting / abstention from energy intake
    plain_language
    A ketone could feed back on its upstream fuel supply.
    primary_references
    (D)-beta-Hydroxybutyrate inhibits adipocyte lipolysis via the nicotinic acid receptor PUMA-G. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15929991/ · DOI 10.1074/jbc.C500213200

    Fasting: fuel switching, nutrient sensing, ketone signaling, nutrient dependencies and refeeding (2026-09-18) · lines 360–366

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse adipocyte experiments. · source_derived_draft · unverified_draft

    ## fast-bhb-lipolysis-feedback A ketone could feed back on its upstream fuel supply. D-beta-hydroxybutyrate inhibited mouse adipocyte lipolysis in an Hcar2-dependent manner. Model: Mouse adipocyte experiments. Limitations: Whole-body ketone feedback was proposed; magnitude in human fasting was not established. Evidence access: Primary abstract (D)-beta-Hydroxybutyrate inhibits adipocyte lipolysis via the nicotinic acid receptor PUMA-G. · 2005 · https://pubmed.ncbi.nlm.nih.gov/15929991/ · DOI 10.1074/jbc.C500213200
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. FGF21 stimulated liver ketogenesis and white-adipose lipolysis.

    Mouse fibroblast growth factor 21 / Fgf21 → Ketone-body production source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse experiments.
    limitations
    Human timing differs; shared pathway labels retain mouse context.
    nutrient_topic
    Fasting physiological-state collection; human protocols, cellular deprivation and refeeding are distinguished. · Fasting / abstention from energy intake
    plain_language
    The endocrine signal altered fuel mobilization.
    primary_references
    Endocrine regulation of the fasting response by PPARalpha-mediated induction of fibroblast growth factor 21. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17550777/ · DOI 10.1016/j.cmet.2007.05.003

    Fasting: fuel switching, nutrient sensing, ketone signaling, nutrient dependencies and refeeding (2026-09-18) · lines 248–254

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse experiments. · source_derived_draft · unverified_draft

    ## fast-mouse-ketones The endocrine signal altered fuel mobilization. FGF21 stimulated liver ketogenesis and white-adipose lipolysis. Model: Mouse experiments. Limitations: Human timing differs; shared pathway labels retain mouse context. Evidence access: Primary abstract Endocrine regulation of the fasting response by PPARalpha-mediated induction of fibroblast growth factor 21. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17550777/ · DOI 10.1016/j.cmet.2007.05.003
    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