Component

Mouse peroxisome proliferator-activated receptor gamma / Pparg

Mouse peroxisome proliferator-activated receptor gamma / Pparg. Species, exposure and limitations are retained in each linked claim.

15 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. Loss of epithelial PPAR-gamma signaling increased Nos2 expression and colonic nitrate availability in the mouse study.

    Mouse peroxisome proliferator-activated receptor gamma / Pparg → Mouse inducible nitric oxide synthase / Nos2 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse epithelial signaling and luminal metabolite experiments.
    limitations
    Nitrate is a downstream electron acceptor; butyrate is not being claimed to chemically remove nitrate.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Changing host signaling supplied a different bacterial respiratory fuel.
    primary_references
    Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28798125/ · DOI 10.1126/science.aam9949
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 222–228

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

    ## butyrate-pparg-nos2 Changing host signaling supplied a different bacterial respiratory fuel. Loss of epithelial PPAR-gamma signaling increased Nos2 expression and colonic nitrate availability in the mouse study. Model: Mouse epithelial signaling and luminal metabolite experiments. Limitations: Nitrate is a downstream electron acceptor; butyrate is not being claimed to chemically remove nitrate. Evidence access: Primary abstract Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28798125/ · DOI 10.1126/science.aam9949
    Complete structured claim and evidence

  2. PPARgamma increased POU2F2 transcription.

    Mouse peroxisome proliferator-activated receptor gamma / Pparg → Mouse POU class 2 homeobox 2 / Pou2f2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/41407214.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08", "start_char": 0, "end_char": 1949, "text_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08"}
    experimental_model
    Mouse transfer/ablation experiments, cell assays and virtual screening
    exposure
    Nasunin intervention reported; exact regimen and binding validation unavailable in the indexed abstract
    limitations
    New preclinical study: virtual screening nomination is not a measured binding affinity. The pathway findings and treatment outcomes are retained separately. No human efficacy or dose inference.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Type 2 diabetic and control mice; mouse primary-cell models
    plain_language
    A second regulator links the upstream signal to cell differentiation.
    primary_references
    [nasunin-p41407214] Neutrophil-derived thrombospondin-1 (THBS1) drives type 2 diabetes-induced osteoporosis via CD36-PPARγ-POU2F2 signaling. (2026). https://pubmed.ncbi.nlm.nih.gov/41407214/ DOI: 10.1016/j.bbadis.2025.168139
    tissue_or_cell_type
    Neutrophil-to-macrophage signaling and osteoclastogenesis

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 445–456

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse transfer/ablation experiments, cell assays and virtual screening · source_derived_draft · unverified_draft

    ### nasunin-pparg-pou2f2 PPARgamma increased POU2F2 transcription. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A second regulator links the upstream signal to cell differentiation. organism: Type 2 diabetic and control mice; mouse primary-cell models tissue_or_cell_type: Neutrophil-to-macrophage signaling and osteoclastogenesis experimental_model: Mouse transfer/ablation experiments, cell assays and virtual screening limitations: New preclinical study: virtual screening nomination is not a measured binding affinity. The pathway findings and treatment outcomes are retained separately. No human efficacy or dose inference. exposure: Nasunin intervention reported; exact regimen and binding validation unavailable in the indexed abstract evidence_span: {"source_cache": "artifacts/nasunin-research/41407214.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08", "start_char": 0, "end_char": 1949, "text_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08"} [nasunin-p41407214] Neutrophil-derived thrombospondin-1 (THBS1) drives type 2 diabetes-induced osteoporosis via CD36-PPARγ-POU2F2 signaling. (2026). https://pubmed.ncbi.nlm.nih.gov/41407214/ DOI: 10.1016/j.bbadis.2025.168139
    Complete structured claim and evidence

  3. Colon-specific Pparg deletion abolished the protective effect of dietary CLA against DSS colitis.

    Mouse peroxisome proliferator-activated receptor gamma / Pparg → Mouse DSS colitis severity source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Conditional mouse deletion and matched littermate feeding study.
    limitations
    Mixture-specific animal result, not a human inflammatory-bowel-disease treatment.
    nutrient_topic
    CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
    plain_language
    Removing the regulator removed protection in this model.
    primary_references
    Activation of PPAR gamma and delta by conjugated linoleic acid mediates protection from experimental inflammatory bowel disease. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15362034/ · DOI 10.1053/j.gastro.2004.06.049

    Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 366–372

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Conditional mouse deletion and matched littermate feeding study. · source_derived_draft · unverified_draft

    ## cla-colitis-deletion Removing the regulator removed protection in this model. Colon-specific Pparg deletion abolished the protective effect of dietary CLA against DSS colitis. Model: Conditional mouse deletion and matched littermate feeding study. Limitations: Mixture-specific animal result, not a human inflammatory-bowel-disease treatment. Evidence access: Primary abstract Activation of PPAR gamma and delta by conjugated linoleic acid mediates protection from experimental inflammatory bowel disease. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15362034/ · DOI 10.1053/j.gastro.2004.06.049
    Complete structured claim and evidence

  4. Macrophage-specific Pparg deletion abolished the CLA-associated protumorigenic effect.

    Mouse peroxisome proliferator-activated receptor gamma / Pparg → Mouse AOM/DSS colorectal tumor burden source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Conditional mouse knockout experiment.
    limitations
    Does not imply all PPAR-gamma activity promotes cancer.
    nutrient_topic
    CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
    plain_language
    The relevant cell type mattered to the tumor response.
    primary_references
    CLA-supplemented diet accelerates experimental colorectal cancer by inducing TGF-β-producing macrophages and T cells. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30279515/ · DOI 10.1038/s41385-018-0090-8

    Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 398–404

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Conditional mouse knockout experiment. · source_derived_draft · unverified_draft

    ## cla-tumor-macrophage-deletion The relevant cell type mattered to the tumor response. Macrophage-specific Pparg deletion abolished the CLA-associated protumorigenic effect. Model: Conditional mouse knockout experiment. Limitations: Does not imply all PPAR-gamma activity promotes cancer. Evidence access: Primary abstract CLA-supplemented diet accelerates experimental colorectal cancer by inducing TGF-β-producing macrophages and T cells. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30279515/ · DOI 10.1038/s41385-018-0090-8
    Complete structured claim and evidence

What acts on it

  1. In mouse 3T3-L1 cells, luteolin suppressed adipogenesis and several PPAR gamma targets while increasing GLUT4 expression.

    Luteolin / 3′,4′,5,7-tetrahydroxyflavone → Mouse peroxisome proliferator-activated receptor gamma / Pparg source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse adipocyte differentiation and gene expression.
    limitations
    GLUT4 expression is not proof of increased glucose uptake in humans.
    nutrient_topic
    Luteolin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Luteolin / 3′,4′,5,7-tetrahydroxyflavone
    plain_language
    One receptor can produce different responses at different genes.
    primary_references
    Mode of peroxisome proliferator-activated receptor γ activation by luteolin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22391103/ · DOI 10.1124/mol.111.076216

    Luteolin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 372–378

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

    ## luteolin-pparg-gene-specific One receptor can produce different responses at different genes. In mouse 3T3-L1 cells, luteolin suppressed adipogenesis and several PPAR gamma targets while increasing GLUT4 expression. Model: Mouse adipocyte differentiation and gene expression. Limitations: GLUT4 expression is not proof of increased glucose uptake in humans. Evidence access: Primary abstract Mode of peroxisome proliferator-activated receptor γ activation by luteolin. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22391103/ · DOI 10.1124/mol.111.076216
    Complete structured claim and evidence

  2. CD36 signaling activated PPARgamma in the reported pathway.

    Mouse fatty-acid translocase / Cd36 → Mouse peroxisome proliferator-activated receptor gamma / Pparg source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/nasunin-research/41407214.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08", "start_char": 0, "end_char": 1949, "text_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08"}
    experimental_model
    Mouse transfer/ablation experiments, cell assays and virtual screening
    exposure
    Nasunin intervention reported; exact regimen and binding validation unavailable in the indexed abstract
    limitations
    New preclinical study: virtual screening nomination is not a measured binding affinity. The pathway findings and treatment outcomes are retained separately. No human efficacy or dose inference.
    nutrient_topic
    Nasunin research collection; topical membership is not evidence of a direct dietary effect. · Nasunin
    organism
    Type 2 diabetic and control mice; mouse primary-cell models
    plain_language
    The receptor response reaches a transcriptional regulator.
    primary_references
    [nasunin-p41407214] Neutrophil-derived thrombospondin-1 (THBS1) drives type 2 diabetes-induced osteoporosis via CD36-PPARγ-POU2F2 signaling. (2026). https://pubmed.ncbi.nlm.nih.gov/41407214/ DOI: 10.1016/j.bbadis.2025.168139
    tissue_or_cell_type
    Neutrophil-to-macrophage signaling and osteoclastogenesis

    Nasunin: identity, redox chemistry and nutrient connections (2026-09-17) · lines 432–443

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse transfer/ablation experiments, cell assays and virtual screening · source_derived_draft · unverified_draft

    ### nasunin-cd36-pparg CD36 signaling activated PPARgamma in the reported pathway. Condition category: normal nutrient_topic: Nasunin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor response reaches a transcriptional regulator. organism: Type 2 diabetic and control mice; mouse primary-cell models tissue_or_cell_type: Neutrophil-to-macrophage signaling and osteoclastogenesis experimental_model: Mouse transfer/ablation experiments, cell assays and virtual screening limitations: New preclinical study: virtual screening nomination is not a measured binding affinity. The pathway findings and treatment outcomes are retained separately. No human efficacy or dose inference. exposure: Nasunin intervention reported; exact regimen and binding validation unavailable in the indexed abstract evidence_span: {"source_cache": "artifacts/nasunin-research/41407214.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08", "start_char": 0, "end_char": 1949, "text_sha256": "e0958157d5bc8c5df908b6d7ff18348c83726b06b63d2dc6953ebfd2ffdf0a08"} [nasunin-p41407214] Neutrophil-derived thrombospondin-1 (THBS1) drives type 2 diabetes-induced osteoporosis via CD36-PPARγ-POU2F2 signaling. (2026). https://pubmed.ncbi.nlm.nih.gov/41407214/ DOI: 10.1016/j.bbadis.2025.168139
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The mouse experiments linked increased luminal respiratory electron acceptors to expansion of Escherichia and Salmonella when the PPAR-gamma homeostatic pathway was disrupted.

    Mouse colonic luminal nitrate availability → Mouse colonic Enterobacteriaceae expansion source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse microbiota perturbation and bacterial respiration experiments.
    limitations
    The pathway is not a universal explanation for every case of dysbiosis.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Host metabolism changed which bacteria could expand.
    primary_references
    Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28798125/ · DOI 10.1126/science.aam9949

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 230–236

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

    ## butyrate-electron-acceptor-growth Host metabolism changed which bacteria could expand. The mouse experiments linked increased luminal respiratory electron acceptors to expansion of Escherichia and Salmonella when the PPAR-gamma homeostatic pathway was disrupted. Model: Mouse microbiota perturbation and bacterial respiration experiments. Limitations: The pathway is not a universal explanation for every case of dysbiosis. Evidence access: Primary abstract Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28798125/ · DOI 10.1126/science.aam9949
    Complete structured claim and evidence

  2. Microbiota-supported PPAR-gamma signaling drove mouse colonocytes toward beta-oxidation, limiting oxygen available to bacteria in the colonic lumen.

    Butyrate → Mouse colonic epithelial oxygen consumption source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse antibiotic, epithelial Pparg and microbial respiration experiments.
    limitations
    Pathway dependence does not establish direct binding of butyrate to PPAR-gamma.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Colon-cell fuel use helped keep the neighboring microbial environment low in oxygen.
    primary_references
    Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28798125/ · DOI 10.1126/science.aam9949

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 214–220

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

    ## butyrate-pparg-oxygen Colon-cell fuel use helped keep the neighboring microbial environment low in oxygen. Microbiota-supported PPAR-gamma signaling drove mouse colonocytes toward beta-oxidation, limiting oxygen available to bacteria in the colonic lumen. Model: Mouse antibiotic, epithelial Pparg and microbial respiration experiments. Limitations: Pathway dependence does not establish direct binding of butyrate to PPAR-gamma. Evidence access: Primary abstract Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28798125/ · DOI 10.1126/science.aam9949
    Complete structured claim and evidence

  3. Cars2-derived cysteine persulfide/H2S signaling promoted EBF2 persulfidation and interaction with PPARgamma or BRG1, supporting thermogenic gene recruitment.

    Mouse mitochondrial cysteinyl-tRNA synthetase / Cars2 → Mouse early B-cell factor 2 / Ebf2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse-centered brown-adipocyte and in vivo experimental program.
    limitations
    Abstract does not fully resolve each chemical intermediate; do not equate free H2S, CysSSH and protein-bound persulfides.
    nutrient_topic
    L-Cysteine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Cysteine
    plain_language
    Sulfur chemistry fed back to the transcription machinery.
    primary_references
    Cars2-Mediated Cysteine Catabolism Drives Brown Fat Development and Thermogenesis Through Persulfidating EBF2. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41849685/ · DOI 10.1002/advs.202522690

    L-Cysteine: sulfur allocation, redox supply and cross-nutrient mechanisms (2026-09-19) · lines 396–402

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse-centered brown-adipocyte and in vivo experimental program. · source_derived_draft · unverified_draft

    ## l-cysteine-cars2-ebf2-persulfidation Sulfur chemistry fed back to the transcription machinery. Cars2-derived cysteine persulfide/H2S signaling promoted EBF2 persulfidation and interaction with PPARgamma or BRG1, supporting thermogenic gene recruitment. Model: Mouse-centered brown-adipocyte and in vivo experimental program. Limitations: Abstract does not fully resolve each chemical intermediate; do not equate free H2S, CysSSH and protein-bound persulfides. Evidence access: Primary abstract Cars2-Mediated Cysteine Catabolism Drives Brown Fat Development and Thermogenesis Through Persulfidating EBF2. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41849685/ · DOI 10.1002/advs.202522690
    Complete structured claim and evidence

  4. Astaxanthin opposed rosiglitazone-stimulated differentiation and lipid accumulation in mouse 3T3-L1 cells.

    Astaxanthin → Rosiglitazone-stimulated mouse 3T3-L1 differentiation source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse 3T3-L1 differentiation experiment.
    limitations
    This does not show that astaxanthin inhibits every PPAR-gamma response or causes weight loss in people.
    nutrient_topic
    Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
    plain_language
    A stimulated fat-cell program was reduced in culture.
    primary_references
    Astaxanthin functions differently as a selective peroxisome proliferator-activated receptor γ modulator in adipocytes and macrophages. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22732454/ · DOI 10.1016/j.bcp.2012.05.021

    Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 278–284

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse 3T3-L1 differentiation experiment. · source_derived_draft · unverified_draft

    ## astaxanthin-adipogenesis A stimulated fat-cell program was reduced in culture. Astaxanthin opposed rosiglitazone-stimulated differentiation and lipid accumulation in mouse 3T3-L1 cells. Model: Mouse 3T3-L1 differentiation experiment. Limitations: This does not show that astaxanthin inhibits every PPAR-gamma response or causes weight loss in people. Evidence access: Primary abstract Astaxanthin functions differently as a selective peroxisome proliferator-activated receptor γ modulator in adipocytes and macrophages. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22732454/ · DOI 10.1016/j.bcp.2012.05.021
    Complete structured claim and evidence

  5. Astaxanthin increased Cd36 and Abca1 transcripts in elicited mouse peritoneal macrophages, despite different effects on the adipocyte program.

    Astaxanthin → Mouse fatty-acid translocase / Cd36 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse macrophage expression assays.
    limitations
    Expression does not measure net cholesterol clearance or prove clinical antiatherosclerotic efficacy.
    nutrient_topic
    Astaxanthin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Astaxanthin
    plain_language
    The same treatment produced a different gene response in immune cells.
    primary_references
    Astaxanthin functions differently as a selective peroxisome proliferator-activated receptor γ modulator in adipocytes and macrophages. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22732454/ · DOI 10.1016/j.bcp.2012.05.021

    Astaxanthin: transport, membrane chemistry, signaling and nutrient interactions (2026-09-19) · lines 286–292

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

    ## astaxanthin-macrophage-cd36 The same treatment produced a different gene response in immune cells. Astaxanthin increased Cd36 and Abca1 transcripts in elicited mouse peritoneal macrophages, despite different effects on the adipocyte program. Model: Mouse macrophage expression assays. Limitations: Expression does not measure net cholesterol clearance or prove clinical antiatherosclerotic efficacy. Evidence access: Primary abstract Astaxanthin functions differently as a selective peroxisome proliferator-activated receptor γ modulator in adipocytes and macrophages. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22732454/ · DOI 10.1016/j.bcp.2012.05.021
    Complete structured claim and evidence

  6. Adding t10,c12 CLA inhibited beta-catenin degradation and increased its interaction with PPAR-gamma.

    trans-10,cis-12 conjugated linoleic acid → Mouse beta-catenin / Ctnnb1 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse 3T3-L1 adipocytes.
    limitations
    No universal activation of every Wnt target was observed.
    nutrient_topic
    CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
    plain_language
    A stabilized protein associated with the fat-cell regulator.
    primary_references
    Trans10, cis12 conjugated linoleic acid inhibits 3T3-L1 adipocyte adipogenesis by elevating β-catenin levels. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26780430/ · DOI 10.1016/j.bbalip.2016.01.004

    Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 206–212

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse 3T3-L1 adipocytes. · source_derived_draft · unverified_draft

    ## cla-beta-catenin A stabilized protein associated with the fat-cell regulator. Adding t10,c12 CLA inhibited beta-catenin degradation and increased its interaction with PPAR-gamma. Model: Mouse 3T3-L1 adipocytes. Limitations: No universal activation of every Wnt target was observed. Evidence access: Primary abstract Trans10, cis12 conjugated linoleic acid inhibits 3T3-L1 adipocyte adipogenesis by elevating β-catenin levels. · 2016 · https://pubmed.ncbi.nlm.nih.gov/26780430/ · DOI 10.1016/j.bbalip.2016.01.004
    Complete structured claim and evidence

  7. Feeding 0.4% t10,c12 CLA for four weeks produced fatty liver, hyperinsulinemia and lipoatrophy; c9,t11 and linoleic-acid diets did not show the same effects.

    trans-10,cis-12 conjugated linoleic acid → Mouse hepatic lipid accumulation source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse dietary comparison.
    limitations
    Not a human risk estimate or proof that insulin caused the liver phenotype.
    nutrient_topic
    CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
    plain_language
    Loss of adipose fat coexisted with liver fat accumulation.
    primary_references
    Dietary trans-10,cis-12 conjugated linoleic acid induces hyperinsulinemia and fatty liver in the mouse. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12235171/ · DOI 10.1194/jlr.m20008-jlr200

    Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 214–220

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

    ## cla-mouse-liver Loss of adipose fat coexisted with liver fat accumulation. Feeding 0.4% t10,c12 CLA for four weeks produced fatty liver, hyperinsulinemia and lipoatrophy; c9,t11 and linoleic-acid diets did not show the same effects. Model: Mouse dietary comparison. Limitations: Not a human risk estimate or proof that insulin caused the liver phenotype. Evidence access: Primary abstract Dietary trans-10,cis-12 conjugated linoleic acid induces hyperinsulinemia and fatty liver in the mouse. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12235171/ · DOI 10.1194/jlr.m20008-jlr200
    Complete structured claim and evidence

  8. CLA feeding worsened AOM/DSS tumor formation despite reducing acute DSS colitis.

    Study-specific mixed-isomer CLA preparations → Mouse AOM/DSS colorectal tumor burden source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse colitis and colorectal-tumor models.
    limitations
    Opposite tumor direction to the earlier study; protocol/composition differences require comparison.
    nutrient_topic
    CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
    plain_language
    Reducing inflammation did not guarantee cancer protection.
    primary_references
    CLA-supplemented diet accelerates experimental colorectal cancer by inducing TGF-β-producing macrophages and T cells. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30279515/ · DOI 10.1038/s41385-018-0090-8

    Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 390–396

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

    ## cla-tumor-promotion Reducing inflammation did not guarantee cancer protection. CLA feeding worsened AOM/DSS tumor formation despite reducing acute DSS colitis. Model: Mouse colitis and colorectal-tumor models. Limitations: Opposite tumor direction to the earlier study; protocol/composition differences require comparison. Evidence access: Primary abstract CLA-supplemented diet accelerates experimental colorectal cancer by inducing TGF-β-producing macrophages and T cells. · 2019 · https://pubmed.ncbi.nlm.nih.gov/30279515/ · DOI 10.1038/s41385-018-0090-8
    Complete structured claim and evidence

  9. A 1% CLA diet reduced disease and adenocarcinoma formation in Pparg-expressing mice, but not mice lacking Pparg in immune and epithelial cells.

    Study-specific mixed-isomer CLA preparations → Mouse AOM/DSS colorectal tumor burden source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Azoxymethane followed by 2% DSS; tissue-specific Pparg deletion.
    limitations
    A later AOM/DSS study found tumor promotion; see the unresolved research disagreement.
    nutrient_topic
    CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
    plain_language
    One study found protection dependent on the regulator.
    primary_references
    Conjugated linoleic acid ameliorates inflammation-induced colorectal cancer in mice through activation of PPARgamma. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20089779/ · DOI 10.3945/jn.109.115642

    Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 382–388

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Azoxymethane followed by 2% DSS; tissue-specific Pparg deletion. · source_derived_draft · unverified_draft

    ## cla-tumor-protection One study found protection dependent on the regulator. A 1% CLA diet reduced disease and adenocarcinoma formation in Pparg-expressing mice, but not mice lacking Pparg in immune and epithelial cells. Model: Azoxymethane followed by 2% DSS; tissue-specific Pparg deletion. Limitations: A later AOM/DSS study found tumor promotion; see the unresolved research disagreement. Evidence access: Primary abstract Conjugated linoleic acid ameliorates inflammation-induced colorectal cancer in mice through activation of PPARgamma. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20089779/ · DOI 10.3945/jn.109.115642
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    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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