Component
trans-10,cis-12 conjugated linoleic acid
Context-specific entity; species, compartment and exposure are stated on each claim.
29 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 it acts on
Adding t10,c12 CLA inhibited beta-catenin degradation and increased its interaction with PPAR-gamma.
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 evidenceAdding t10,c12 CLA increased intracellular calcium; BAPTA and the calcium-mobilization inhibitor TMB-8 attenuated the increase.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Primary human adipocytes with pharmacological perturbation.
- limitations
- Does not mean dietary calcium causes the effect or that a unique channel was identified.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- A local calcium signal helped initiate the response.
- primary_references
- Inflammation and insulin resistance induced by trans-10, cis-12 conjugated linoleic acid depend on intracellular calcium levels in primary cultures of human adipocytes. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20154361/ · DOI 10.1194/jlr.M005447
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary human adipocytes with pharmacological perturbation. · source_derived_draft · unverified_draft
## cla-calcium A local calcium signal helped initiate the response. Adding t10,c12 CLA increased intracellular calcium; BAPTA and the calcium-mobilization inhibitor TMB-8 attenuated the increase. Model: Primary human adipocytes with pharmacological perturbation. Limitations: Does not mean dietary calcium causes the effect or that a unique channel was identified. Evidence access: Primary abstract Inflammation and insulin resistance induced by trans-10, cis-12 conjugated linoleic acid depend on intracellular calcium levels in primary cultures of human adipocytes. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20154361/ · DOI 10.1194/jlr.M005447
Complete structured claim and evidenceCLA treatment increased IL-6 and IL-8 secretion from the human adipose culture systems.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human adipocytes, stromal-vascular cells and adipose explants.
- limitations
- Culture concentrations and cell mixtures limit extrapolation.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- The response could signal to neighboring cells.
- primary_references
- Conjugated linoleic acid promotes human adipocyte insulin resistance through NFkappaB-dependent cytokine production. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16155293/ · DOI 10.1074/jbc.M508159200
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 134–140
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human adipocytes, stromal-vascular cells and adipose explants. · source_derived_draft · unverified_draft
## cla-cytokines The response could signal to neighboring cells. CLA treatment increased IL-6 and IL-8 secretion from the human adipose culture systems. Model: Human adipocytes, stromal-vascular cells and adipose explants. Limitations: Culture concentrations and cell mixtures limit extrapolation. Evidence access: Primary abstract Conjugated linoleic acid promotes human adipocyte insulin resistance through NFkappaB-dependent cytokine production. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16155293/ · DOI 10.1074/jbc.M508159200
Complete structured claim and evidenceAdding t10,c12 CLA induced DGK-eta expression in primary human adipocytes.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Primary human adipocyte expression study.
- limitations
- Expression alone does not demonstrate increased catalytic flux.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Another lipid-signaling enzyme responded to CLA.
- primary_references
- Diacylglycerol kinase inhibitor R59022 attenuates conjugated linoleic acid-mediated inflammation in human adipocytes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23264678/ · DOI 10.1194/jlr.M031211
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 182–188
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary human adipocyte expression study. · source_derived_draft · unverified_draft
## cla-dgkh-expression Another lipid-signaling enzyme responded to CLA. Adding t10,c12 CLA induced DGK-eta expression in primary human adipocytes. Model: Primary human adipocyte expression study. Limitations: Expression alone does not demonstrate increased catalytic flux. Evidence access: Primary abstract Diacylglycerol kinase inhibitor R59022 attenuates conjugated linoleic acid-mediated inflammation in human adipocytes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23264678/ · DOI 10.1194/jlr.M031211
Complete structured claim and evidenceAdding t10,c12 CLA reduced GLUT4 gene expression and insulin-stimulated glucose uptake and oxidation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Primary cultures of differentiating human preadipocytes.
- limitations
- Reduced fat storage is not automatically improved metabolic health.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Less glucose entered the fat cells in response to insulin.
- primary_references
- Isomer-specific regulation of metabolism and PPARgamma signaling by CLA in human preadipocytes. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12730300/ · DOI 10.1194/jlr.M300001-JLR200
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary cultures of differentiating human preadipocytes. · source_derived_draft · unverified_draft
## cla-glut4 Less glucose entered the fat cells in response to insulin. Adding t10,c12 CLA reduced GLUT4 gene expression and insulin-stimulated glucose uptake and oxidation. Model: Primary cultures of differentiating human preadipocytes. Limitations: Reduced fat storage is not automatically improved metabolic health. Evidence access: Primary abstract Isomer-specific regulation of metabolism and PPARgamma signaling by CLA in human preadipocytes. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12730300/ · DOI 10.1194/jlr.M300001-JLR200
Complete structured claim and evidenceFat mass and weight fell from baseline in the t10,c12 arm but not significantly more than placebo.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Same 12-week trial.
- limitations
- Do not present within-group loss as superiority over placebo.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- A before-and-after change was not a demonstrated treatment benefit.
- primary_references
- Treatment with dietary trans10cis12 conjugated linoleic acid causes isomer-specific insulin resistance in obese men with the metabolic syndrome. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12196420/ · DOI 10.2337/diacare.25.9.1516
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 422–428
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same 12-week trial. · source_derived_draft · unverified_draft
## cla-human-t10-fat A before-and-after change was not a demonstrated treatment benefit. Fat mass and weight fell from baseline in the t10,c12 arm but not significantly more than placebo. Model: Same 12-week trial. Limitations: Do not present within-group loss as superiority over placebo. Evidence access: Primary abstract Treatment with dietary trans10cis12 conjugated linoleic acid causes isomer-specific insulin resistance in obese men with the metabolic syndrome. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12196420/ · DOI 10.2337/diacare.25.9.1516
Complete structured claim and evidenceThe purified t10,c12 arm increased insulin resistance by 19% and glycemia by 4% versus placebo.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Sixty abdominally obese men with metabolic-syndrome features; 12-week three-arm trial, 3.4 g/day assigned CLA preparation.
- limitations
- The mixed-isomer arm did not show the same glucose effect; formulation and population matter.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- The isolated isomer impaired glucose handling in this population.
- primary_references
- Treatment with dietary trans10cis12 conjugated linoleic acid causes isomer-specific insulin resistance in obese men with the metabolic syndrome. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12196420/ · DOI 10.2337/diacare.25.9.1516
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 414–420
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Sixty abdominally obese men with metabolic-syndrome features; 12-week three-arm trial, 3.4 g/day assigned CLA preparation. · source_derived_draft · unverified_draft
## cla-human-t10-insulin The isolated isomer impaired glucose handling in this population. The purified t10,c12 arm increased insulin resistance by 19% and glycemia by 4% versus placebo. Model: Sixty abdominally obese men with metabolic-syndrome features; 12-week three-arm trial, 3.4 g/day assigned CLA preparation. Limitations: The mixed-isomer arm did not show the same glucose effect; formulation and population matter. Evidence access: Primary abstract Treatment with dietary trans10cis12 conjugated linoleic acid causes isomer-specific insulin resistance in obese men with the metabolic syndrome. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12196420/ · DOI 10.2337/diacare.25.9.1516
Complete structured claim and evidenceFeeding 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.
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 evidenceAdding t10,c12 CLA promoted NF-kappa-B activation, including p65 phosphorylation and nuclear translocation with I-kappa-B-alpha degradation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human adipocyte/stromal-vascular cultures and explants.
- limitations
- Different cell populations contribute to the response.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Inflammatory signaling became active in the fat-cell cultures.
- primary_references
- Conjugated linoleic acid promotes human adipocyte insulin resistance through NFkappaB-dependent cytokine production. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16155293/ · DOI 10.1074/jbc.M508159200
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 126–132
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human adipocyte/stromal-vascular cultures and explants. · source_derived_draft · unverified_draft
## cla-nfkb Inflammatory signaling became active in the fat-cell cultures. Adding t10,c12 CLA promoted NF-kappa-B activation, including p65 phosphorylation and nuclear translocation with I-kappa-B-alpha degradation. Model: Human adipocyte/stromal-vascular cultures and explants. Limitations: Different cell populations contribute to the response. Evidence access: Primary abstract Conjugated linoleic acid promotes human adipocyte insulin resistance through NFkappaB-dependent cytokine production. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16155293/ · DOI 10.1074/jbc.M508159200
Complete structured claim and evidenceAdding t10,c12 CLA reduced oleic-acid uptake and oxidation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Primary cultures of differentiating human preadipocytes.
- limitations
- Does not determine whole-body fuel oxidation.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- This fat-cell result was not increased fat burning.
- primary_references
- Isomer-specific regulation of metabolism and PPARgamma signaling by CLA in human preadipocytes. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12730300/ · DOI 10.1194/jlr.M300001-JLR200
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 78–84
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary cultures of differentiating human preadipocytes. · source_derived_draft · unverified_draft
## cla-oleate This fat-cell result was not increased fat burning. Adding t10,c12 CLA reduced oleic-acid uptake and oxidation. Model: Primary cultures of differentiating human preadipocytes. Limitations: Does not determine whole-body fuel oxidation. Evidence access: Primary abstract Isomer-specific regulation of metabolism and PPARgamma signaling by CLA in human preadipocytes. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12730300/ · DOI 10.1194/jlr.M300001-JLR200
Complete structured claim and evidenceThe isomer inhibited arachidonic-acid- and collagen-induced platelet aggregation in the 5–7 micromolar I50 range.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human platelet preparation.
- limitations
- Reversible, timing-dependent effects; no clinical antithrombotic benefit or drug interaction quantified.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Platelet activation changed in a laboratory assay.
- primary_references
- Antiplatelet effects of conjugated linoleic acid isomers. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10320806/ · DOI 10.1016/s1388-1981(99)00055-4
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 278–284
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human platelet preparation. · source_derived_draft · unverified_draft
## cla-platelets-t10 Platelet activation changed in a laboratory assay. The isomer inhibited arachidonic-acid- and collagen-induced platelet aggregation in the 5–7 micromolar I50 range. Model: Human platelet preparation. Limitations: Reversible, timing-dependent effects; no clinical antithrombotic benefit or drug interaction quantified. Evidence access: Primary abstract Antiplatelet effects of conjugated linoleic acid isomers. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10320806/ · DOI 10.1016/s1388-1981(99)00055-4
Complete structured claim and evidenceAdding t10,c12 CLA increased plasma-membrane PLC-gamma1 abundance within three minutes.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Primary human adipocyte localization experiment.
- limitations
- Localization is not proof of direct CLA binding or identification of its receptor.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- A lipid-signaling enzyme moved toward the membrane.
- primary_references
- The phospholipase C inhibitor U73122 attenuates trans-10, cis-12 conjugated linoleic acid-mediated inflammatory signaling and insulin resistance in human adipocytes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23468551/ · DOI 10.3945/jn.112.173161
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 166–172
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary human adipocyte localization experiment. · source_derived_draft · unverified_draft
## cla-plc-location A lipid-signaling enzyme moved toward the membrane. Adding t10,c12 CLA increased plasma-membrane PLC-gamma1 abundance within three minutes. Model: Primary human adipocyte localization experiment. Limitations: Localization is not proof of direct CLA binding or identification of its receptor. Evidence access: Primary abstract The phospholipase C inhibitor U73122 attenuates trans-10, cis-12 conjugated linoleic acid-mediated inflammatory signaling and insulin resistance in human adipocytes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23468551/ · DOI 10.3945/jn.112.173161
Complete structured claim and evidenceAdding t10,c12, but not c9,t11 CLA, suppressed ligand-stimulated PPAR-gamma reporter activation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Primary human adipocyte culture and reporter experiments.
- limitations
- The 2003 transient-transfection study reported antagonism with both isomers; assay context remains relevant.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- An isomer could interfere with activation of the regulator.
- primary_references
- Trans-10, cis-12 conjugated linoleic acid antagonizes ligand-dependent PPARgamma activity in primary cultures of human adipocytes. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18287349/ · DOI 10.1093/jn/138.3.455
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 102–108
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary human adipocyte culture and reporter experiments. · source_derived_draft · unverified_draft
## cla-pparg-antagonism An isomer could interfere with activation of the regulator. Adding t10,c12, but not c9,t11 CLA, suppressed ligand-stimulated PPAR-gamma reporter activation. Model: Primary human adipocyte culture and reporter experiments. Limitations: The 2003 transient-transfection study reported antagonism with both isomers; assay context remains relevant. Evidence access: Primary abstract Trans-10, cis-12 conjugated linoleic acid antagonizes ligand-dependent PPARgamma activity in primary cultures of human adipocytes. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18287349/ · DOI 10.1093/jn/138.3.455
Complete structured claim and evidenceAdding t10,c12 CLA lowered PPAR-gamma and several target-gene transcripts.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Primary cultures of differentiating human preadipocytes.
- limitations
- Expression and direct ligand binding are different measurements.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- A regulator of fat-cell identity was suppressed.
- primary_references
- Isomer-specific regulation of metabolism and PPARgamma signaling by CLA in human preadipocytes. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12730300/ · DOI 10.1194/jlr.M300001-JLR200
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary cultures of differentiating human preadipocytes. · source_derived_draft · unverified_draft
## cla-pparg-expression-t10 A regulator of fat-cell identity was suppressed. Adding t10,c12 CLA lowered PPAR-gamma and several target-gene transcripts. Model: Primary cultures of differentiating human preadipocytes. Limitations: Expression and direct ligand binding are different measurements. Evidence access: Primary abstract Isomer-specific regulation of metabolism and PPARgamma signaling by CLA in human preadipocytes. · 2003 · https://pubmed.ncbi.nlm.nih.gov/12730300/ · DOI 10.1194/jlr.M300001-JLR200
Complete structured claim and evidenceAdding t10,c12 CLA increased PPAR-gamma and ERK1/2 phosphorylation before PPAR-gamma protein declined.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human adipocyte time-course experiments.
- limitations
- ERK causation of the PPAR-gamma phosphorylation was proposed rather than isolated here.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Signaling changed before the regulator became less abundant.
- primary_references
- Trans-10, cis-12 conjugated linoleic acid antagonizes ligand-dependent PPARgamma activity in primary cultures of human adipocytes. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18287349/ · DOI 10.1093/jn/138.3.455
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 110–116
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human adipocyte time-course experiments. · source_derived_draft · unverified_draft
## cla-pparg-phosphorylation Signaling changed before the regulator became less abundant. Adding t10,c12 CLA increased PPAR-gamma and ERK1/2 phosphorylation before PPAR-gamma protein declined. Model: Human adipocyte time-course experiments. Limitations: ERK causation of the PPAR-gamma phosphorylation was proposed rather than isolated here. Evidence access: Primary abstract Trans-10, cis-12 conjugated linoleic acid antagonizes ligand-dependent PPARgamma activity in primary cultures of human adipocytes. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18287349/ · DOI 10.1093/jn/138.3.455
Complete structured claim and evidenceOnly the t10,c12 preparation increased hepatic retinol secretion and serum retinol/RBP.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse dietary comparison.
- limitations
- Retinoid oxidation was only proposed; no demonstrated human deficiency or toxicity.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Vitamin A distribution changed beyond liver storage.
- primary_references
- Hepatic retinol secretion and storage are altered by dietary CLA: common and distinct actions of CLA c9,t11 and t10,c12 isomers. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19454764/ · DOI 10.1194/jlr.M900054-JLR200
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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-retinol-release Vitamin A distribution changed beyond liver storage. Only the t10,c12 preparation increased hepatic retinol secretion and serum retinol/RBP. Model: Mouse dietary comparison. Limitations: Retinoid oxidation was only proposed; no demonstrated human deficiency or toxicity. Evidence access: Primary abstract Hepatic retinol secretion and storage are altered by dietary CLA: common and distinct actions of CLA c9,t11 and t10,c12 isomers. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19454764/ · DOI 10.1194/jlr.M900054-JLR200
Complete structured claim and evidenceFeeding the enriched isomer preparation increased hepatic retinyl ester accumulation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse dietary isomer comparison.
- limitations
- Accumulation does not establish improved vitamin A function.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- CLA altered a vitamin A storage compartment.
- primary_references
- Hepatic retinol secretion and storage are altered by dietary CLA: common and distinct actions of CLA c9,t11 and t10,c12 isomers. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19454764/ · DOI 10.1194/jlr.M900054-JLR200
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 246–252
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse dietary isomer comparison. · source_derived_draft · unverified_draft
## cla-retinyl-t10 CLA altered a vitamin A storage compartment. Feeding the enriched isomer preparation increased hepatic retinyl ester accumulation. Model: Mouse dietary isomer comparison. Limitations: Accumulation does not establish improved vitamin A function. Evidence access: Primary abstract Hepatic retinol secretion and storage are altered by dietary CLA: common and distinct actions of CLA c9,t11 and t10,c12 isomers. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19454764/ · DOI 10.1194/jlr.M900054-JLR200
Complete structured claim and evidenceAt 45 micromolar, the isomer reduced SCD activity in MDA-MB-231 and MCF-7 cells; protein fell only in MDA-MB-231, while mRNA was not repressed.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human breast-cancer cell lines.
- limitations
- Cell-line biochemistry does not establish anticancer benefit or ordinary dietary exposure.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- The same enzyme changed through different regulatory levels.
- primary_references
- Inhibition of stearoyl-CoA desaturase activity by the cis-9,trans-11 isomer and the trans-10,cis-12 isomer of conjugated linoleic acid in MDA-MB-231 and MCF-7 human breast cancer cells. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12061775/ · DOI 10.1016/S0006-291X(02)00554-5
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 62–68
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human breast-cancer cell lines. · source_derived_draft · unverified_draft
## cla-scd-t10 The same enzyme changed through different regulatory levels. At 45 micromolar, the isomer reduced SCD activity in MDA-MB-231 and MCF-7 cells; protein fell only in MDA-MB-231, while mRNA was not repressed. Model: Human breast-cancer cell lines. Limitations: Cell-line biochemistry does not establish anticancer benefit or ordinary dietary exposure. Evidence access: Primary abstract Inhibition of stearoyl-CoA desaturase activity by the cis-9,trans-11 isomer and the trans-10,cis-12 isomer of conjugated linoleic acid in MDA-MB-231 and MCF-7 human breast cancer cells. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12061775/ · DOI 10.1016/S0006-291X(02)00554-5
Complete structured claim and evidence
Where it participates (unsigned role)
CaMKII inhibitor KN-62 attenuated CLA-induced stress/inflammatory responses and loss of insulin-stimulated glucose uptake.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human adipocyte pharmacology; CaMKII-beta induction also measured.
- limitations
- Inhibitor data alone do not prove CAMK2B is the sole required isoform.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Blocking a calcium-responsive kinase pathway weakened the response.
- primary_references
- Inflammation and insulin resistance induced by trans-10, cis-12 conjugated linoleic acid depend on intracellular calcium levels in primary cultures of human adipocytes. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20154361/ · DOI 10.1194/jlr.M005447
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human adipocyte pharmacology; CaMKII-beta induction also measured. · source_derived_draft · unverified_draft
## cla-camk Blocking a calcium-responsive kinase pathway weakened the response. CaMKII inhibitor KN-62 attenuated CLA-induced stress/inflammatory responses and loss of insulin-stimulated glucose uptake. Model: Human adipocyte pharmacology; CaMKII-beta induction also measured. Limitations: Inhibitor data alone do not prove CAMK2B is the sole required isoform. Evidence access: Primary abstract Inflammation and insulin resistance induced by trans-10, cis-12 conjugated linoleic acid depend on intracellular calcium levels in primary cultures of human adipocytes. · 2010 · https://pubmed.ncbi.nlm.nih.gov/20154361/ · DOI 10.1194/jlr.M005447
Complete structured claim and evidenceDGK inhibitor R59022 attenuated CLA-induced calcium accumulation and reductions in glucose/fatty-acid uptake.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Primary human adipocytes, R59022 pretreatment.
- limitations
- The inhibitor does not establish DGK-eta as the calcium-controlling isoform.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Pharmacological results connected lipid signaling and calcium.
- primary_references
- Diacylglycerol kinase inhibitor R59022 attenuates conjugated linoleic acid-mediated inflammation in human adipocytes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23264678/ · DOI 10.1194/jlr.M031211
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Primary human adipocytes, R59022 pretreatment. · source_derived_draft · unverified_draft
## cla-dgk-inhibitor Pharmacological results connected lipid signaling and calcium. DGK inhibitor R59022 attenuated CLA-induced calcium accumulation and reductions in glucose/fatty-acid uptake. Model: Primary human adipocytes, R59022 pretreatment. Limitations: The inhibitor does not establish DGK-eta as the calcium-controlling isoform. Evidence access: Primary abstract Diacylglycerol kinase inhibitor R59022 attenuates conjugated linoleic acid-mediated inflammation in human adipocytes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23264678/ · DOI 10.1194/jlr.M031211
Complete structured claim and evidenceDGK-eta siRNA reduced CLA-induced IL-8 and MCP-1 expression and JNK/c-Jun activation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human adipocyte RNA-interference experiment.
- limitations
- Partial effects do not establish an exclusive pathway.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Gene depletion supported a contribution by a specific enzyme.
- primary_references
- Diacylglycerol kinase inhibitor R59022 attenuates conjugated linoleic acid-mediated inflammation in human adipocytes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23264678/ · DOI 10.1194/jlr.M031211
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human adipocyte RNA-interference experiment. · source_derived_draft · unverified_draft
## cla-dgkh-knockdown Gene depletion supported a contribution by a specific enzyme. DGK-eta siRNA reduced CLA-induced IL-8 and MCP-1 expression and JNK/c-Jun activation. Model: Human adipocyte RNA-interference experiment. Limitations: Partial effects do not establish an exclusive pathway. Evidence access: Primary abstract Diacylglycerol kinase inhibitor R59022 attenuates conjugated linoleic acid-mediated inflammation in human adipocytes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23264678/ · DOI 10.1194/jlr.M031211
Complete structured claim and evidenceDHA co-feeding did not prevent CLA-associated loss of adipose mass or its gene-expression changes.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Same four-week mouse experiment.
- limitations
- Liver and adipose outcomes must remain distinct.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- The same combination did not rescue every tissue.
- primary_references
- The effect of docosahexaenoic acid on t10, c12-conjugated linoleic acid-induced changes in fatty acid composition of mouse liver, adipose, and muscle. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23170930/ · DOI 10.1089/met.2012.0116
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same four-week mouse experiment. · source_derived_draft · unverified_draft
## cla-dha-adipose The same combination did not rescue every tissue. DHA co-feeding did not prevent CLA-associated loss of adipose mass or its gene-expression changes. Model: Same four-week mouse experiment. Limitations: Liver and adipose outcomes must remain distinct. Evidence access: Primary abstract The effect of docosahexaenoic acid on t10, c12-conjugated linoleic acid-induced changes in fatty acid composition of mouse liver, adipose, and muscle. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23170930/ · DOI 10.1089/met.2012.0116
Complete structured claim and evidenceAdding 1.5% DHA to 0.5% t10,c12 CLA prevented the CLA-associated increase in liver fat.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Female C57BL/6N mice; four-week feeding study.
- limitations
- High experimental diet proportions; not established human supplement protection.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Another fatty acid changed the liver response.
- primary_references
- The effect of docosahexaenoic acid on t10, c12-conjugated linoleic acid-induced changes in fatty acid composition of mouse liver, adipose, and muscle. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23170930/ · DOI 10.1089/met.2012.0116
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Female C57BL/6N mice; four-week feeding study. · source_derived_draft · unverified_draft
## cla-dha-liver Another fatty acid changed the liver response. Adding 1.5% DHA to 0.5% t10,c12 CLA prevented the CLA-associated increase in liver fat. Model: Female C57BL/6N mice; four-week feeding study. Limitations: High experimental diet proportions; not established human supplement protection. Evidence access: Primary abstract The effect of docosahexaenoic acid on t10, c12-conjugated linoleic acid-induced changes in fatty acid composition of mouse liver, adipose, and muscle. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23170930/ · DOI 10.1089/met.2012.0116
Complete structured claim and evidenceAt 100 micromolar, c9,t11 inhibited endothelial eicosanoid production, whereas t10,c12 stimulated it.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human saphenous-vein endothelial cells with calcium-ionophore stimulation.
- limitations
- Lower-concentration results differed; no universal anti-inflammatory label.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Isomer and concentration changed the direction of the response.
- primary_references
- The effect of conjugated linoleic acid on arachidonic acid metabolism and eicosanoid production in human saphenous vein endothelial cells. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11880240/ · DOI 10.1016/s1388-1981(01)00198-6
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human saphenous-vein endothelial cells with calcium-ionophore stimulation. · source_derived_draft · unverified_draft
## cla-endothelium-c9 Isomer and concentration changed the direction of the response. At 100 micromolar, c9,t11 inhibited endothelial eicosanoid production, whereas t10,c12 stimulated it. Model: Human saphenous-vein endothelial cells with calcium-ionophore stimulation. Limitations: Lower-concentration results differed; no universal anti-inflammatory label. Evidence access: Primary abstract The effect of conjugated linoleic acid on arachidonic acid metabolism and eicosanoid production in human saphenous vein endothelial cells. · 2002 · https://pubmed.ncbi.nlm.nih.gov/11880240/ · DOI 10.1016/s1388-1981(01)00198-6
Complete structured claim and evidenceBRL co-treatment rescued FABP4, LPL and perilipin transcripts but did not prevent reduced GLUT4, glucose uptake or triglyceride content.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- One-week co-treatment of primary human adipocyte cultures.
- limitations
- Transcript rescue did not restore all downstream functions.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Restoring some target genes did not restore the whole response.
- primary_references
- Trans-10, cis-12 conjugated linoleic acid antagonizes ligand-dependent PPARgamma activity in primary cultures of human adipocytes. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18287349/ · DOI 10.1093/jn/138.3.455
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · One-week co-treatment of primary human adipocyte cultures. · source_derived_draft · unverified_draft
## cla-partial-rescue Restoring some target genes did not restore the whole response. BRL co-treatment rescued FABP4, LPL and perilipin transcripts but did not prevent reduced GLUT4, glucose uptake or triglyceride content. Model: One-week co-treatment of primary human adipocyte cultures. Limitations: Transcript rescue did not restore all downstream functions. Evidence access: Primary abstract Trans-10, cis-12 conjugated linoleic acid antagonizes ligand-dependent PPARgamma activity in primary cultures of human adipocytes. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18287349/ · DOI 10.1093/jn/138.3.455
Complete structured claim and evidencePLC inhibitor U73122 attenuated CLA-induced calcium accumulation, inflammatory signaling and impaired glucose uptake.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human adipocyte inhibitor experiment.
- limitations
- Broad inhibitor evidence does not isolate PLC-gamma1 as necessary.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- A phospholipase-sensitive step linked membrane signaling to calcium.
- primary_references
- The phospholipase C inhibitor U73122 attenuates trans-10, cis-12 conjugated linoleic acid-mediated inflammatory signaling and insulin resistance in human adipocytes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23468551/ · DOI 10.3945/jn.112.173161
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human adipocyte inhibitor experiment. · source_derived_draft · unverified_draft
## cla-plc-block A phospholipase-sensitive step linked membrane signaling to calcium. PLC inhibitor U73122 attenuated CLA-induced calcium accumulation, inflammatory signaling and impaired glucose uptake. Model: Human adipocyte inhibitor experiment. Limitations: Broad inhibitor evidence does not isolate PLC-gamma1 as necessary. Evidence access: Primary abstract The phospholipase C inhibitor U73122 attenuates trans-10, cis-12 conjugated linoleic acid-mediated inflammatory signaling and insulin resistance in human adipocytes. · 2013 · https://pubmed.ncbi.nlm.nih.gov/23468551/ · DOI 10.3945/jn.112.173161
Complete structured claim and evidenceRBP-deficient mice supported an RBP-dependent mechanism for CLA-induced hepatic retinol secretion and redistribution toward adipose tissue.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- RBP-loss mouse comparison with t10,c12 supplementation.
- limitations
- Genetic model, not evidence that RBP abundance alone predicts a human response.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- A transport protein helped determine where vitamin A went.
- primary_references
- Hepatic retinol secretion and storage are altered by dietary CLA: common and distinct actions of CLA c9,t11 and t10,c12 isomers. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19454764/ · DOI 10.1194/jlr.M900054-JLR200
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · RBP-loss mouse comparison with t10,c12 supplementation. · source_derived_draft · unverified_draft
## cla-rbp-loss A transport protein helped determine where vitamin A went. RBP-deficient mice supported an RBP-dependent mechanism for CLA-induced hepatic retinol secretion and redistribution toward adipose tissue. Model: RBP-loss mouse comparison with t10,c12 supplementation. Limitations: Genetic model, not evidence that RBP abundance alone predicts a human response. Evidence access: Primary abstract Hepatic retinol secretion and storage are altered by dietary CLA: common and distinct actions of CLA c9,t11 and t10,c12 isomers. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19454764/ · DOI 10.1194/jlr.M900054-JLR200
Complete structured claim and evidencep65 siRNA depletion attenuated CLA-induced loss of GLUT4 and PPAR-gamma proteins and suppression of glucose uptake.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human adipocyte RNA-interference experiment.
- limitations
- Supports a contribution in this model, not universal necessity in all tissues.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Removing a signaling component weakened the adverse response.
- primary_references
- Conjugated linoleic acid promotes human adipocyte insulin resistance through NFkappaB-dependent cytokine production. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16155293/ · DOI 10.1074/jbc.M508159200
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human adipocyte RNA-interference experiment. · source_derived_draft · unverified_draft
## cla-rela-knockdown Removing a signaling component weakened the adverse response. p65 siRNA depletion attenuated CLA-induced loss of GLUT4 and PPAR-gamma proteins and suppression of glucose uptake. Model: Human adipocyte RNA-interference experiment. Limitations: Supports a contribution in this model, not universal necessity in all tissues. Evidence access: Primary abstract Conjugated linoleic acid promotes human adipocyte insulin resistance through NFkappaB-dependent cytokine production. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16155293/ · DOI 10.1074/jbc.M508159200
Complete structured claim and evidenceThe mixture and individual isomers reduced arachidonate-derived TXB2 formation, while platelet 12-HETE formation was not inhibited.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human platelet radiotracer assay.
- limitations
- TXB2 is the measured readout of TXA2 formation.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Two branches from the same fatty acid responded differently.
- primary_references
- Antiplatelet effects of conjugated linoleic acid isomers. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10320806/ · DOI 10.1016/s1388-1981(99)00055-4
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human platelet radiotracer assay. · source_derived_draft · unverified_draft
## cla-txb2 Two branches from the same fatty acid responded differently. The mixture and individual isomers reduced arachidonate-derived TXB2 formation, while platelet 12-HETE formation was not inhibited. Model: Human platelet radiotracer assay. Limitations: TXB2 is the measured readout of TXA2 formation. Evidence access: Primary abstract Antiplatelet effects of conjugated linoleic acid isomers. · 1999 · https://pubmed.ncbi.nlm.nih.gov/10320806/ · DOI 10.1016/s1388-1981(99)00055-4
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.