Nutrient chapter
Conjugated linoleic acid / CLA isomer family
CLA is a family of fatty-acid isomers. This chapter keeps cis-9,trans-11, trans-10,cis-12 and mixed preparations separate while tracing fat-cell signaling, vitamin A transport, calcium, omega-3 interactions, nitrite chemistry and human trial outcomes. Plain explanations accompany full technical records and exact sources.
64 recorded mechanisms · 0 availability situations · 4 preserved sources. Draft and verified records are labeled separately.
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The mechanisms
What the sources say this nutrient does, one relationship at a time. Plain wording comes first; the technical statement follows.
Deuterated trans-vaccenic acid administered as triglyceride produced labeled cis-9,trans-11 CLA in human serum lipids.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Reanalysis of four historical single-person tracer experiments.
- limitations
- Small tracer evidence; enrichment is not a universal dietary conversion fraction.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- The body can make one CLA isomer from a distinct dietary precursor.
- primary_references
- Biosynthesis of conjugated linoleic acid in humans. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10757542/ · DOI 10.1007/BF02664761
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Reanalysis of four historical single-person tracer experiments. · source_derived_draft · unverified_draft
## cla-vaccenic-tracer The body can make one CLA isomer from a distinct dietary precursor. Deuterated trans-vaccenic acid administered as triglyceride produced labeled cis-9,trans-11 CLA in human serum lipids. Model: Reanalysis of four historical single-person tracer experiments. Limitations: Small tracer evidence; enrichment is not a universal dietary conversion fraction. Evidence access: Primary abstract Biosynthesis of conjugated linoleic acid in humans. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10757542/ · DOI 10.1007/BF02664761
Complete structured claim and evidenceFeeding increasing vaccenic-acid intakes gave an estimated mean conversion to rumenic acid of 19%, with substantial individual variation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Thirty healthy adults; 1.5, 3 or 4.5 g/day vaccenic acid for nine days.
- limitations
- Protocol-specific estimate; not an instruction to consume these amounts.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Food-derived precursor supply contributes to measured CLA.
- primary_references
- Bioconversion of vaccenic acid to conjugated linoleic acid in humans. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12197992/ · DOI 10.1093/ajcn/76.3.504
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Thirty healthy adults; 1.5, 3 or 4.5 g/day vaccenic acid for nine days. · source_derived_draft · unverified_draft
## cla-conversion-rate Food-derived precursor supply contributes to measured CLA. Feeding increasing vaccenic-acid intakes gave an estimated mean conversion to rumenic acid of 19%, with substantial individual variation. Model: Thirty healthy adults; 1.5, 3 or 4.5 g/day vaccenic acid for nine days. Limitations: Protocol-specific estimate; not an instruction to consume these amounts. Evidence access: Primary abstract Bioconversion of vaccenic acid to conjugated linoleic acid in humans. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12197992/ · DOI 10.1093/ajcn/76.3.504
Complete structured claim and evidenceEnriched dairy increased c9,t11 CLA in plasma phosphatidylcholine, triglycerides, cholesteryl esters and peripheral blood mononuclear cells.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Double-blind crossover in healthy men; enriched products supplied both CLA and vaccenic acid for six weeks.
- limitations
- Cannot separate direct CLA intake from precursor conversion or infer health benefit.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- CLA reached several lipid compartments.
- primary_references
- Incorporation of cis-9, trans-11 conjugated linoleic acid and vaccenic acid (trans-11 18 : 1) into plasma and leucocyte lipids in healthy men consuming dairy products naturally enriched in these fatty acids. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16115358/ · DOI 10.1079/bjn20051506
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Double-blind crossover in healthy men; enriched products supplied both CLA and vaccenic acid for six weeks. · source_derived_draft · unverified_draft
## cla-incorporation CLA reached several lipid compartments. Enriched dairy increased c9,t11 CLA in plasma phosphatidylcholine, triglycerides, cholesteryl esters and peripheral blood mononuclear cells. Model: Double-blind crossover in healthy men; enriched products supplied both CLA and vaccenic acid for six weeks. Limitations: Cannot separate direct CLA intake from precursor conversion or infer health benefit. Evidence access: Primary abstract Incorporation of cis-9, trans-11 conjugated linoleic acid and vaccenic acid (trans-11 18 : 1) into plasma and leucocyte lipids in healthy men consuming dairy products naturally enriched in these fatty acids. · 2005 · https://pubmed.ncbi.nlm.nih.gov/16115358/ · DOI 10.1079/bjn20051506
Complete structured claim and evidenceReconstituting the non-heme iron and heme sites of a human SCD/cytochrome-b5 proteoliposome complex restored conversion of stearoyl-CoA to oleoyl-CoA.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human proteins translated in wheat-germ extract and assembled in liposomes.
- limitations
- The tested substrate was stearoyl-CoA, not vaccenic acid; nutrient status was not tested.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- The desaturation machinery needs metal-containing partners.
- primary_references
- Wheat germ cell-free translation, purification, and assembly of a functional human stearoyl-CoA desaturase complex. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18765284/ · DOI 10.1016/j.pep.2008.08.002
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human proteins translated in wheat-germ extract and assembled in liposomes. · source_derived_draft · unverified_draft
## cla-scd-cofactors The desaturation machinery needs metal-containing partners. Reconstituting the non-heme iron and heme sites of a human SCD/cytochrome-b5 proteoliposome complex restored conversion of stearoyl-CoA to oleoyl-CoA. Model: Human proteins translated in wheat-germ extract and assembled in liposomes. Limitations: The tested substrate was stearoyl-CoA, not vaccenic acid; nutrient status was not tested. Evidence access: Primary abstract Wheat germ cell-free translation, purification, and assembly of a functional human stearoyl-CoA desaturase complex. · 2008 · https://pubmed.ncbi.nlm.nih.gov/18765284/ · DOI 10.1016/j.pep.2008.08.002
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
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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-c9 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 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
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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 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 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
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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-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 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 c9,t11 CLA increased PPAR-gamma and several target-gene transcripts relative to vehicle.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Primary cultures of differentiating human preadipocytes.
- limitations
- Not proof of improved insulin sensitivity in humans.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- The other isomer gave a different transcriptional response.
- 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-c9 The other isomer gave a different transcriptional response. Adding c9,t11 CLA increased PPAR-gamma and several target-gene transcripts relative to vehicle. Model: Primary cultures of differentiating human preadipocytes. Limitations: Not proof of improved insulin sensitivity in humans. 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, 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
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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 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
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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 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 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
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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 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
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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 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 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 evidenceCaMKII 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 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 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
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 174–180
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 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 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 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
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 198–204
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 evidenceAdding 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 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 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 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
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 230–236
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 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
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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-c9 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 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
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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 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 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 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 270–276
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-c9 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 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 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
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 286–292
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 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
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 294–300
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 evidencec9,t11 increased arachidonate incorporation into phosphatidylcholine despite lower overall incorporation into membrane phospholipids.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human endothelial radiotracer experiment.
- limitations
- Does not show that extra choline reproduces the effect.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- A fatty acid was redistributed between membrane lipid pools.
- 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 endothelial radiotracer experiment. · source_derived_draft · unverified_draft
## cla-aa-pc A fatty acid was redistributed between membrane lipid pools. c9,t11 increased arachidonate incorporation into phosphatidylcholine despite lower overall incorporation into membrane phospholipids. Model: Human endothelial radiotracer experiment. Limitations: Does not show that extra choline reproduces the effect. 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 evidenceCLA yielded substantially more nitration products than nonconjugated linoleic acid under the tested nitrogen-oxide reactions.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Chemical, cellular and in-vivo nitration experiments.
- limitations
- This is formation of a different molecule, not evidence that plain CLA has every nitro-lipid action.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Its double-bond arrangement changes its chemical reactivity.
- primary_references
- Conjugated linoleic acid is a preferential substrate for fatty acid nitration. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23144452/ · DOI 10.1074/jbc.M112.401356
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Chemical, cellular and in-vivo nitration experiments. · source_derived_draft · unverified_draft
## cla-nitration Its double-bond arrangement changes its chemical reactivity. CLA yielded substantially more nitration products than nonconjugated linoleic acid under the tested nitrogen-oxide reactions. Model: Chemical, cellular and in-vivo nitration experiments. Limitations: This is formation of a different molecule, not evidence that plain CLA has every nitro-lipid action. Evidence access: Primary abstract Conjugated linoleic acid is a preferential substrate for fatty acid nitration. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23144452/ · DOI 10.1074/jbc.M112.401356
Complete structured claim and evidenceAdding CLA during labeled oral nitrite administration increased plasma 9-nitro-CLA formation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Healthy-volunteer crossover; five returned for CLA coadministration.
- limitations
- Small acute study using investigational formulations; not a dosing recommendation.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Dietary lipid changed which nitrogen-oxide products formed.
- primary_references
- Conjugated Linoleic Acid Modulates Clinical Responses to Oral Nitrite and Nitrate. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28739973/ · DOI 10.1161/HYPERTENSIONAHA.117.09016
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Healthy-volunteer crossover; five returned for CLA coadministration. · source_derived_draft · unverified_draft
## cla-human-nitro-9 Dietary lipid changed which nitrogen-oxide products formed. Adding CLA during labeled oral nitrite administration increased plasma 9-nitro-CLA formation. Model: Healthy-volunteer crossover; five returned for CLA coadministration. Limitations: Small acute study using investigational formulations; not a dosing recommendation. Evidence access: Primary abstract Conjugated Linoleic Acid Modulates Clinical Responses to Oral Nitrite and Nitrate. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28739973/ · DOI 10.1161/HYPERTENSIONAHA.117.09016
Complete structured claim and evidenceAdding CLA during labeled oral nitrite administration increased plasma 12-nitro-CLA formation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Same five-person paired coadministration study.
- limitations
- Same dataset as the 9-nitro product, not an independent replication.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- A second nitrated product was detected separately.
- primary_references
- Conjugated Linoleic Acid Modulates Clinical Responses to Oral Nitrite and Nitrate. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28739973/ · DOI 10.1161/HYPERTENSIONAHA.117.09016
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same five-person paired coadministration study. · source_derived_draft · unverified_draft
## cla-human-nitro-12 A second nitrated product was detected separately. Adding CLA during labeled oral nitrite administration increased plasma 12-nitro-CLA formation. Model: Same five-person paired coadministration study. Limitations: Same dataset as the 9-nitro product, not an independent replication. Evidence access: Primary abstract Conjugated Linoleic Acid Modulates Clinical Responses to Oral Nitrite and Nitrate. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28739973/ · DOI 10.1161/HYPERTENSIONAHA.117.09016
Complete structured claim and evidenceCLA coadministration reduced labeled NO–deoxyhemoglobin formation and attenuated nitrite-associated vasodilation and platelet inhibition.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Acute labeled-nitrite human study.
- limitations
- Does not quantify interactions with prescription nitrates or prove long-term harm.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Making more nitrated lipid coincided with less of another NO response.
- primary_references
- Conjugated Linoleic Acid Modulates Clinical Responses to Oral Nitrite and Nitrate. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28739973/ · DOI 10.1161/HYPERTENSIONAHA.117.09016
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Acute labeled-nitrite human study. · source_derived_draft · unverified_draft
## cla-no-diversion Making more nitrated lipid coincided with less of another NO response. CLA coadministration reduced labeled NO–deoxyhemoglobin formation and attenuated nitrite-associated vasodilation and platelet inhibition. Model: Acute labeled-nitrite human study. Limitations: Does not quantify interactions with prescription nitrates or prove long-term harm. Evidence access: Primary abstract Conjugated Linoleic Acid Modulates Clinical Responses to Oral Nitrite and Nitrate. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28739973/ · DOI 10.1161/HYPERTENSIONAHA.117.09016
Complete structured claim and evidenceNO2-CLA reacted reversibly with glutathione and other low-molecular-weight thiols through electrophilic beta and delta carbons.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Biochemical kinetic and mass-spectrometric studies.
- limitations
- Adduct formation is not proof of systemic glutathione depletion.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Glutathione can temporarily bind a CLA-derived metabolite.
- primary_references
- The Chemical Basis of Thiol Addition to Nitro-conjugated Linoleic Acid, a Protective Cell-signaling Lipid. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27923813/ · DOI 10.1074/jbc.M116.756288
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Biochemical kinetic and mass-spectrometric studies. · source_derived_draft · unverified_draft
## cla-gsh-adduct Glutathione can temporarily bind a CLA-derived metabolite. NO2-CLA reacted reversibly with glutathione and other low-molecular-weight thiols through electrophilic beta and delta carbons. Model: Biochemical kinetic and mass-spectrometric studies. Limitations: Adduct formation is not proof of systemic glutathione depletion. Evidence access: Primary abstract The Chemical Basis of Thiol Addition to Nitro-conjugated Linoleic Acid, a Protective Cell-signaling Lipid. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27923813/ · DOI 10.1074/jbc.M116.756288
Complete structured claim and evidenceHuman albumin bound NO2-CLA noncovalently and formed covalent adducts at Cys34.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Purified protein and chemical assays.
- limitations
- Distribution was a mechanistic implication, not a measured clinical outcome.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- A circulating carrier can bind the modified lipid in two ways.
- primary_references
- The Chemical Basis of Thiol Addition to Nitro-conjugated Linoleic Acid, a Protective Cell-signaling Lipid. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27923813/ · DOI 10.1074/jbc.M116.756288
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Purified protein and chemical assays. · source_derived_draft · unverified_draft
## cla-albumin A circulating carrier can bind the modified lipid in two ways. Human albumin bound NO2-CLA noncovalently and formed covalent adducts at Cys34. Model: Purified protein and chemical assays. Limitations: Distribution was a mechanistic implication, not a measured clinical outcome. Evidence access: Primary abstract The Chemical Basis of Thiol Addition to Nitro-conjugated Linoleic Acid, a Protective Cell-signaling Lipid. · 2017 · https://pubmed.ncbi.nlm.nih.gov/27923813/ · DOI 10.1074/jbc.M116.756288
Complete structured claim and evidenceAdding CLA inhibited conversion of 8-iso-PGF2alpha to its dinor metabolite in normal and adrenoleukodystrophy fibroblasts.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human fibroblasts; accompanying rat experiments showed reduced dinor products.
- limitations
- Does not prove all CLA-associated isoprostane increases are harmless or unrelated to oxidation.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- A higher oxidation marker can reflect slower removal.
- primary_references
- Impairment of 8-iso-PGF(2ALPHA) isoprostane metabolism by dietary conjugated linoleic acid (CLA). · 2009 · https://pubmed.ncbi.nlm.nih.gov/19403295/ · DOI 10.1016/j.plefa.2009.02.008
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 358–364
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human fibroblasts; accompanying rat experiments showed reduced dinor products. · source_derived_draft · unverified_draft
## cla-isoprostane-catabolism A higher oxidation marker can reflect slower removal. Adding CLA inhibited conversion of 8-iso-PGF2alpha to its dinor metabolite in normal and adrenoleukodystrophy fibroblasts. Model: Human fibroblasts; accompanying rat experiments showed reduced dinor products. Limitations: Does not prove all CLA-associated isoprostane increases are harmless or unrelated to oxidation. Evidence access: Primary abstract Impairment of 8-iso-PGF(2ALPHA) isoprostane metabolism by dietary conjugated linoleic acid (CLA). · 2009 · https://pubmed.ncbi.nlm.nih.gov/19403295/ · DOI 10.1016/j.plefa.2009.02.008
Complete structured claim and evidenceColon-specific Pparg deletion abolished the protective effect of dietary CLA against DSS colitis.
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
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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 evidenceCLA increased TFF3 in human SW480 cells; PPAR-gamma antagonist GW9662 prevented this induction.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Human colorectal cell line, 0–2.5 micromolar CLA.
- limitations
- Pharmacological support does not identify the active isomer or prove human mucosal healing.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- A mucosal-repair protein responded through a receptor-sensitive pathway.
- primary_references
- Dietary conjugated linoleic acid activates PPARγ and the intestinal trefoil factor in SW480 cells and mice with dextran sulfate sodium-induced colitis. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23077197/ · DOI 10.3945/jn.112.163931
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human colorectal cell line, 0–2.5 micromolar CLA. · source_derived_draft · unverified_draft
## cla-tff3 A mucosal-repair protein responded through a receptor-sensitive pathway. CLA increased TFF3 in human SW480 cells; PPAR-gamma antagonist GW9662 prevented this induction. Model: Human colorectal cell line, 0–2.5 micromolar CLA. Limitations: Pharmacological support does not identify the active isomer or prove human mucosal healing. Evidence access: Primary abstract Dietary conjugated linoleic acid activates PPARγ and the intestinal trefoil factor in SW480 cells and mice with dextran sulfate sodium-induced colitis. · 2012 · https://pubmed.ncbi.nlm.nih.gov/23077197/ · DOI 10.3945/jn.112.163931
Complete structured claim and evidenceA 1% CLA diet reduced disease and adenocarcinoma formation in Pparg-expressing mice, but not mice lacking Pparg in immune and epithelial cells.
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
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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
Complete structured claim and evidenceCLA feeding worsened AOM/DSS tumor formation despite reducing acute DSS colitis.
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
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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 evidenceMacrophage-specific Pparg deletion abolished the CLA-associated protumorigenic effect.
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
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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 evidenceIn-vivo neutralization of LAP-expressing cells abolished CLA-associated tumor promotion.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse antibody-intervention experiment targeting latency-associated peptide-expressing cells.
- limitations
- Not equivalent to proving that every TGF-beta signal was blocked or identifying a human treatment.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Perturbing the TGF-beta-associated cell population changed the result.
- 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
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse antibody-intervention experiment targeting latency-associated peptide-expressing cells. · source_derived_draft · unverified_draft
## cla-tgf-neutralization Perturbing the TGF-beta-associated cell population changed the result. In-vivo neutralization of LAP-expressing cells abolished CLA-associated tumor promotion. Model: Mouse antibody-intervention experiment targeting latency-associated peptide-expressing cells. Limitations: Not equivalent to proving that every TGF-beta signal was blocked or identifying a human treatment. 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 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
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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 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
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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 evidenceThree grams/day c9,t11 CLA for three months reduced insulin sensitivity 15% versus placebo, without a body-composition difference.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Twenty-five abdominally obese men; randomized placebo-controlled clamp study.
- limitations
- Does not establish effects from ordinary dairy intake or in other populations.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- The food-predominant isomer was not uniformly favorable at supplemental exposure.
- primary_references
- Effects of cis-9,trans-11 conjugated linoleic acid supplementation on insulin sensitivity, lipid peroxidation, and proinflammatory markers in obese men. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15277146/ · DOI 10.1093/ajcn/80.2.279
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Twenty-five abdominally obese men; randomized placebo-controlled clamp study. · source_derived_draft · unverified_draft
## cla-human-c9-insulin The food-predominant isomer was not uniformly favorable at supplemental exposure. Three grams/day c9,t11 CLA for three months reduced insulin sensitivity 15% versus placebo, without a body-composition difference. Model: Twenty-five abdominally obese men; randomized placebo-controlled clamp study. Limitations: Does not establish effects from ordinary dairy intake or in other populations. Evidence access: Primary abstract Effects of cis-9,trans-11 conjugated linoleic acid supplementation on insulin sensitivity, lipid peroxidation, and proinflammatory markers in obese men. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15277146/ · DOI 10.1093/ajcn/80.2.279
Complete structured claim and evidenceUrinary 8-iso-PGF2alpha increased 50% versus placebo with c9,t11 supplementation.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Same three-month trial.
- limitations
- Other experiments show CLA can alter marker catabolism; concentration alone does not isolate formation rate.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- A measured lipid-oxidation marker changed.
- primary_references
- Effects of cis-9,trans-11 conjugated linoleic acid supplementation on insulin sensitivity, lipid peroxidation, and proinflammatory markers in obese men. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15277146/ · DOI 10.1093/ajcn/80.2.279
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Same three-month trial. · source_derived_draft · unverified_draft
## cla-human-c9-marker A measured lipid-oxidation marker changed. Urinary 8-iso-PGF2alpha increased 50% versus placebo with c9,t11 supplementation. Model: Same three-month trial. Limitations: Other experiments show CLA can alter marker catabolism; concentration alone does not isolate formation rate. Evidence access: Primary abstract Effects of cis-9,trans-11 conjugated linoleic acid supplementation on insulin sensitivity, lipid peroxidation, and proinflammatory markers in obese men. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15277146/ · DOI 10.1093/ajcn/80.2.279
Complete structured claim and evidenceSix months of mixed-isomer CLA produced no significant clamp-measured insulin-sensitivity difference from placebo.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Substudy of a 118-person trial; 49 entered clamp substudy and 41 completed paired clamps.
- limitations
- A nonsignificant result is not proof of equivalence or universal safety.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- Another preparation and population gave a different result.
- primary_references
- The effect of 6 months supplementation with conjugated linoleic acid on insulin resistance in overweight and obese. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17031391/ · DOI 10.1038/sj.ijo.0803482
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AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Substudy of a 118-person trial; 49 entered clamp substudy and 41 completed paired clamps. · source_derived_draft · unverified_draft
## cla-mixed-clamp Another preparation and population gave a different result. Six months of mixed-isomer CLA produced no significant clamp-measured insulin-sensitivity difference from placebo. Model: Substudy of a 118-person trial; 49 entered clamp substudy and 41 completed paired clamps. Limitations: A nonsignificant result is not proof of equivalence or universal safety. Evidence access: Primary abstract The effect of 6 months supplementation with conjugated linoleic acid on insulin resistance in overweight and obese. · 2007 · https://pubmed.ncbi.nlm.nih.gov/17031391/ · DOI 10.1038/sj.ijo.0803482
Complete structured claim and evidenceAt one year, body fat mass was lower than placebo in CLA-triglyceride and free-fatty-acid groups by 8.7% and 6.9%, respectively.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- 180 overweight adults randomized to two formulations or olive oil.
- limitations
- These are fat-mass comparisons, not percentage-point body-fat changes or proven disease prevention.
- nutrient_topic
- CLA collection; isomer, preparation, species, exposure and manipulation remain explicit. · Conjugated linoleic acid / CLA isomer family
- plain_language
- A longer mixed-preparation trial found a body-composition effect.
- primary_references
- Conjugated linoleic acid supplementation for 1 y reduces body fat mass in healthy overweight humans. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15159244/ · DOI 10.1093/ajcn/79.6.1118
Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19) · lines 454–460
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · 180 overweight adults randomized to two formulations or olive oil. · source_derived_draft · unverified_draft
## cla-year-fat A longer mixed-preparation trial found a body-composition effect. At one year, body fat mass was lower than placebo in CLA-triglyceride and free-fatty-acid groups by 8.7% and 6.9%, respectively. Model: 180 overweight adults randomized to two formulations or olive oil. Limitations: These are fat-mass comparisons, not percentage-point body-fat changes or proven disease prevention. Evidence access: Primary abstract Conjugated linoleic acid supplementation for 1 y reduces body fat mass in healthy overweight humans. · 2004 · https://pubmed.ncbi.nlm.nih.gov/15159244/ · DOI 10.1093/ajcn/79.6.1118
Complete structured claim and evidenceHuman placental phosphatidylinositol synthase used myo-inositol and CDP-diacylglycerol to form phosphatidylinositol.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/8110188.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c05bb5272b443bde4f99d4af375d31988a4812150450d6c4462059a59aa8a09e", "start_char": 0, "end_char": 940, "text_sha256": "c05bb5272b443bde4f99d4af375d31988a4812150450d6c4462059a59aa8a09e"}
- experimental_model
- Purification and kinetics of placental PI synthase
- exposure
- Substrate and ion titrations
- limitations
- Assay optima and inhibitory concentrations are not dietary advice or proof of in vivo nutrient competition.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Homo sapiens
- plain_language
- This step attaches the inositol head group to a membrane lipid.
- primary_references
- [ino-p8110188] Purification and characterization of phosphatidylinositol synthase from human placenta. (1994). https://pubmed.ncbi.nlm.nih.gov/8110188/ DOI: 10.1042/bj2970517
- tissue_or_cell_type
- Placental microsomal enzyme
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 496–507
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Purification and kinetics of placental PI synthase · source_derived_draft · unverified_draft
### ino-cdipt-synthesis Human placental phosphatidylinositol synthase used myo-inositol and CDP-diacylglycerol to form phosphatidylinositol. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: This step attaches the inositol head group to a membrane lipid. organism: Homo sapiens tissue_or_cell_type: Placental microsomal enzyme experimental_model: Purification and kinetics of placental PI synthase limitations: Assay optima and inhibitory concentrations are not dietary advice or proof of in vivo nutrient competition. exposure: Substrate and ion titrations evidence_span: {"source_cache": "artifacts/inositol-research/8110188.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c05bb5272b443bde4f99d4af375d31988a4812150450d6c4462059a59aa8a09e", "start_char": 0, "end_char": 940, "text_sha256": "c05bb5272b443bde4f99d4af375d31988a4812150450d6c4462059a59aa8a09e"} [ino-p8110188] Purification and characterization of phosphatidylinositol synthase from human placenta. (1994). https://pubmed.ncbi.nlm.nih.gov/8110188/ DOI: 10.1042/bj2970517
Complete structured claim and evidencePLCB3 hydrolyzed PI(4,5)P2 to produce soluble IP3 and membrane-associated diacylglycerol.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/inositol-research/37991948.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7", "start_char": 0, "end_char": 1735, "text_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7"}
- experimental_model
- Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis
- exposure
- G-alpha-q and G-beta-gamma stimulation
- limitations
- Reconstituted biochemical regulation; not an oral inositol intervention. Product generation and lipid depletion occur in the same reaction.
- nutrient_topic
- Inositol research collection; topical membership is not evidence of a direct dietary effect. · Inositol (stereoisomer family)
- organism
- Recombinant mammalian signaling proteins
- plain_language
- Splitting one membrane lipid creates two different signaling products.
- primary_references
- [ino-p37991948] The mechanism of Gαq regulation of PLCβ3-catalyzed PIP2 hydrolysis. (2023). https://pubmed.ncbi.nlm.nih.gov/37991948/ DOI: 10.1073/pnas.2315011120
- tissue_or_cell_type
- Defined membrane bilayers
Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17) · lines 626–637
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis · source_derived_draft · unverified_draft
### ino-plc-ip3 PLCB3 hydrolyzed PI(4,5)P2 to produce soluble IP3 and membrane-associated diacylglycerol. Condition category: normal nutrient_topic: Inositol research collection; topical membership is not evidence of a direct dietary effect. plain_language: Splitting one membrane lipid creates two different signaling products. organism: Recombinant mammalian signaling proteins tissue_or_cell_type: Defined membrane bilayers experimental_model: Reconstituted lipid-bilayer kinetics and membrane-bound structural analysis limitations: Reconstituted biochemical regulation; not an oral inositol intervention. Product generation and lipid depletion occur in the same reaction. exposure: G-alpha-q and G-beta-gamma stimulation evidence_span: {"source_cache": "artifacts/inositol-research/37991948.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7", "start_char": 0, "end_char": 1735, "text_sha256": "fa553185ea3f13a8af7be9a548de14cd13ebe22ff307635fb76675ddc64347d7"} [ino-p37991948] The mechanism of Gαq regulation of PLCβ3-catalyzed PIP2 hydrolysis. (2023). https://pubmed.ncbi.nlm.nih.gov/37991948/ DOI: 10.1073/pnas.2315011120
Complete structured claim and evidenceHuman ITPR3 forms a calcium-release channel with an open pore in the IP3/ATP/Ca2+-bound structural state.
Experimental context and source evidence
- compartment_description
- ER membrane
- experimental_model
- Recombinant human ITPR3; cryo-EM in ligand-bound gating states
- limitations
- Structure specifies ITPR3; it must not be relabeled as ITPR1 or a measurement of every receptor subtype.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Homo sapiens
- plain_language
- ITPR3 provides a route for calcium to leave the ER.
- primary_references
- [ca-schmitz2022] Structural basis for activation and gating of IP3 receptors (2022). https://pubmed.ncbi.nlm.nih.gov/35301323/ DOI: 10.1038/s41467-022-29073-2
- research_relationship_category
- transport
- tissue_or_cell_type
- Recombinant ITPR3
- transport_effect
- raises A calcium-release channel: the recorded direction is ER lumen to cytosol.
- transport_or_reaction_direction
- ER lumen to cytosol
- transport_pool
- cytosolic calcium A calcium-release channel: the recorded direction is ER lumen to cytosol.
Calcium: mechanism-first literature curation (2026-09-17) · lines 478–490
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human ITPR3; cryo-EM in ligand-bound gating states · source_derived_draft · unverified_draft
### ca-itpr3-er-calcium-channel Human ITPR3 forms a calcium-release channel with an open pore in the IP3/ATP/Ca2+-bound structural state. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: ITPR3 provides a route for calcium to leave the ER. organism: Homo sapiens tissue_or_cell_type: Recombinant ITPR3 experimental_model: Recombinant human ITPR3; cryo-EM in ligand-bound gating states limitations: Structure specifies ITPR3; it must not be relabeled as ITPR1 or a measurement of every receptor subtype. research_relationship_category: transport transport_or_reaction_direction: ER lumen to cytosol compartment_description: ER membrane [ca-schmitz2022] Structural basis for activation and gating of IP3 receptors (2022). https://pubmed.ncbi.nlm.nih.gov/35301323/ DOI: 10.1038/s41467-022-29073-2
Complete structured claim and evidenceCalcium binding participates in ITPR3 gating after IP3/ATP priming, with both active and inactive calcium-bound conformations resolved.
Experimental context and source evidence
- compartment_description
- Cytosolic regulatory regions of ER channel
- experimental_model
- Recombinant human ITPR3; cryo-EM in ligand-bound gating states
- limitations
- Structural populations do not define a universal calcium threshold or prove all calcium-bound channels are active.
- nutrient_topic
- Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
- organism
- Homo sapiens
- plain_language
- Calcium helps control ITPR3 opening; binding does not guarantee that the channel stays open.
- primary_references
- [ca-schmitz2022] Structural basis for activation and gating of IP3 receptors (2022). https://pubmed.ncbi.nlm.nih.gov/35301323/ DOI: 10.1038/s41467-022-29073-2
- research_relationship_category
- regulation
- tissue_or_cell_type
- Recombinant ITPR3
Calcium: mechanism-first literature curation (2026-09-17) · lines 492–503
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human ITPR3; cryo-EM in ligand-bound gating states · source_derived_draft · unverified_draft
### ca-itpr3-calcium-coactivation Calcium binding participates in ITPR3 gating after IP3/ATP priming, with both active and inactive calcium-bound conformations resolved. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Calcium helps control ITPR3 opening; binding does not guarantee that the channel stays open. organism: Homo sapiens tissue_or_cell_type: Recombinant ITPR3 experimental_model: Recombinant human ITPR3; cryo-EM in ligand-bound gating states limitations: Structural populations do not define a universal calcium threshold or prove all calcium-bound channels are active. research_relationship_category: regulation compartment_description: Cytosolic regulatory regions of ER channel [ca-schmitz2022] Structural basis for activation and gating of IP3 receptors (2022). https://pubmed.ncbi.nlm.nih.gov/35301323/ DOI: 10.1038/s41467-022-29073-2
Complete structured claim and evidenceRbp4-null mice acquired hepatic vitamin A stores but could not mobilize them normally.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_location
- Abstract
- experimental_model
- Rbp4-knockout mice on vitamin A-sufficient and deficient diets.
- exposure
- Rbp4 knockout under sufficient and deficient feeding.
- limitations
- Alternative delivery operates with adequate intake; RBP4 is not the sole tissue supply route.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Mus musculus
- outcome
- Rbp4-null mice acquired hepatic vitamin A stores but could not mobilize them normally.
- plain_language
- Stored vitamin A can remain inaccessible when its transport protein is absent.
- primary_references
- [va-quadro-1999] Impaired retinal function and vitamin A availability in mice lacking retinol-binding protein (1999). https://pmc.ncbi.nlm.nih.gov/articles/PMC1171537/ DOI: 10.1093/emboj/18.17.4633
- tissue_or_cell_type
- Liver and circulation
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 374–386
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rbp4-knockout mice on vitamin A-sufficient and deficient diets. · source_derived_draft · unverified_draft
### va-rbp4-store-mobilization Rbp4-null mice acquired hepatic vitamin A stores but could not mobilize them normally. Condition category: machinery_impairment nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Stored vitamin A can remain inaccessible when its transport protein is absent. organism: Mus musculus tissue_or_cell_type: Liver and circulation experimental_model: Rbp4-knockout mice on vitamin A-sufficient and deficient diets. limitations: Alternative delivery operates with adequate intake; RBP4 is not the sole tissue supply route. exposure: Rbp4 knockout under sufficient and deficient feeding. outcome: Rbp4-null mice acquired hepatic vitamin A stores but could not mobilize them normally. evidence_location: Abstract [va-quadro-1999] Impaired retinal function and vitamin A availability in mice lacking retinol-binding protein (1999). https://pmc.ncbi.nlm.nih.gov/articles/PMC1171537/ DOI: 10.1093/emboj/18.17.4633
Complete structured claim and evidenceSTRA6 accelerated retinol release from extracellular RBP in real-time assays.
Experimental context and source evidence
- evidence_location
- Abstract
- experimental_model
- Transfected-cell radioretinol uptake and real-time retinol-release assays.
- exposure
- Retinol-loaded RBP and STRA6 expression.
- limitations
- In vitro transport mechanism; no organism-wide flux estimate. Cell-line species were not resolved in the retrieved abstract/figure evidence; no species-specific extension is asserted.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Mammalian transfected-cell preparations
- outcome
- STRA6 accelerated retinol release from extracellular RBP in real-time assays.
- plain_language
- The receptor unloads retinol from its blood carrier.
- primary_references
- [va-kawaguchi-2011] Receptor-mediated cellular uptake mechanism that couples to intracellular storage (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3199320/ DOI: 10.1021/cb200178w
- tissue_or_cell_type
- Plasma membrane
- transport_direction
- extracellular holo-RBP4 to membrane/cell
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 444–457
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected-cell radioretinol uptake and real-time retinol-release assays. · source_derived_draft · unverified_draft
### va-stra6-retinol-release STRA6 accelerated retinol release from extracellular RBP in real-time assays. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor unloads retinol from its blood carrier. organism: Mammalian transfected-cell preparations tissue_or_cell_type: Plasma membrane experimental_model: Transfected-cell radioretinol uptake and real-time retinol-release assays. limitations: In vitro transport mechanism; no organism-wide flux estimate. Cell-line species were not resolved in the retrieved abstract/figure evidence; no species-specific extension is asserted. exposure: Retinol-loaded RBP and STRA6 expression. outcome: STRA6 accelerated retinol release from extracellular RBP in real-time assays. evidence_location: Abstract transport_direction: extracellular holo-RBP4 to membrane/cell [va-kawaguchi-2011] Receptor-mediated cellular uptake mechanism that couples to intracellular storage (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3199320/ DOI: 10.1021/cb200178w
Complete structured claim and evidenceCoexpression of LRAT enhanced STRA6-mediated retinol uptake by coupling transport to ester storage.
Experimental context and source evidence
- evidence_location
- Figure 1
- experimental_model
- Transfected-cell radioretinol uptake and real-time retinol-release assays.
- exposure
- STRA6 with or without LRAT; radiolabeled holo-RBP uptake.
- limitations
- No single intracellular protein was absolutely required for STRA6 activity. Cell-line species were not resolved in the retrieved abstract/figure evidence; no species-specific extension is asserted.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Mammalian transfected cells
- outcome
- Coexpression of LRAT enhanced STRA6-mediated retinol uptake by coupling transport to ester storage.
- plain_language
- Retinol esterification helps keep inward uptake moving.
- primary_references
- [va-kawaguchi-2011] Receptor-mediated cellular uptake mechanism that couples to intracellular storage (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3199320/ DOI: 10.1021/cb200178w
- tissue_or_cell_type
- Plasma membrane and intracellular retinoid compartment
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 459–471
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected-cell radioretinol uptake and real-time retinol-release assays. · source_derived_draft · unverified_draft
### va-lrat-couples-stra6 Coexpression of LRAT enhanced STRA6-mediated retinol uptake by coupling transport to ester storage. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Retinol esterification helps keep inward uptake moving. organism: Mammalian transfected cells tissue_or_cell_type: Plasma membrane and intracellular retinoid compartment experimental_model: Transfected-cell radioretinol uptake and real-time retinol-release assays. limitations: No single intracellular protein was absolutely required for STRA6 activity. Cell-line species were not resolved in the retrieved abstract/figure evidence; no species-specific extension is asserted. exposure: STRA6 with or without LRAT; radiolabeled holo-RBP uptake. outcome: Coexpression of LRAT enhanced STRA6-mediated retinol uptake by coupling transport to ester storage. evidence_location: Figure 1 [va-kawaguchi-2011] Receptor-mediated cellular uptake mechanism that couples to intracellular storage (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3199320/ DOI: 10.1021/cb200178w
Complete structured claim and evidenceCellular RBP1 enhanced STRA6-mediated uptake of RBP-bound retinol.
Experimental context and source evidence
- evidence_location
- Figure 1
- experimental_model
- Transfected-cell radioretinol uptake and real-time retinol-release assays.
- exposure
- STRA6 plus CRBP-I compared with STRA6 alone.
- limitations
- Coupling is supported, but absolute RBP1 dependence is not. Cell-line species were not resolved in the retrieved abstract/figure evidence; no species-specific extension is asserted.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Mammalian transfected cells
- outcome
- Cellular RBP1 enhanced STRA6-mediated uptake of RBP-bound retinol.
- plain_language
- An intracellular retinol-binding protein helps retain delivered vitamin A.
- primary_references
- [va-kawaguchi-2011] Receptor-mediated cellular uptake mechanism that couples to intracellular storage (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3199320/ DOI: 10.1021/cb200178w
- tissue_or_cell_type
- Plasma membrane and cytoplasm
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 473–485
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected-cell radioretinol uptake and real-time retinol-release assays. · source_derived_draft · unverified_draft
### va-rbp1-couples-stra6 Cellular RBP1 enhanced STRA6-mediated uptake of RBP-bound retinol. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: An intracellular retinol-binding protein helps retain delivered vitamin A. organism: Mammalian transfected cells tissue_or_cell_type: Plasma membrane and cytoplasm experimental_model: Transfected-cell radioretinol uptake and real-time retinol-release assays. limitations: Coupling is supported, but absolute RBP1 dependence is not. Cell-line species were not resolved in the retrieved abstract/figure evidence; no species-specific extension is asserted. exposure: STRA6 plus CRBP-I compared with STRA6 alone. outcome: Cellular RBP1 enhanced STRA6-mediated uptake of RBP-bound retinol. evidence_location: Figure 1 [va-kawaguchi-2011] Receptor-mediated cellular uptake mechanism that couples to intracellular storage (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3199320/ DOI: 10.1021/cb200178w
Complete structured claim and evidenceHuman and rat liver LRAT activity transferred the sn-1 acyl group of phosphatidylcholine to CRBP-bound retinol.
Experimental context and source evidence
- cross_nutrient
- Phosphatidylcholine-dependent retinol storage links retinoid metabolism to choline-containing phospholipid availability.
- evidence_location
- Abstract
- experimental_model
- Human and rat liver microsomes supplied phosphatidylcholine and CRBP-bound retinol.
- exposure
- Exogenous phosphatidylcholine plus CRBP-bound retinol.
- limitations
- Biochemical donor requirement; dietary choline deficiency was not tested.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Homo sapiens and Rattus norvegicus
- outcome
- Human and rat liver LRAT activity transferred the sn-1 acyl group of phosphatidylcholine to CRBP-bound retinol.
- plain_language
- A membrane choline phospholipid supplies the fatty-acid group used to store vitamin A.
- primary_references
- [va-macdonald-1988] A lecithin:retinol acyltransferase activity in human and rat liver (1988). https://pubmed.ncbi.nlm.nih.gov/3178828/ DOI: 10.1016/S0006-291X(88)80818-0
- tissue_or_cell_type
- Liver microsomes
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 317–330
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and rat liver microsomes supplied phosphatidylcholine and CRBP-bound retinol. · source_derived_draft · unverified_draft
### va-lrat-phosphatidylcholine-donor Human and rat liver LRAT activity transferred the sn-1 acyl group of phosphatidylcholine to CRBP-bound retinol. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: A membrane choline phospholipid supplies the fatty-acid group used to store vitamin A. organism: Homo sapiens and Rattus norvegicus tissue_or_cell_type: Liver microsomes experimental_model: Human and rat liver microsomes supplied phosphatidylcholine and CRBP-bound retinol. limitations: Biochemical donor requirement; dietary choline deficiency was not tested. exposure: Exogenous phosphatidylcholine plus CRBP-bound retinol. outcome: Human and rat liver LRAT activity transferred the sn-1 acyl group of phosphatidylcholine to CRBP-bound retinol. evidence_location: Abstract cross_nutrient: Phosphatidylcholine-dependent retinol storage links retinoid metabolism to choline-containing phospholipid availability. [va-macdonald-1988] A lecithin:retinol acyltransferase activity in human and rat liver (1988). https://pubmed.ncbi.nlm.nih.gov/3178828/ DOI: 10.1016/S0006-291X(88)80818-0
Complete structured claim and evidence
Availability and dependencies
Each situation shows the normal role first, then what the sources report under a specific condition. A shortfall in the diet, a fault in the machinery, and a low blood reading are kept separate because they are not the same thing.
The sources
Every document behind this chapter is preserved word for word. Open one to read it in full with its recorded conflicts marked in place.
- Calcium: mechanism-first literature curation (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
- Conjugated linoleic acid: isomers, signaling, nutrient interactions and discovery (2026-09-19)AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · unverified_draftRead preserved source
- Inositol: synthesis, signaling, mineral interactions and conditional deficiency (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
- Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17)AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · unverified_draftRead preserved source
Recorded disagreements
Where two sources say different things, both are kept and the difference is explained. You can discuss a disagreement or propose a mechanism that might account for it.
- CLA and mouse colorectal tumors: protection versus promotionTwo primary AOM/DSS mouse studies report opposite tumor directions under CLA feeding: the 2010 study found reduced adenocarcinoma formation, whereas the 2018 study found increased tumor formation despite less acute colitis. This is an unresolved research disagreement, not an error corrected in a ledger draft. The protocols and cell-specific deletions are not identical.Read the recorded disagreement
Open questions in this collection
Questions the curators could not answer from the sources in front of them, kept here with the reason each one is still open. These are gaps in this collection, not findings or proof that no one has studied them.
Chapters are assembled from supplied drafts and curated literature summaries. Statements remain unverified against the primary studies, and the ledger is not medical advice.