Component

Vitamin A

Vitamin A is a family of nutrient activities involved in vision, gene regulation and tissue function. Retinol, retinal isomers, retinoic acid, retinyl esters and provitamin carotenoids have separate records because they perform different roles.

56 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. Vitamin-A-deficient wild-type mice accumulated more hepatic lycopene than vitamin-A-sufficient mice.

    Vitamin A → Mouse hepatic lycopene content source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/lycopene-research/37269907.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "36b39754d4d3b4ed8721a15f8dffe03bfd387dcbef3ff50918daabb45c48e756", "start_char": 0, "end_char": 1986, "text_sha256": "36b39754d4d3b4ed8721a15f8dffe03bfd387dcbef3ff50918daabb45c48e756"}
    experimental_model
    Carotenoid-enzyme knockout comparison and vitamin-A diet experiment
    exposure
    1 mg lycopene in cottonseed oil daily for two weeks; separate vitamin-A-deficient versus sufficient diets
    limitations
    Mouse knockout distribution does not directly quantify human cleavage; increased ISX signaling does not prove conversion to vitamin A.
    nutrient_topic
    Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene
    organism
    Mouse
    plain_language
    A shortage of one nutrient can change the handling of another compound.
    primary_references
    [lycopene-p37269907] Lycopene Accumulation in Transgenic Mice Lacking One or Both Carotenoid Cleaving Enzymes. (2023). https://pubmed.ncbi.nlm.nih.gov/37269907/ DOI: 10.1016/j.tjnut.2023.05.025
    tissue_or_cell_type
    Liver, other tissues and intestinal gene expression
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 806–817

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Carotenoid-enzyme knockout comparison and vitamin-A diet experiment · source_derived_draft · unverified_draft

    ### lycopene-vitamin-a-status Vitamin-A-deficient wild-type mice accumulated more hepatic lycopene than vitamin-A-sufficient mice. Condition category: nutrient_deficiency nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: A shortage of one nutrient can change the handling of another compound. organism: Mouse tissue_or_cell_type: Liver, other tissues and intestinal gene expression experimental_model: Carotenoid-enzyme knockout comparison and vitamin-A diet experiment limitations: Mouse knockout distribution does not directly quantify human cleavage; increased ISX signaling does not prove conversion to vitamin A. exposure: 1 mg lycopene in cottonseed oil daily for two weeks; separate vitamin-A-deficient versus sufficient diets evidence_span: {"source_cache": "artifacts/lycopene-research/37269907.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "36b39754d4d3b4ed8721a15f8dffe03bfd387dcbef3ff50918daabb45c48e756", "start_char": 0, "end_char": 1986, "text_sha256": "36b39754d4d3b4ed8721a15f8dffe03bfd387dcbef3ff50918daabb45c48e756"} [lycopene-p37269907] Lycopene Accumulation in Transgenic Mice Lacking One or Both Carotenoid Cleaving Enzymes. (2023). https://pubmed.ncbi.nlm.nih.gov/37269907/ DOI: 10.1016/j.tjnut.2023.05.025
    Complete structured claim and evidence
  2. Visual function normalized within eight days of vitamin A treatment in the three reported deficient patients.

    Vitamin A → Visual sensitivity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    Before/after repletion follow-up
    limitations
    Uncontrolled treatment observation; no dose recommendation.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    plain_language
    Repletion reversed the measured visual deficit in this series.
    primary_references
    [kemp-1988] Visual function and rhodopsin levels in humans with vitamin A deficiency (1988). https://pubmed.ncbi.nlm.nih.gov/3350064/ DOI: 10.1016/S0014-4835(88)80076-9
    tissue_or_cell_type
    Retina
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1019–1028

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Before/after repletion follow-up · source_derived_draft · unverified_draft

    ### a-vision-deficiency-repletion Visual function normalized within eight days of vitamin A treatment in the three reported deficient patients. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Repletion reversed the measured visual deficit in this series. organism: Homo sapiens tissue_or_cell_type: Retina experimental_model: Before/after repletion follow-up limitations: Uncontrolled treatment observation; no dose recommendation. [kemp-1988] Visual function and rhodopsin levels in humans with vitamin A deficiency (1988). https://pubmed.ncbi.nlm.nih.gov/3350064/ DOI: 10.1016/S0014-4835(88)80076-9
    Complete structured claim and evidence
  3. In three vitamin A-deficient patients, slow rod dark adaptation accompanied abnormally slow rhodopsin regeneration.

    Vitamin A → Rhodopsin regeneration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    Adaptometry and fundus reflectometry
    limitations
    Disease-associated deficiency; no general threshold or intake estimate.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    plain_language
    Pigment recovery slowed when vitamin A was depleted.
    primary_references
    [kemp-1988] Visual function and rhodopsin levels in humans with vitamin A deficiency (1988). https://pubmed.ncbi.nlm.nih.gov/3350064/ DOI: 10.1016/S0014-4835(88)80076-9
    tissue_or_cell_type
    Mid-peripheral retina
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 997–1006

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adaptometry and fundus reflectometry · source_derived_draft · unverified_draft

    ### a-vision-deficiency-rhodopsin In three vitamin A-deficient patients, slow rod dark adaptation accompanied abnormally slow rhodopsin regeneration. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Pigment recovery slowed when vitamin A was depleted. organism: Homo sapiens tissue_or_cell_type: Mid-peripheral retina experimental_model: Adaptometry and fundus reflectometry limitations: Disease-associated deficiency; no general threshold or intake estimate. [kemp-1988] Visual function and rhodopsin levels in humans with vitamin A deficiency (1988). https://pubmed.ncbi.nlm.nih.gov/3350064/ DOI: 10.1016/S0014-4835(88)80076-9
    Complete structured claim and evidence
  4. All three deficient patients initially lacked measurable rod function and had delayed cone adaptation.

    Vitamin A → Visual sensitivity source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    Baseline visual function
    limitations
    Clinical series of three, not a population effect size.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    plain_language
    Severe depletion impaired night vision and also slowed cone recovery.
    primary_references
    [kemp-1988] Visual function and rhodopsin levels in humans with vitamin A deficiency (1988). https://pubmed.ncbi.nlm.nih.gov/3350064/ DOI: 10.1016/S0014-4835(88)80076-9
    tissue_or_cell_type
    Retina
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1008–1017

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Baseline visual function · source_derived_draft · unverified_draft

    ### a-vision-deficiency-sensitivity All three deficient patients initially lacked measurable rod function and had delayed cone adaptation. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Severe depletion impaired night vision and also slowed cone recovery. organism: Homo sapiens tissue_or_cell_type: Retina experimental_model: Baseline visual function limitations: Clinical series of three, not a population effect size. [kemp-1988] Visual function and rhodopsin levels in humans with vitamin A deficiency (1988). https://pubmed.ncbi.nlm.nih.gov/3350064/ DOI: 10.1016/S0014-4835(88)80076-9
    Complete structured claim and evidence
  5. Vitamin A-supplemented diets increased ocular A2E/bisretinoid accumulation in wild-type and Abca4-null mice relative to control diets.

    Vitamin A → A2E bisretinoid source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Dietary supplementation versus control; biochemical and morphologic endpoints
    exposure
    dietary vitamin A excess/supplementation
    genotype
    wild type and Abca4-null
    limitations
    Mouse exposure; no human dose or treatment recommendation follows. Degeneration depended on pigmentation and occurred on both diets.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Extra vitamin A increased visual-cycle by-products in these mice.
    primary_references
    [radu-2008] Accelerated accumulation of lipofuscin pigments in the RPE of a mouse model for ABCA4-mediated retinal dystrophies following Vitamin A supplementation (2008). https://pubmed.ncbi.nlm.nih.gov/18515570/ DOI: 10.1167/iovs.07-1470
    tissue_or_cell_type
    Eye/RPE

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 847–858

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary supplementation versus control; biochemical and morphologic endpoints · source_derived_draft · unverified_draft

    ### a-vision-excess-bisretinoids Vitamin A-supplemented diets increased ocular A2E/bisretinoid accumulation in wild-type and Abca4-null mice relative to control diets. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Extra vitamin A increased visual-cycle by-products in these mice. organism: Mus musculus tissue_or_cell_type: Eye/RPE experimental_model: Dietary supplementation versus control; biochemical and morphologic endpoints limitations: Mouse exposure; no human dose or treatment recommendation follows. Degeneration depended on pigmentation and occurred on both diets. exposure: dietary vitamin A excess/supplementation genotype: wild type and Abca4-null [radu-2008] Accelerated accumulation of lipofuscin pigments in the RPE of a mouse model for ABCA4-mediated retinal dystrophies following Vitamin A supplementation (2008). https://pubmed.ncbi.nlm.nih.gov/18515570/ DOI: 10.1167/iovs.07-1470
    Complete structured claim and evidence
  6. Chronic vitamin A hepatotoxicity cases included cirrhosis and portal hypertension with characteristic hepatic storage-cell changes.

    Vitamin A → Liver fibrosis source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    41 selected clinical cases with liver histology.
    exposure
    Chronic preformed-vitamin-A exposure; excess, not deficiency.
    limitations
    Case series cannot estimate population incidence or define a safe-dose threshold.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    plain_language
    Prolonged excess can damage the organ that stores vitamin A.
    primary_references
    [va-geubel1991] Liver damage caused by therapeutic vitamin A administration: estimate of dose-related toxicity in 41 cases (1991). https://pubmed.ncbi.nlm.nih.gov/2019375/ DOI: 10.1016/0016-5085(91)90672-8
    tissue_or_cell_type
    Liver

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1834–1844

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 41 selected clinical cases with liver histology. · source_derived_draft · unverified_draft

    ### va-chronic-excess-liver-injury Chronic vitamin A hepatotoxicity cases included cirrhosis and portal hypertension with characteristic hepatic storage-cell changes. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Prolonged excess can damage the organ that stores vitamin A. organism: Homo sapiens tissue_or_cell_type: Liver experimental_model: 41 selected clinical cases with liver histology. limitations: Case series cannot estimate population incidence or define a safe-dose threshold. exposure: Chronic preformed-vitamin-A exposure; excess, not deficiency. [va-geubel1991] Liver damage caused by therapeutic vitamin A administration: estimate of dose-related toxicity in 41 cases (1991). https://pubmed.ncbi.nlm.nih.gov/2019375/ DOI: 10.1016/0016-5085(91)90672-8
    Complete structured claim and evidence
  7. Vitamin A deficiency reduced renal Epo mRNA in the rat experiment.

    Vitamin A → EPO mRNA source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    Renal gene-expression assay.
    limitations
    Does not by itself measure circulating EPO or prove ineffective erythropoiesis mediation.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Rattus norvegicus
    plain_language
    A shortage affected expression of an erythropoietic signal.
    primary_references
    [va-cunha2014] Vitamin A deficiency modulates iron metabolism via ineffective erythropoiesis (2014). https://pubmed.ncbi.nlm.nih.gov/24998947/ DOI: 10.1016/j.jnutbio.2014.05.005
    tissue_or_cell_type
    Kidney
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1755–1764

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Renal gene-expression assay. · source_derived_draft · unverified_draft

    ### va-deficiency-epo-transcript Vitamin A deficiency reduced renal Epo mRNA in the rat experiment. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: A shortage affected expression of an erythropoietic signal. organism: Rattus norvegicus tissue_or_cell_type: Kidney experimental_model: Renal gene-expression assay. limitations: Does not by itself measure circulating EPO or prove ineffective erythropoiesis mediation. [va-cunha2014] Vitamin A deficiency modulates iron metabolism via ineffective erythropoiesis (2014). https://pubmed.ncbi.nlm.nih.gov/24998947/ DOI: 10.1016/j.jnutbio.2014.05.005
    Complete structured claim and evidence
  8. Vitamin A deficiency reduced intestinal Fpn1 transcripts in the same rat study.

    Vitamin A → SLC40A1 mRNA source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    Intestinal mRNA assay.
    limitations
    Does not quantify ferroportin membrane protein or iron-export flux.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Rattus norvegicus
    plain_language
    Expression of an iron-export component changed alongside systemic signals.
    primary_references
    [va-cunha2016] Vitamin A deficiency modulates iron metabolism independent of hemojuvelin (Hfe2) and bone morphogenetic protein 6 (Bmp6) transcript levels (2016). https://pubmed.ncbi.nlm.nih.gov/27551308/ DOI: 10.1186/s12263-016-0519-4
    tissue_or_cell_type
    Small intestine
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1778–1787

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestinal mRNA assay. · source_derived_draft · unverified_draft

    ### va-deficiency-ferroportin-transcript Vitamin A deficiency reduced intestinal Fpn1 transcripts in the same rat study. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Expression of an iron-export component changed alongside systemic signals. organism: Rattus norvegicus tissue_or_cell_type: Small intestine experimental_model: Intestinal mRNA assay. limitations: Does not quantify ferroportin membrane protein or iron-export flux. [va-cunha2016] Vitamin A deficiency modulates iron metabolism independent of hemojuvelin (Hfe2) and bone morphogenetic protein 6 (Bmp6) transcript levels (2016). https://pubmed.ncbi.nlm.nih.gov/27551308/ DOI: 10.1186/s12263-016-0519-4
    Complete structured claim and evidence
  9. Vitamin A-deficient rats showed lower hepatic Hamp transcripts despite increased Bmp6 and Hfe2 transcripts.

    Vitamin A → HAMP mRNA source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Vitamin A/iron -> hepcidin regulation.
    experimental_model
    Dietary comparison; hepatic mRNA.
    limitations
    Not a direct demonstration of BMP signaling flux or circulating hepcidin.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Rattus norvegicus
    plain_language
    The measured regulatory signals did not all move in the same direction.
    primary_references
    [va-cunha2016] Vitamin A deficiency modulates iron metabolism independent of hemojuvelin (Hfe2) and bone morphogenetic protein 6 (Bmp6) transcript levels (2016). https://pubmed.ncbi.nlm.nih.gov/27551308/ DOI: 10.1186/s12263-016-0519-4
    tissue_or_cell_type
    Liver
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1766–1776

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Dietary comparison; hepatic mRNA. · source_derived_draft · unverified_draft

    ### va-deficiency-hepcidin-transcript Vitamin A-deficient rats showed lower hepatic Hamp transcripts despite increased Bmp6 and Hfe2 transcripts. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The measured regulatory signals did not all move in the same direction. organism: Rattus norvegicus tissue_or_cell_type: Liver experimental_model: Dietary comparison; hepatic mRNA. limitations: Not a direct demonstration of BMP signaling flux or circulating hepcidin. cross_nutrient: Vitamin A/iron -> hepcidin regulation. [va-cunha2016] Vitamin A deficiency modulates iron metabolism independent of hemojuvelin (Hfe2) and bone morphogenetic protein 6 (Bmp6) transcript levels (2016). https://pubmed.ncbi.nlm.nih.gov/27551308/ DOI: 10.1186/s12263-016-0519-4
    Complete structured claim and evidence
  10. Vitamin A-deficient rats had more splenic iron but lower serum iron and transferrin saturation.

    Vitamin A → Splenic iron storage source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Vitamin A deficiency -> iron distribution.
    experimental_model
    Controlled rat dietary groups.
    limitations
    Erythrophagocytosis is a proposed explanation, not a fully isolated causal sequence.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Rattus norvegicus
    plain_language
    Iron could be retained in one tissue while circulating availability fell.
    primary_references
    [va-cunha2014] Vitamin A deficiency modulates iron metabolism via ineffective erythropoiesis (2014). https://pubmed.ncbi.nlm.nih.gov/24998947/ DOI: 10.1016/j.jnutbio.2014.05.005
    tissue_or_cell_type
    Spleen and serum
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1743–1753

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled rat dietary groups. · source_derived_draft · unverified_draft

    ### va-deficiency-iron-sequestration Vitamin A-deficient rats had more splenic iron but lower serum iron and transferrin saturation. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Iron could be retained in one tissue while circulating availability fell. organism: Rattus norvegicus tissue_or_cell_type: Spleen and serum experimental_model: Controlled rat dietary groups. limitations: Erythrophagocytosis is a proposed explanation, not a fully isolated causal sequence. cross_nutrient: Vitamin A deficiency -> iron distribution. [va-cunha2014] Vitamin A deficiency modulates iron metabolism via ineffective erythropoiesis (2014). https://pubmed.ncbi.nlm.nih.gov/24998947/ DOI: 10.1016/j.jnutbio.2014.05.005
    Complete structured claim and evidence
  11. Vitamin A and beta-carotene increased labelled nonheme iron absorption from tested cereal meals.

    Vitamin A → Nonheme iron absorption source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Vitamin A/carotene -> iron absorption; contested.
    experimental_model
    Six human cereal-meal studies.
    limitations
    Not consistently replicated; the claimed iron-complex mechanism was proposed rather than structurally demonstrated.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    plain_language
    This study found that the meal additives made more iron available.
    primary_references
    [va-garciacasal1998] Vitamin A and beta-carotene can improve nonheme iron absorption from rice, wheat and corn by humans (1998). https://pubmed.ncbi.nlm.nih.gov/9482776/ DOI: 10.1093/jn/128.3.646
    tissue_or_cell_type
    Intestinal absorption

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1542–1552

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six human cereal-meal studies. · source_derived_draft · unverified_draft

    ### va-iron-absorption-positive1998 Vitamin A and beta-carotene increased labelled nonheme iron absorption from tested cereal meals. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: This study found that the meal additives made more iron available. organism: Homo sapiens tissue_or_cell_type: Intestinal absorption experimental_model: Six human cereal-meal studies. limitations: Not consistently replicated; the claimed iron-complex mechanism was proposed rather than structurally demonstrated. cross_nutrient: Vitamin A/carotene -> iron absorption; contested. [va-garciacasal1998] Vitamin A and beta-carotene can improve nonheme iron absorption from rice, wheat and corn by humans (1998). https://pubmed.ncbi.nlm.nih.gov/9482776/ DOI: 10.1093/jn/128.3.646
    Complete structured claim and evidence
  12. Combined vitamin A and iron produced the largest hemoglobin response in the factorial pregnancy trial.

    Vitamin A → Blood hemoglobin concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Vitamin A/iron -> hemoglobin response.
    experimental_model
    Eight-week randomized trial.
    limitations
    Combined benefit does not prove a biochemical synergy or specify the cellular mediator.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    plain_language
    Correcting more than one shortage improved the measured response in this population.
    primary_references
    [va-suharno1993] Supplementation with vitamin A and iron for nutritional anaemia in pregnant women in West Java, Indonesia (1993). https://pubmed.ncbi.nlm.nih.gov/7901636/ DOI: 10.1016/0140-6736(93)92246-p
    tissue_or_cell_type
    Blood
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1448–1458

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Eight-week randomized trial. · source_derived_draft · unverified_draft

    ### va-iron-combined-hemoglobin Combined vitamin A and iron produced the largest hemoglobin response in the factorial pregnancy trial. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Correcting more than one shortage improved the measured response in this population. organism: Homo sapiens tissue_or_cell_type: Blood experimental_model: Eight-week randomized trial. limitations: Combined benefit does not prove a biochemical synergy or specify the cellular mediator. cross_nutrient: Vitamin A/iron -> hemoglobin response. [va-suharno1993] Supplementation with vitamin A and iron for nutritional anaemia in pregnant women in West Java, Indonesia (1993). https://pubmed.ncbi.nlm.nih.gov/7901636/ DOI: 10.1016/0140-6736(93)92246-p
    Complete structured claim and evidence
  13. Vitamin A increased circulating EPO and hemoglobin in schoolchildren with poor nutrient status.

    Vitamin A → Circulating erythropoietin concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Vitamin A -> EPO/iron use.
    experimental_model
    Randomized ten-month follow-up.
    limitations
    EPO was measured, not blocked; its mediation of the hemoglobin response remains inferred.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    plain_language
    Vitamin A can influence the signal that supports red-cell production.
    primary_references
    [va-zimmermann2006-iron] Vitamin A supplementation in children with poor vitamin A and iron status increases erythropoietin and hemoglobin concentrations without changing total body iron (2006). https://pubmed.ncbi.nlm.nih.gov/16960172/ DOI: 10.1093/ajcn/84.3.580
    tissue_or_cell_type
    Blood
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1460–1470

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized ten-month follow-up. · source_derived_draft · unverified_draft

    ### va-repletion-erythropoietin Vitamin A increased circulating EPO and hemoglobin in schoolchildren with poor nutrient status. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin A can influence the signal that supports red-cell production. organism: Homo sapiens tissue_or_cell_type: Blood experimental_model: Randomized ten-month follow-up. limitations: EPO was measured, not blocked; its mediation of the hemoglobin response remains inferred. cross_nutrient: Vitamin A -> EPO/iron use. [va-zimmermann2006-iron] Vitamin A supplementation in children with poor vitamin A and iron status increases erythropoietin and hemoglobin concentrations without changing total body iron (2006). https://pubmed.ncbi.nlm.nih.gov/16960172/ DOI: 10.1093/ajcn/84.3.580
    Complete structured claim and evidence
  14. Ferritin fell while calculated total-body iron remained unchanged in the same trial, consistent with redistribution of existing iron.

    Vitamin A → Serum ferritin concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    experimental_model
    Ferritin/transferrin-receptor-based estimates.
    limitations
    Redistribution is an interpretation; liver iron was not directly biopsied.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    plain_language
    A better blood count did not require a measured increase in total-body iron.
    primary_references
    [va-zimmermann2006-iron] Vitamin A supplementation in children with poor vitamin A and iron status increases erythropoietin and hemoglobin concentrations without changing total body iron (2006). https://pubmed.ncbi.nlm.nih.gov/16960172/ DOI: 10.1093/ajcn/84.3.580
    tissue_or_cell_type
    Blood; inferred storage
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1472–1481

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Ferritin/transferrin-receptor-based estimates. · source_derived_draft · unverified_draft

    ### va-repletion-iron-store-redistribution Ferritin fell while calculated total-body iron remained unchanged in the same trial, consistent with redistribution of existing iron. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: A better blood count did not require a measured increase in total-body iron. organism: Homo sapiens tissue_or_cell_type: Blood; inferred storage experimental_model: Ferritin/transferrin-receptor-based estimates. limitations: Redistribution is an interpretation; liver iron was not directly biopsied. [va-zimmermann2006-iron] Vitamin A supplementation in children with poor vitamin A and iron status increases erythropoietin and hemoglobin concentrations without changing total body iron (2006). https://pubmed.ncbi.nlm.nih.gov/16960172/ DOI: 10.1093/ajcn/84.3.580
    Complete structured claim and evidence
  15. Vitamin A-deficient mice lacked IgA-secreting cells in the small intestine.

    Vitamin A → Intestinal IgA-secreting cell abundance source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_locator
    Abstract
    experimental_model
    Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice.
    exposure
    Vitamin A-deficient diet
    limitations
    Migration and differentiation contributions are not interchangeable.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Depletion reduced the local antibody-secreting cell compartment.
    primary_references
    [va-mora-2006] Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006). https://pubmed.ncbi.nlm.nih.gov/17110582/ DOI: 10.1126/science.1132742
    tissue_or_cell_type
    Small intestine
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1240–1251

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice. · source_derived_draft · unverified_draft

    ### va-sig-deficient-intestinal-iga Vitamin A-deficient mice lacked IgA-secreting cells in the small intestine. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Depletion reduced the local antibody-secreting cell compartment. organism: Mus musculus tissue_or_cell_type: Small intestine experimental_model: Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice. limitations: Migration and differentiation contributions are not interchangeable. evidence_locator: Abstract exposure: Vitamin A-deficient diet [va-mora-2006] Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006). https://pubmed.ncbi.nlm.nih.gov/17110582/ DOI: 10.1126/science.1132742
    Complete structured claim and evidence
  16. Vitamin A-deficient mice had depleted intestinal lamina propria T cells.

    Vitamin A → Intestinal T-cell abundance source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_locator
    Abstract
    experimental_model
    Mouse activated T cells, gut dendritic cells and vitamin A-deficient mice.
    exposure
    Vitamin A-deficient diet
    limitations
    Does not isolate trafficking from all other deficiency effects.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Dietary depletion changed the intestinal T-cell compartment.
    primary_references
    [va-iwata-2004] Retinoic acid imprints gut-homing specificity on T cells (2004). https://pubmed.ncbi.nlm.nih.gov/15485630/ DOI: 10.1016/j.immuni.2004.08.011
    tissue_or_cell_type
    Intestinal lamina propria
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1201–1212

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse activated T cells, gut dendritic cells and vitamin A-deficient mice. · source_derived_draft · unverified_draft

    ### va-sig-deficient-intestinal-t-cells Vitamin A-deficient mice had depleted intestinal lamina propria T cells. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Dietary depletion changed the intestinal T-cell compartment. organism: Mus musculus tissue_or_cell_type: Intestinal lamina propria experimental_model: Mouse activated T cells, gut dendritic cells and vitamin A-deficient mice. limitations: Does not isolate trafficking from all other deficiency effects. evidence_locator: Abstract exposure: Vitamin A-deficient diet [va-iwata-2004] Retinoic acid imprints gut-homing specificity on T cells (2004). https://pubmed.ncbi.nlm.nih.gov/15485630/ DOI: 10.1016/j.immuni.2004.08.011
    Complete structured claim and evidence
  17. The six-patient abetalipoproteinemia report noted that vitamin A alone had not prevented or arrested the retinal lesion, whereas long-term regimens including vitamin E modified its course.

    Vitamin A → Retinal function in abetalipoproteinemia source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    true
    experimental_model
    Six-patient long-term abetalipoproteinemia case series
    exposure
    Large oral vitamin E doses for 12–18 years alongside low-fat diet and other fat-soluble vitamins; exact dose absent from the abstract.
    limitations
    Uncontrolled co-treatment series; cannot isolate vitamin E effect or demonstrate nutrient synergy. Genetic lipid transport disease differs from simple low intake.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    In this transport disease, vitamin A alone did not substitute for the broader treatment that included vitamin E.
    primary_references
    [e-clin-retina1986] Oral vitamin E supplements can prevent the retinopathy of abetalipoproteinaemia. (1986). https://pubmed.ncbi.nlm.nih.gov/3954973/ DOI: 10.1136/bjo.70.3.166
    tissue_or_cell_type
    Retina
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1453–1464

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-patient long-term abetalipoproteinemia case series · source_derived_draft · unverified_draft

    ### e-clin-abetalipo-a-alone The six-patient abetalipoproteinemia report noted that vitamin A alone had not prevented or arrested the retinal lesion, whereas long-term regimens including vitamin E modified its course. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this transport disease, vitamin A alone did not substitute for the broader treatment that included vitamin E. organism: Homo sapiens tissue_or_cell_type: Retina experimental_model: Six-patient long-term abetalipoproteinemia case series limitations: Uncontrolled co-treatment series; cannot isolate vitamin E effect or demonstrate nutrient synergy. Genetic lipid transport disease differs from simple low intake. exposure: Large oral vitamin E doses for 12–18 years alongside low-fat diet and other fat-soluble vitamins; exact dose absent from the abstract. cross_nutrient: true [e-clin-retina1986] Oral vitamin E supplements can prevent the retinopathy of abetalipoproteinaemia. (1986). https://pubmed.ncbi.nlm.nih.gov/3954973/ DOI: 10.1136/bjo.70.3.166
    Complete structured claim and evidence

What acts on it

  1. In fifteen well-nourished young children, intrinsically labeled beta-carotene from pureed Moringa leaves had 28% relative bioefficacy and an estimated vitamin A equivalence of 3.3:1 by weight.

    All-trans-beta-carotene → Vitamin A source_derived_draftungraded
    Experimental context and source evidence
    dose
    Pureed labeled Moringa leaves providing 1 mg beta-carotene plus a reference retinyl-acetate dose
    duration
    Thirty-five-day isotope sampling
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Fifteen Mexican children aged 17-35 months
    limitations
    Children were well nourished with adequate vitamin A stores; the estimate may differ with deficiency, food matrix, genetics and infection.
    nutrient_topic
    Moringa oleifera chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Moringa oleifera
    organism
    Fifteen Mexican children aged 17-35 months
    plain_language
    In fifteen well-nourished young children, intrinsically labeled beta-carotene from pureed Moringa leaves had 28% relative bioefficacy and an estimated vitamin A equivalence of 3.3:1 by weight.
    primary_references
    Use of a "Super-child" Approach to Assess the Vitamin A Equivalence of Moringa oleifera Leaves, Develop a Compartmental Model for Vitamin A Kinetics, and Estimate Vitamin A Total Body Stores in Young Mexican Children. (2017). https://pubmed.ncbi.nlm.nih.gov/28931584/ DOI: 10.3945/jn.117.256974
    route
    Oral
    tissue
    Stable-isotope plasma retinol kinetics

    Moringa oleifera: mechanism of action and interactions (2026-09-20) · lines 233–242

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Fifteen Mexican children aged 17-35 months · source_derived_draft · unverified_draft

    ## moringa-child-vitamin-a-equivalence In fifteen well-nourished young children, intrinsically labeled beta-carotene from pureed Moringa leaves had 28% relative bioefficacy and an estimated vitamin A equivalence of 3.3:1 by weight. Model/species: Fifteen Mexican children aged 17-35 months Tissue/system: Stable-isotope plasma retinol kinetics Exposure: Pureed labeled Moringa leaves providing 1 mg beta-carotene plus a reference retinyl-acetate dose Route: Oral Duration: Thirty-five-day isotope sampling Limits: Children were well nourished with adequate vitamin A stores; the estimate may differ with deficiency, food matrix, genetics and infection. Primary reference: Use of a "Super-child" Approach to Assess the Vitamin A Equivalence of Moringa oleifera Leaves, Develop a Compartmental Model for Vitamin A Kinetics, and Estimate Vitamin A Total Body Stores in Young Mexican Children. (2017). https://pubmed.ncbi.nlm.nih.gov/28931584/ DOI: 10.3945/jn.117.256974 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. In a six-week pilot feeding study, Moringa-fortified complementary foods produced only marginal, nonsignificant blood-retinol increases, and all infants remained vitamin A deficient.

    Experimental context and source evidence
    dose
    Two Moringa-fortified foods versus a cereal-legume control
    duration
    Six weeks
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Sixty-five completing infant-mother pairs in Ghana
    limitations
    The pilot had substantial attrition and short follow-up; its null result does not contradict measured carotenoid conversion in well-nourished children.
    nutrient_topic
    Moringa oleifera chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Moringa oleifera
    organism
    Sixty-five completing infant-mother pairs in Ghana
    plain_language
    In a six-week pilot feeding study, Moringa-fortified complementary foods produced only marginal, nonsignificant blood-retinol increases, and all infants remained vitamin A deficient.
    primary_references
    Improving Blood Retinol Concentrations with Complementary Foods Fortified with Moringa oleifera Leaf Powder - A Pilot Study. (2018). https://pubmed.ncbi.nlm.nih.gov/29962920/
    route
    Oral feeding
    tissue
    Whole-blood retinol

    Moringa oleifera: mechanism of action and interactions (2026-09-20) · lines 244–253

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Sixty-five completing infant-mother pairs in Ghana · source_derived_draft · unverified_draft

    ## moringa-infant-retinol-null In a six-week pilot feeding study, Moringa-fortified complementary foods produced only marginal, nonsignificant blood-retinol increases, and all infants remained vitamin A deficient. Model/species: Sixty-five completing infant-mother pairs in Ghana Tissue/system: Whole-blood retinol Exposure: Two Moringa-fortified foods versus a cereal-legume control Route: Oral feeding Duration: Six weeks Limits: The pilot had substantial attrition and short follow-up; its null result does not contradict measured carotenoid conversion in well-nourished children. Primary reference: Improving Blood Retinol Concentrations with Complementary Foods Fortified with Moringa oleifera Leaf Powder - A Pilot Study. (2018). https://pubmed.ncbi.nlm.nih.gov/29962920/ Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence
  2. In a three-month cluster-randomized pilot, 20 g/day maternal Moringa leaf powder did not change human-milk vitamin A concentration or maternal and infant serum vitamin A status, although milk alpha-carotene rose modestly.

    Experimental context and source evidence
    dose
    Corn porridge with or without 20 g/day leaf powder
    duration
    Three months
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Forty-four completing Kenyan breastfeeding mother-infant pairs
    limitations
    The small pilot had baseline alpha-carotene imbalance and was not powered to establish clinical infant benefit.
    nutrient_topic
    Moringa oleifera chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Moringa oleifera
    organism
    Forty-four completing Kenyan breastfeeding mother-infant pairs
    plain_language
    In a three-month cluster-randomized pilot, 20 g/day maternal Moringa leaf powder did not change human-milk vitamin A concentration or maternal and infant serum vitamin A status, although milk alpha-carotene rose modestly.
    primary_references
    Impact of Maternal Moringa oleifera Leaf Supplementation on Milk and Serum Vitamin A and Carotenoid Concentrations in a Cohort of Breastfeeding Kenyan Women and Their Infants. (2024). https://pubmed.ncbi.nlm.nih.gov/39408390/ DOI: 10.3390/nu16193425
    route
    Maternal oral feeding
    tissue
    Milk retinol/carotenoids and serum retinol-binding protein

    Moringa oleifera: mechanism of action and interactions (2026-09-20) · lines 255–264

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Forty-four completing Kenyan breastfeeding mother-infant pairs · source_derived_draft · unverified_draft

    ## moringa-maternal-milk-retinol-null In a three-month cluster-randomized pilot, 20 g/day maternal Moringa leaf powder did not change human-milk vitamin A concentration or maternal and infant serum vitamin A status, although milk alpha-carotene rose modestly. Model/species: Forty-four completing Kenyan breastfeeding mother-infant pairs Tissue/system: Milk retinol/carotenoids and serum retinol-binding protein Exposure: Corn porridge with or without 20 g/day leaf powder Route: Maternal oral feeding Duration: Three months Limits: The small pilot had baseline alpha-carotene imbalance and was not powered to establish clinical infant benefit. Primary reference: Impact of Maternal Moringa oleifera Leaf Supplementation on Milk and Serum Vitamin A and Carotenoid Concentrations in a Cohort of Breastfeeding Kenyan Women and Their Infants. (2024). https://pubmed.ncbi.nlm.nih.gov/39408390/ DOI: 10.3390/nu16193425 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence
  3. Olestra lowered serum lycopene by 12 weeks, persisting after cholesterol or BMI adjustment; the multivitamin did not prevent this.

    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/lycopene-research/15930452.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3a90148eb83ff18442e37f9fd5ed31f44acbf8d7616ef05ff1e65e6e2d64e84f", "start_char": 0, "end_char": 1595, "text_sha256": "3a90148eb83ff18442e37f9fd5ed31f44acbf8d7616ef05ff1e65e6e2d64e84f"}
    experimental_model
    Randomized 36-week controlled diet study
    exposure
    Olestra substituted for one-third of fat energy; daily multivitamin and vitamin-E-fortified olestra
    limitations
    Exposure-specific depletion, not an established lycopene deficiency syndrome; reference-range limits are not clinical deficiency thresholds.
    nutrient_topic
    Lycopene research collection; topical membership is not evidence of a direct dietary effect. · Lycopene
    organism
    Human, 37 healthy men
    plain_language
    Replacing dietary fat with a nonabsorbed substitute changed carotenoid exposure.
    primary_references
    [lycopene-p15930452] Daily intake of multivitamins during long-term intake of olestra in men prevents declines in serum vitamins A and E but not carotenoids. (2005). https://pubmed.ncbi.nlm.nih.gov/15930452/ DOI: 10.1093/jn/135.6.1456
    tissue_or_cell_type
    Serum carotenoids and fat-soluble vitamins
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Lycopene: absorption, metabolism, nutrient connections and human outcomes (2026-09-17) · lines 858–869

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized 36-week controlled diet study · source_derived_draft · unverified_draft

    ### lycopene-olestra-lycopene Olestra lowered serum lycopene by 12 weeks, persisting after cholesterol or BMI adjustment; the multivitamin did not prevent this. Condition category: biomarker_context nutrient_topic: Lycopene research collection; topical membership is not evidence of a direct dietary effect. plain_language: Replacing dietary fat with a nonabsorbed substitute changed carotenoid exposure. organism: Human, 37 healthy men tissue_or_cell_type: Serum carotenoids and fat-soluble vitamins experimental_model: Randomized 36-week controlled diet study limitations: Exposure-specific depletion, not an established lycopene deficiency syndrome; reference-range limits are not clinical deficiency thresholds. exposure: Olestra substituted for one-third of fat energy; daily multivitamin and vitamin-E-fortified olestra evidence_span: {"source_cache": "artifacts/lycopene-research/15930452.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "3a90148eb83ff18442e37f9fd5ed31f44acbf8d7616ef05ff1e65e6e2d64e84f", "start_char": 0, "end_char": 1595, "text_sha256": "3a90148eb83ff18442e37f9fd5ed31f44acbf8d7616ef05ff1e65e6e2d64e84f"} [lycopene-p15930452] Daily intake of multivitamins during long-term intake of olestra in men prevents declines in serum vitamins A and E but not carotenoids. (2005). https://pubmed.ncbi.nlm.nih.gov/15930452/ DOI: 10.1093/jn/135.6.1456
    Complete structured claim and evidence
  4. Acetate promoted B-cell IgA class switching and IgA production in vitro in the presence of wild-type but not GPR43 knockout dendritic cells, and mechanistically acetate induced dendritic-cell expression of Aldh1a2, which converts vitamin A into retinoic acid, with blockade of retinoic acid signalling inhibiting the acetate-induced IgA production.

    Acetate → Aldehyde dehydrogenase 1A2 / ALDH1A2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/acetate-research/27966553.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac", "start_char": 0, "end_char": 1363, "text_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac"}
    experimental_model
    GPR43 knockout mice with B-cell and dendritic-cell coculture and retinoic acid signalling blockade
    exposure
    Dietary acetate or butyrate in wild-type and GPR43 knockout mice, with in vitro IgA class switching assays
    limitations
    A clean set of controls: butyrate did not substitute for acetate, the effect was independent of T cells, and blocking the downstream vitamin A metabolite removed it.
    nutrient_topic
    Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
    organism
    Mouse
    plain_language
    Acetate works by switching on the enzyme that turns vitamin A into its active form; block that and the effect is gone.
    primary_references
    [acetate-p27966553] Microbiota metabolite short-chain fatty acid acetate promotes intestinal IgA response to microbiota which is mediated by GPR43. (2017). https://pubmed.ncbi.nlm.nih.gov/27966553/ DOI: 10.1038/mi.2016.114
    tissue_or_cell_type
    Intestinal mucosa

    Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 394–405

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · GPR43 knockout mice with B-cell and dendritic-cell coculture and retinoic acid signalling blockade · source_derived_draft · unverified_draft

    ### acetate-acetate-vitamin-a-route Acetate promoted B-cell IgA class switching and IgA production in vitro in the presence of wild-type but not GPR43 knockout dendritic cells, and mechanistically acetate induced dendritic-cell expression of Aldh1a2, which converts vitamin A into retinoic acid, with blockade of retinoic acid signalling inhibiting the acetate-induced IgA production. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: Acetate works by switching on the enzyme that turns vitamin A into its active form; block that and the effect is gone. organism: Mouse tissue_or_cell_type: Intestinal mucosa experimental_model: GPR43 knockout mice with B-cell and dendritic-cell coculture and retinoic acid signalling blockade limitations: A clean set of controls: butyrate did not substitute for acetate, the effect was independent of T cells, and blocking the downstream vitamin A metabolite removed it. exposure: Dietary acetate or butyrate in wild-type and GPR43 knockout mice, with in vitro IgA class switching assays evidence_span: {"source_cache": "artifacts/acetate-research/27966553.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac", "start_char": 0, "end_char": 1363, "text_sha256": "25ef476e62dd28f354099501d2919c3f765aaddd89d1a05739e3e0dc703d11ac"} [acetate-p27966553] Microbiota metabolite short-chain fatty acid acetate promotes intestinal IgA response to microbiota which is mediated by GPR43. (2017). https://pubmed.ncbi.nlm.nih.gov/27966553/ DOI: 10.1038/mi.2016.114
    Complete structured claim and evidence
  5. Adding beta-carotene or vitamin A retained more iron in solution when the assay pH rose from acidic toward near-neutral.

    All-trans-beta-carotene → Iron solubility source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Retinoid/iron chemistry; hypothesis boundary retained.
    experimental_model
    Cell-free pH-shift experiment.
    limitations
    Solubility alone neither proves a defined retinoid-iron complex nor absorption in vivo.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    plain_language
    A laboratory solubility result supported a proposed explanation for the meal findings.
    primary_references
    [va-garciacasal1998] Vitamin A and beta-carotene can improve nonheme iron absorption from rice, wheat and corn by humans (1998). https://pubmed.ncbi.nlm.nih.gov/9482776/ DOI: 10.1093/jn/128.3.646
    tissue_or_cell_type
    Cell-free chemistry

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1554–1564

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell-free pH-shift experiment. · source_derived_draft · unverified_draft

    ### va-retinoid-iron-solubility-assay Adding beta-carotene or vitamin A retained more iron in solution when the assay pH rose from acidic toward near-neutral. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: A laboratory solubility result supported a proposed explanation for the meal findings. organism: Homo sapiens tissue_or_cell_type: Cell-free chemistry experimental_model: Cell-free pH-shift experiment. limitations: Solubility alone neither proves a defined retinoid-iron complex nor absorption in vivo. cross_nutrient: Retinoid/iron chemistry; hypothesis boundary retained. [va-garciacasal1998] Vitamin A and beta-carotene can improve nonheme iron absorption from rice, wheat and corn by humans (1998). https://pubmed.ncbi.nlm.nih.gov/9482776/ DOI: 10.1093/jn/128.3.646
    Complete structured claim and evidence
  6. 9-cis RA also bound RAR alpha, beta and gamma; it was not RXR-selective.

    9-cis-retinoic acid → Retinoic acid receptor family source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Transfected COS-1 nucleosol; ligand competition and chimeric receptor reporters.
    exposure
    Isomer competition
    limitations
    Does not establish endogenous tissue concentrations.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Recombinant receptors in COS-1 cells
    plain_language
    An RXR-binding retinoid can also activate RAR pathways.
    primary_references
    [va-allenby-1993] Retinoic acid receptors and retinoid X receptors: interactions with endogenous retinoic acids (1993). https://pubmed.ncbi.nlm.nih.gov/8380496/ DOI: 10.1073/pnas.90.1.30
    tissue_or_cell_type
    Nuclear extracts

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1043–1054

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected COS-1 nucleosol; ligand competition and chimeric receptor reporters. · source_derived_draft · unverified_draft

    ### va-sig-9cis-rar-binding 9-cis RA also bound RAR alpha, beta and gamma; it was not RXR-selective. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: An RXR-binding retinoid can also activate RAR pathways. organism: Recombinant receptors in COS-1 cells tissue_or_cell_type: Nuclear extracts experimental_model: Transfected COS-1 nucleosol; ligand competition and chimeric receptor reporters. limitations: Does not establish endogenous tissue concentrations. evidence_locator: Abstract exposure: Isomer competition [va-allenby-1993] Retinoic acid receptors and retinoid X receptors: interactions with endogenous retinoic acids (1993). https://pubmed.ncbi.nlm.nih.gov/8380496/ DOI: 10.1073/pnas.90.1.30
    Complete structured claim and evidence
  7. 9-cis RA bound the tested RXR preparation with high affinity and activated RXR-dependent reporter responses.

    9-cis-retinoic acid → Retinoid X receptor family source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Receptor binding and cell transfection assays.
    exposure
    9-cis RA exposure
    limitations
    Its biochemical activity does not establish a universal physiological RXR ligand pool.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Recombinant/cultured-cell system
    plain_language
    The 9-cis isomer supplies a direct experimental RXR ligand.
    primary_references
    [va-heyman-1992] 9-cis retinoic acid is a high affinity ligand for the retinoid X receptor (1992). https://pubmed.ncbi.nlm.nih.gov/1310260/ DOI: 10.1016/0092-8674(92)90479-v
    tissue_or_cell_type
    Receptor-binding preparations

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1069–1080

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Receptor binding and cell transfection assays. · source_derived_draft · unverified_draft

    ### va-sig-9cis-rxr-binding 9-cis RA bound the tested RXR preparation with high affinity and activated RXR-dependent reporter responses. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The 9-cis isomer supplies a direct experimental RXR ligand. organism: Recombinant/cultured-cell system tissue_or_cell_type: Receptor-binding preparations experimental_model: Receptor binding and cell transfection assays. limitations: Its biochemical activity does not establish a universal physiological RXR ligand pool. evidence_locator: Abstract exposure: 9-cis RA exposure [va-heyman-1992] 9-cis retinoic acid is a high affinity ligand for the retinoid X receptor (1992). https://pubmed.ncbi.nlm.nih.gov/1310260/ DOI: 10.1016/0092-8674(92)90479-v
    Complete structured claim and evidence
  8. All-trans RA bound the tested RAR alpha, beta and gamma preparations with high affinity.

    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Transfected COS-1 nucleosol; ligand competition and chimeric receptor reporters.
    exposure
    Radioligand competition
    limitations
    Binding affinity is not a dietary threshold.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Recombinant receptors in African green monkey COS-1 cells
    plain_language
    The all-trans isomer directly engages RAR proteins.
    primary_references
    [va-allenby-1993] Retinoic acid receptors and retinoid X receptors: interactions with endogenous retinoic acids (1993). https://pubmed.ncbi.nlm.nih.gov/8380496/ DOI: 10.1073/pnas.90.1.30
    tissue_or_cell_type
    Nuclear extracts

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1030–1041

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected COS-1 nucleosol; ligand competition and chimeric receptor reporters. · source_derived_draft · unverified_draft

    ### va-sig-atra-rar-binding All-trans RA bound the tested RAR alpha, beta and gamma preparations with high affinity. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The all-trans isomer directly engages RAR proteins. organism: Recombinant receptors in African green monkey COS-1 cells tissue_or_cell_type: Nuclear extracts experimental_model: Transfected COS-1 nucleosol; ligand competition and chimeric receptor reporters. limitations: Binding affinity is not a dietary threshold. evidence_locator: Abstract exposure: Radioligand competition [va-allenby-1993] Retinoic acid receptors and retinoid X receptors: interactions with endogenous retinoic acids (1993). https://pubmed.ncbi.nlm.nih.gov/8380496/ DOI: 10.1073/pnas.90.1.30
    Complete structured claim and evidence
  9. All-trans RA did not effectively compete for RXR binding in the tested isomer assay.

    All-trans-retinoic acid → Retinoid X receptor family source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Transfected COS-1 nucleosol; ligand competition and chimeric receptor reporters.
    exposure
    Isomer competition
    limitations
    Cell metabolism can alter apparent reporter responses.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Recombinant receptors in COS-1 cells
    plain_language
    RAR and RXR cannot be treated as interchangeable RA receptors.
    primary_references
    [va-allenby-1993] Retinoic acid receptors and retinoid X receptors: interactions with endogenous retinoic acids (1993). https://pubmed.ncbi.nlm.nih.gov/8380496/ DOI: 10.1073/pnas.90.1.30
    tissue_or_cell_type
    Nuclear extracts

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1056–1067

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected COS-1 nucleosol; ligand competition and chimeric receptor reporters. · source_derived_draft · unverified_draft

    ### va-sig-atra-rxr-selectivity All-trans RA did not effectively compete for RXR binding in the tested isomer assay. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: RAR and RXR cannot be treated as interchangeable RA receptors. organism: Recombinant receptors in COS-1 cells tissue_or_cell_type: Nuclear extracts experimental_model: Transfected COS-1 nucleosol; ligand competition and chimeric receptor reporters. limitations: Cell metabolism can alter apparent reporter responses. evidence_locator: Abstract exposure: Isomer competition [va-allenby-1993] Retinoic acid receptors and retinoid X receptors: interactions with endogenous retinoic acids (1993). https://pubmed.ncbi.nlm.nih.gov/8380496/ DOI: 10.1073/pnas.90.1.30
    Complete structured claim and evidence
  10. FRET sensors visualized an endogenous RA concentration gradient during zebrafish gastrulation and somitogenesis.

    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Genetically encoded FRET RA sensors in living zebrafish embryos.
    exposure
    Genetically encoded RA sensors
    limitations
    Sensor affinity, developmental stage and model constrain interpretation.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Danio rerio
    plain_language
    Embryonic cells encounter different local amounts of signaling RA.
    primary_references
    [va-shimozono-2013] Visualization of an endogenous retinoic acid gradient across embryonic development (2013). https://pubmed.ncbi.nlm.nih.gov/23563268/ DOI: 10.1038/nature12037
    tissue_or_cell_type
    Living early embryos

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1409–1420

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genetically encoded FRET RA sensors in living zebrafish embryos. · source_derived_draft · unverified_draft

    ### va-sig-embryonic-ra-gradient FRET sensors visualized an endogenous RA concentration gradient during zebrafish gastrulation and somitogenesis. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Embryonic cells encounter different local amounts of signaling RA. organism: Danio rerio tissue_or_cell_type: Living early embryos experimental_model: Genetically encoded FRET RA sensors in living zebrafish embryos. limitations: Sensor affinity, developmental stage and model constrain interpretation. evidence_locator: Abstract exposure: Genetically encoded RA sensors [va-shimozono-2013] Visualization of an endogenous retinoic acid gradient across embryonic development (2013). https://pubmed.ncbi.nlm.nih.gov/23563268/ DOI: 10.1038/nature12037
    Complete structured claim and evidence
  11. The exposed embryos showed rhombomere 2/3 transformation toward 4/5 identity with matching anatomical changes.

    All-trans-retinoic acid → Hindbrain segment identity source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    RA-exposed preheadfold transgenic mouse embryos; lacZ and anatomy.
    exposure
    Experimental excess RA exposure
    limitations
    Not a quantitative human teratogenic threshold.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Excess developmental signaling changed segment identity.
    primary_references
    [va-marshall-1992] Retinoic acid alters hindbrain Hox code and induces transformation of rhombomeres 2/3 into a 4/5 identity (1992). https://www.nature.com/articles/360737a0 DOI: 10.1038/360737a0
    tissue_or_cell_type
    Embryonic hindbrain

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1435–1446

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · RA-exposed preheadfold transgenic mouse embryos; lacZ and anatomy. · source_derived_draft · unverified_draft

    ### va-sig-excess-ra-hindbrain-identity The exposed embryos showed rhombomere 2/3 transformation toward 4/5 identity with matching anatomical changes. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Excess developmental signaling changed segment identity. organism: Mus musculus tissue_or_cell_type: Embryonic hindbrain experimental_model: RA-exposed preheadfold transgenic mouse embryos; lacZ and anatomy. limitations: Not a quantitative human teratogenic threshold. evidence_locator: Abstract exposure: Experimental excess RA exposure [va-marshall-1992] Retinoic acid alters hindbrain Hox code and induces transformation of rhombomeres 2/3 into a 4/5 identity (1992). https://www.nature.com/articles/360737a0 DOI: 10.1038/360737a0
    Complete structured claim and evidence
  12. Preheadfold RA exposure altered segmental Hoxb1 reporter expression in mouse hindbrain.

    All-trans-retinoic acid → Hoxb1 gene source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    RA-exposed preheadfold transgenic mouse embryos; lacZ and anatomy.
    exposure
    Experimental excess RA exposure
    limitations
    Timing-specific teratogenic experiment, not ordinary dietary intake.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Excess RA can shift where an embryonic patterning gene is active.
    primary_references
    [va-marshall-1992] Retinoic acid alters hindbrain Hox code and induces transformation of rhombomeres 2/3 into a 4/5 identity (1992). https://www.nature.com/articles/360737a0 DOI: 10.1038/360737a0
    tissue_or_cell_type
    Preheadfold embryos/hindbrain

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1422–1433

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · RA-exposed preheadfold transgenic mouse embryos; lacZ and anatomy. · source_derived_draft · unverified_draft

    ### va-sig-excess-ra-hox-pattern Preheadfold RA exposure altered segmental Hoxb1 reporter expression in mouse hindbrain. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Excess RA can shift where an embryonic patterning gene is active. organism: Mus musculus tissue_or_cell_type: Preheadfold embryos/hindbrain experimental_model: RA-exposed preheadfold transgenic mouse embryos; lacZ and anatomy. limitations: Timing-specific teratogenic experiment, not ordinary dietary intake. evidence_locator: Abstract exposure: Experimental excess RA exposure [va-marshall-1992] Retinoic acid alters hindbrain Hox code and induces transformation of rhombomeres 2/3 into a 4/5 identity (1992). https://www.nature.com/articles/360737a0 DOI: 10.1038/360737a0
    Complete structured claim and evidence
  13. A conserved Hoxb1 enhancer containing a RARE mediated RA responsiveness and early neuroectodermal expression.

    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Mouse Hoxb1 enhancer transgenes; homologous chicken and pufferfish elements.
    exposure
    Enhancer transgenes and RA exposure
    limitations
    Enhancer behavior is not a maternal serum-retinol threshold.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus; comparative chicken/pufferfish enhancer sequences
    plain_language
    Embryonic RA signaling connects to a spatial developmental gene program.
    primary_references
    [va-marshall-1994] A conserved retinoic acid response element required for early expression of the homeobox gene Hoxb-1 (1994). https://www.nature.com/articles/370567a0 DOI: 10.1038/370567a0
    tissue_or_cell_type
    Early embryonic neuroectoderm

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1396–1407

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse Hoxb1 enhancer transgenes; homologous chicken and pufferfish elements. · source_derived_draft · unverified_draft

    ### va-sig-hoxb1-ra-enhancer A conserved Hoxb1 enhancer containing a RARE mediated RA responsiveness and early neuroectodermal expression. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Embryonic RA signaling connects to a spatial developmental gene program. organism: Mus musculus; comparative chicken/pufferfish enhancer sequences tissue_or_cell_type: Early embryonic neuroectoderm experimental_model: Mouse Hoxb1 enhancer transgenes; homologous chicken and pufferfish elements. limitations: Enhancer behavior is not a maternal serum-retinol threshold. evidence_locator: Abstract exposure: Enhancer transgenes and RA exposure [va-marshall-1994] A conserved retinoic acid response element required for early expression of the homeobox gene Hoxb-1 (1994). https://www.nature.com/articles/370567a0 DOI: 10.1038/370567a0
    Complete structured claim and evidence
  14. Ligand destabilized SMRT association with retinoid receptor complexes, including DNA-bound receptors.

    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Biochemical interactions and engineered cellular transcription reporters.
    exposure
    Ligand addition
    limitations
    Cofactor exchange varies by promoter and cell.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Biochemical receptor system
    plain_language
    Ligand binding can release a transcriptional brake.
    primary_references
    [va-chen-1995] A transcriptional co-repressor that interacts with nuclear hormone receptors (1995). https://pubmed.ncbi.nlm.nih.gov/7566127/ DOI: 10.1038/377454a0
    tissue_or_cell_type
    Receptor complexes

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1149–1160

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical interactions and engineered cellular transcription reporters. · source_derived_draft · unverified_draft

    ### va-sig-ligand-smrt-release Ligand destabilized SMRT association with retinoid receptor complexes, including DNA-bound receptors. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Ligand binding can release a transcriptional brake. organism: Biochemical receptor system tissue_or_cell_type: Receptor complexes experimental_model: Biochemical interactions and engineered cellular transcription reporters. limitations: Cofactor exchange varies by promoter and cell. evidence_locator: Abstract exposure: Ligand addition [va-chen-1995] A transcriptional co-repressor that interacts with nuclear hormone receptors (1995). https://pubmed.ncbi.nlm.nih.gov/7566127/ DOI: 10.1038/377454a0
    Complete structured claim and evidence
  15. Removing RA from airway epithelial culture medium sharply reduced mucin secretion.

    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_locator
    Abstract
    experimental_model
    Human normal tracheobronchial epithelial air-liquid interface cultures.
    exposure
    RA withdrawal
    limitations
    Does not demonstrate airway infection protection.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    plain_language
    RA availability helps maintain the secretory phenotype in cultured airway cells.
    primary_references
    [va-yoon-1997] Regulation of the secretory phenotype of human airway epithelium by retinoic acid, triiodothyronine, and extracellular matrix (1997). https://pubmed.ncbi.nlm.nih.gov/9191474/ DOI: 10.1165/ajrcmb.16.6.9191474
    tissue_or_cell_type
    Normal tracheobronchial epithelial air-liquid interface culture
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1383–1394

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human normal tracheobronchial epithelial air-liquid interface cultures. · source_derived_draft · unverified_draft

    ### va-sig-ra-airway-secretion Removing RA from airway epithelial culture medium sharply reduced mucin secretion. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: RA availability helps maintain the secretory phenotype in cultured airway cells. organism: Homo sapiens tissue_or_cell_type: Normal tracheobronchial epithelial air-liquid interface culture experimental_model: Human normal tracheobronchial epithelial air-liquid interface cultures. limitations: Does not demonstrate airway infection protection. evidence_locator: Abstract exposure: RA withdrawal [va-yoon-1997] Regulation of the secretory phenotype of human airway epithelium by retinoic acid, triiodothyronine, and extracellular matrix (1997). https://pubmed.ncbi.nlm.nih.gov/9191474/ DOI: 10.1165/ajrcmb.16.6.9191474
    Complete structured claim and evidence
  16. RA during T-cell activation increased the alpha4beta7 gut-homing integrin.

    All-trans-retinoic acid → Integrin alpha4beta7 source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Mouse activated T cells, gut dendritic cells and vitamin A-deficient mice.
    exposure
    Added RA
    limitations
    Does not establish independent transcriptional induction of each subunit.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    RA helps activated T cells acquire an intestinal adhesion complex.
    primary_references
    [va-iwata-2004] Retinoic acid imprints gut-homing specificity on T cells (2004). https://pubmed.ncbi.nlm.nih.gov/15485630/ DOI: 10.1016/j.immuni.2004.08.011
    tissue_or_cell_type
    Activated T cells

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1188–1199

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse activated T cells, gut dendritic cells and vitamin A-deficient mice. · source_derived_draft · unverified_draft

    ### va-sig-ra-alpha4beta7 RA during T-cell activation increased the alpha4beta7 gut-homing integrin. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: RA helps activated T cells acquire an intestinal adhesion complex. organism: Mus musculus tissue_or_cell_type: Activated T cells experimental_model: Mouse activated T cells, gut dendritic cells and vitamin A-deficient mice. limitations: Does not establish independent transcriptional induction of each subunit. evidence_locator: Abstract exposure: Added RA [va-iwata-2004] Retinoic acid imprints gut-homing specificity on T cells (2004). https://pubmed.ncbi.nlm.nih.gov/15485630/ DOI: 10.1016/j.immuni.2004.08.011
    Complete structured claim and evidence
  17. Dendritic-cell-derived RA conferred gut tropism on activated B cells.

    All-trans-retinoic acid → B-cell gut homing source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice.
    exposure
    Gut dendritic-cell-derived RA
    limitations
    Gut tropism alone is not IgA secretion.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    RA helps route antibody-producing cell precursors to the intestine.
    primary_references
    [va-mora-2006] Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006). https://pubmed.ncbi.nlm.nih.gov/17110582/ DOI: 10.1126/science.1132742
    tissue_or_cell_type
    B-cell cultures

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1214–1225

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice. · source_derived_draft · unverified_draft

    ### va-sig-ra-b-cell-homing Dendritic-cell-derived RA conferred gut tropism on activated B cells. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: RA helps route antibody-producing cell precursors to the intestine. organism: Mus musculus tissue_or_cell_type: B-cell cultures experimental_model: Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice. limitations: Gut tropism alone is not IgA secretion. evidence_locator: Abstract exposure: Gut dendritic-cell-derived RA [va-mora-2006] Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006). https://pubmed.ncbi.nlm.nih.gov/17110582/ DOI: 10.1126/science.1132742
    Complete structured claim and evidence
  18. RA during mouse T-cell activation increased CCR9 expression.

    All-trans-retinoic acid → C-C chemokine receptor 9 source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Mouse activated T cells, gut dendritic cells and vitamin A-deficient mice.
    exposure
    Added RA
    limitations
    Receptor expression is distinct from clinical infection protection.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Activated cells acquire a receptor associated with gut entry.
    primary_references
    [va-iwata-2004] Retinoic acid imprints gut-homing specificity on T cells (2004). https://pubmed.ncbi.nlm.nih.gov/15485630/ DOI: 10.1016/j.immuni.2004.08.011
    tissue_or_cell_type
    Activated T cells

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1175–1186

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse activated T cells, gut dendritic cells and vitamin A-deficient mice. · source_derived_draft · unverified_draft

    ### va-sig-ra-ccr9 RA during mouse T-cell activation increased CCR9 expression. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Activated cells acquire a receptor associated with gut entry. organism: Mus musculus tissue_or_cell_type: Activated T cells experimental_model: Mouse activated T cells, gut dendritic cells and vitamin A-deficient mice. limitations: Receptor expression is distinct from clinical infection protection. evidence_locator: Abstract exposure: Added RA [va-iwata-2004] Retinoic acid imprints gut-homing specificity on T cells (2004). https://pubmed.ncbi.nlm.nih.gov/15485630/ DOI: 10.1016/j.immuni.2004.08.011
    Complete structured claim and evidence
  19. RA alone was insufficient for IgA secretion but cooperated with IL-6 or IL-5 to induce it.

    All-trans-retinoic acid → Immunoglobulin A source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice.
    exposure
    RA with IL-6 or IL-5
    limitations
    Cannot generalize to every IgA-switching pathway.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    IgA output required additional immune signals in this experiment.
    primary_references
    [va-mora-2006] Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006). https://pubmed.ncbi.nlm.nih.gov/17110582/ DOI: 10.1126/science.1132742
    tissue_or_cell_type
    B-cell cultures

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1227–1238

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice. · source_derived_draft · unverified_draft

    ### va-sig-ra-cytokine-iga RA alone was insufficient for IgA secretion but cooperated with IL-6 or IL-5 to induce it. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: IgA output required additional immune signals in this experiment. organism: Mus musculus tissue_or_cell_type: B-cell cultures experimental_model: Mouse B-cell/dendritic-cell systems and vitamin A-deficient mice. limitations: Cannot generalize to every IgA-switching pathway. evidence_locator: Abstract exposure: RA with IL-6 or IL-5 [va-mora-2006] Generation of gut-homing IgA-secreting B cells by intestinal dendritic cells (2006). https://pubmed.ncbi.nlm.nih.gov/17110582/ DOI: 10.1126/science.1132742
    Complete structured claim and evidence
  20. RA with IL-15 promoted dendritic-cell IL-12p70 release.

    All-trans-retinoic acid → Interleukin-12 p70 source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract and Figure 3
    experimental_model
    Mouse dendritic-cell/T-cell experiments and IL-15-rich intestinal models.
    exposure
    RA plus IL-15
    limitations
    No claim that dietary vitamin A causes coeliac disease.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    An inflammatory cytokine can redirect RA-associated immune signaling.
    primary_references
    [va-depaolo-2011] Co-adjuvant effects of retinoic acid and IL-15 induce inflammatory immunity to dietary antigens (2011). https://www.nature.com/articles/nature09849 DOI: 10.1038/nature09849
    tissue_or_cell_type
    Dendritic cells

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1292–1303

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse dendritic-cell/T-cell experiments and IL-15-rich intestinal models. · source_derived_draft · unverified_draft

    ### va-sig-ra-il15-il12 RA with IL-15 promoted dendritic-cell IL-12p70 release. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inflammatory cytokine can redirect RA-associated immune signaling. organism: Mus musculus tissue_or_cell_type: Dendritic cells experimental_model: Mouse dendritic-cell/T-cell experiments and IL-15-rich intestinal models. limitations: No claim that dietary vitamin A causes coeliac disease. evidence_locator: Abstract and Figure 3 exposure: RA plus IL-15 [va-depaolo-2011] Co-adjuvant effects of retinoic acid and IL-15 induce inflammatory immunity to dietary antigens (2011). https://www.nature.com/articles/nature09849 DOI: 10.1038/nature09849
    Complete structured claim and evidence
  21. RA with IL-15 promoted dendritic-cell IL-23 release.

    All-trans-retinoic acid → Interleukin-23 source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract and Figure 3
    experimental_model
    Mouse dendritic-cell/T-cell experiments and IL-15-rich intestinal models.
    exposure
    RA plus IL-15
    limitations
    Different context from isolated naive T-cell induction.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    RA participates in a proinflammatory response in this cytokine setting.
    primary_references
    [va-depaolo-2011] Co-adjuvant effects of retinoic acid and IL-15 induce inflammatory immunity to dietary antigens (2011). https://www.nature.com/articles/nature09849 DOI: 10.1038/nature09849
    tissue_or_cell_type
    Dendritic cells

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1305–1316

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse dendritic-cell/T-cell experiments and IL-15-rich intestinal models. · source_derived_draft · unverified_draft

    ### va-sig-ra-il15-il23 RA with IL-15 promoted dendritic-cell IL-23 release. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: RA participates in a proinflammatory response in this cytokine setting. organism: Mus musculus tissue_or_cell_type: Dendritic cells experimental_model: Mouse dendritic-cell/T-cell experiments and IL-15-rich intestinal models. limitations: Different context from isolated naive T-cell induction. evidence_locator: Abstract and Figure 3 exposure: RA plus IL-15 [va-depaolo-2011] Co-adjuvant effects of retinoic acid and IL-15 induce inflammatory immunity to dietary antigens (2011). https://www.nature.com/articles/nature09849 DOI: 10.1038/nature09849
    Complete structured claim and evidence
  22. RA promoted regulatory T-cell differentiation under the tested TGF-beta-dependent conditions.

    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Mouse naive T-cell differentiation under TGF-beta and inflammatory cytokine conditions.
    exposure
    Added RA in TGF-beta-driven differentiation
    limitations
    Not an unconditional anti-inflammatory effect or human dietary outcome.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    RA can cooperate with TGF-beta to favor regulatory cells.
    primary_references
    [va-mucida-2007] Reciprocal TH17 and regulatory T cell differentiation mediated by retinoic acid (2007). https://pubmed.ncbi.nlm.nih.gov/17569825/ DOI: 10.1126/science.1145697
    tissue_or_cell_type
    Naive T-cell cultures

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1253–1264

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse naive T-cell differentiation under TGF-beta and inflammatory cytokine conditions. · source_derived_draft · unverified_draft

    ### va-sig-ra-tgfb-foxp3 RA promoted regulatory T-cell differentiation under the tested TGF-beta-dependent conditions. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: RA can cooperate with TGF-beta to favor regulatory cells. organism: Mus musculus tissue_or_cell_type: Naive T-cell cultures experimental_model: Mouse naive T-cell differentiation under TGF-beta and inflammatory cytokine conditions. limitations: Not an unconditional anti-inflammatory effect or human dietary outcome. evidence_locator: Abstract exposure: Added RA in TGF-beta-driven differentiation [va-mucida-2007] Reciprocal TH17 and regulatory T cell differentiation mediated by retinoic acid (2007). https://pubmed.ncbi.nlm.nih.gov/17569825/ DOI: 10.1126/science.1145697
    Complete structured claim and evidence
  23. Added RA inhibited IL-6-driven Th17 induction in the tested TGF-beta context.

    All-trans-retinoic acid → Th17 differentiation source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Mouse naive T-cell differentiation under TGF-beta and inflammatory cytokine conditions.
    exposure
    RA with IL-6/TGF-beta
    limitations
    New lineage induction differs from established intestinal Th17 effector function.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    The cytokine environment determines which T-cell differentiation program RA modifies.
    primary_references
    [va-mucida-2007] Reciprocal TH17 and regulatory T cell differentiation mediated by retinoic acid (2007). https://pubmed.ncbi.nlm.nih.gov/17569825/ DOI: 10.1126/science.1145697
    tissue_or_cell_type
    Naive T-cell cultures

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1266–1277

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse naive T-cell differentiation under TGF-beta and inflammatory cytokine conditions. · source_derived_draft · unverified_draft

    ### va-sig-ra-th17-differentiation Added RA inhibited IL-6-driven Th17 induction in the tested TGF-beta context. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cytokine environment determines which T-cell differentiation program RA modifies. organism: Mus musculus tissue_or_cell_type: Naive T-cell cultures experimental_model: Mouse naive T-cell differentiation under TGF-beta and inflammatory cytokine conditions. limitations: New lineage induction differs from established intestinal Th17 effector function. evidence_locator: Abstract exposure: RA with IL-6/TGF-beta [va-mucida-2007] Reciprocal TH17 and regulatory T cell differentiation mediated by retinoic acid (2007). https://pubmed.ncbi.nlm.nih.gov/17569825/ DOI: 10.1126/science.1145697
    Complete structured claim and evidence
  24. RAR alpha-selective pharmacology supported RAR alpha-mediated induction of airway mucin transcripts, including MUC5AC.

    Retinoic acid receptor alpha → MUC5AC gene source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Normal human tracheobronchial epithelial cultures with receptor-selective agonists/antagonists.
    exposure
    Receptor-selective agonists/antagonists
    limitations
    Transcript changes do not establish improved mucus clearance.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    plain_language
    RAR signaling helps cultured airway cells adopt a mucus-producing program.
    primary_references
    [va-koo-1999] Role of retinoid receptors in the regulation of mucin gene expression by retinoic acid in human tracheobronchial epithelial cells (1999). https://pubmed.ncbi.nlm.nih.gov/10024510/ DOI: 10.1042/bj3380351
    tissue_or_cell_type
    Normal tracheobronchial epithelial cells

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1357–1368

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Normal human tracheobronchial epithelial cultures with receptor-selective agonists/antagonists. · source_derived_draft · unverified_draft

    ### va-sig-rara-airway-mucin RAR alpha-selective pharmacology supported RAR alpha-mediated induction of airway mucin transcripts, including MUC5AC. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: RAR signaling helps cultured airway cells adopt a mucus-producing program. organism: Homo sapiens tissue_or_cell_type: Normal tracheobronchial epithelial cells experimental_model: Normal human tracheobronchial epithelial cultures with receptor-selective agonists/antagonists. limitations: Transcript changes do not establish improved mucus clearance. evidence_locator: Abstract exposure: Receptor-selective agonists/antagonists [va-koo-1999] Role of retinoid receptors in the regulation of mucin gene expression by retinoic acid in human tracheobronchial epithelial cells (1999). https://pubmed.ncbi.nlm.nih.gov/10024510/ DOI: 10.1042/bj3380351
    Complete structured claim and evidence
  25. RXRA associated with RARA and cooperatively bound retinoid response DNA.

    Experimental context and source evidence
    evidence_locator
    Figure 2
    experimental_model
    Recombinant receptors, gel shifts, coimmunoprecipitation and CV-1 reporters.
    exposure
    Receptor coexpression/reconstitution
    limitations
    Synthetic response elements; not every genomic site.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Recombinant receptors
    plain_language
    Two distinct receptor proteins assemble a DNA-binding complex.
    primary_references
    [va-kliewer-1992] Retinoid X receptor interacts with nuclear receptors in retinoic acid, thyroid hormone and vitamin D3 signalling (1992). https://pubmed.ncbi.nlm.nih.gov/1310351/ DOI: 10.1038/355446a0
    tissue_or_cell_type
    Cell-free DNA-binding assay

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1082–1093

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant receptors, gel shifts, coimmunoprecipitation and CV-1 reporters. · source_derived_draft · unverified_draft

    ### va-sig-rara-rxra-cooperative-binding RXRA associated with RARA and cooperatively bound retinoid response DNA. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Two distinct receptor proteins assemble a DNA-binding complex. organism: Recombinant receptors tissue_or_cell_type: Cell-free DNA-binding assay experimental_model: Recombinant receptors, gel shifts, coimmunoprecipitation and CV-1 reporters. limitations: Synthetic response elements; not every genomic site. evidence_locator: Figure 2 exposure: Receptor coexpression/reconstitution [va-kliewer-1992] Retinoid X receptor interacts with nuclear receptors in retinoic acid, thyroid hormone and vitamin D3 signalling (1992). https://pubmed.ncbi.nlm.nih.gov/1310351/ DOI: 10.1038/355446a0
    Complete structured claim and evidence
  26. Rara-deficient or RAR-antagonized T cells proliferated less efficiently after stimulation.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_locator
    Discussion and T-cell activation experiments
    experimental_model
    Vitamin A-insufficient and Rara-deficient mice; stimulated CD4 T cells.
    exposure
    Rara loss or RAR antagonism
    limitations
    Does not negate RA effects on Treg differentiation.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Loss of receptor signaling can weaken effector-cell expansion.
    primary_references
    [va-hall-2011] Essential role for retinoic acid in the promotion of CD4(+) T cell effector responses via retinoic acid receptor alpha (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3415227/ DOI: 10.1016/j.immuni.2011.03.003
    tissue_or_cell_type
    CD4 T cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1279–1290

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Vitamin A-insufficient and Rara-deficient mice; stimulated CD4 T cells. · source_derived_draft · unverified_draft

    ### va-sig-rara-t-cell-proliferation Rara-deficient or RAR-antagonized T cells proliferated less efficiently after stimulation. Condition category: machinery_impairment nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of receptor signaling can weaken effector-cell expansion. organism: Mus musculus tissue_or_cell_type: CD4 T cells experimental_model: Vitamin A-insufficient and Rara-deficient mice; stimulated CD4 T cells. limitations: Does not negate RA effects on Treg differentiation. evidence_locator: Discussion and T-cell activation experiments exposure: Rara loss or RAR antagonism [va-hall-2011] Essential role for retinoic acid in the promotion of CD4(+) T cell effector responses via retinoic acid receptor alpha (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3415227/ DOI: 10.1016/j.immuni.2011.03.003
    Complete structured claim and evidence
  27. The agonist-bound RAR ligand-binding domain interacted with TIF2 in an AF-2-dependent manner.

    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Human TIF2 cloning; in vitro receptor-domain interactions and cellular reporters.
    exposure
    Agonist versus control; AF-2 mutants
    limitations
    Domain assays do not resolve every endogenous chromatin complex.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Human TIF2 and engineered receptor domains
    plain_language
    An activated receptor gains a binding surface for a transcriptional coactivator.
    primary_references
    [va-voegel-1996] TIF2, a 160 kDa transcriptional mediator for the ligand-dependent activation function AF-2 of nuclear receptors (1996). https://pubmed.ncbi.nlm.nih.gov/8670870/ DOI: 10.1002/j.1460-2075.1996.tb00736.x
    tissue_or_cell_type
    Cell-free and cellular interaction assays

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1162–1173

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human TIF2 cloning; in vitro receptor-domain interactions and cellular reporters. · source_derived_draft · unverified_draft

    ### va-sig-rara-tif2-recruitment The agonist-bound RAR ligand-binding domain interacted with TIF2 in an AF-2-dependent manner. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: An activated receptor gains a binding surface for a transcriptional coactivator. organism: Human TIF2 and engineered receptor domains tissue_or_cell_type: Cell-free and cellular interaction assays experimental_model: Human TIF2 cloning; in vitro receptor-domain interactions and cellular reporters. limitations: Domain assays do not resolve every endogenous chromatin complex. evidence_locator: Abstract exposure: Agonist versus control; AF-2 mutants [va-voegel-1996] TIF2, a 160 kDa transcriptional mediator for the ligand-dependent activation function AF-2 of nuclear receptors (1996). https://pubmed.ncbi.nlm.nih.gov/8670870/ DOI: 10.1002/j.1460-2075.1996.tb00736.x
    Complete structured claim and evidence
  28. RAR beta occupied the mouse Saa3 promoter; mutation of RARE -224 abolished reporter activity.

    Retinoic acid receptor beta → Mouse Saa3 gene source_derived_draftungraded
    Experimental context and source evidence
    evidence_locator
    Figure 2; Methods
    experimental_model
    Mouse MODE-K cells and intestinal epithelial Rarb deletion.
    exposure
    100 nM retinol plus 100 ng/mL LPS for 24 h
    limitations
    Direct binding to Saa1/Saa2 was predicted, not demonstrated here.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Epithelial retinoid sensing directly controls this mouse immune gene.
    primary_references
    [va-gattu-2019] Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6561173/ DOI: 10.1073/pnas.1812069116
    tissue_or_cell_type
    MODE-K intestinal epithelial cells

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1318–1329

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse MODE-K cells and intestinal epithelial Rarb deletion. · source_derived_draft · unverified_draft

    ### va-sig-rarb-saa3-promoter RAR beta occupied the mouse Saa3 promoter; mutation of RARE -224 abolished reporter activity. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Epithelial retinoid sensing directly controls this mouse immune gene. organism: Mus musculus tissue_or_cell_type: MODE-K intestinal epithelial cells experimental_model: Mouse MODE-K cells and intestinal epithelial Rarb deletion. limitations: Direct binding to Saa1/Saa2 was predicted, not demonstrated here. evidence_locator: Figure 2; Methods exposure: 100 nM retinol plus 100 ng/mL LPS for 24 h [va-gattu-2019] Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6561173/ DOI: 10.1073/pnas.1812069116
    Complete structured claim and evidence
  29. Epithelial Rarb deletion reduced intestinal Th17 IL-17A production without reducing overall Th17 frequency.

    Retinoic acid receptor beta → Interleukin 17A source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_locator
    Figure 4A-D
    experimental_model
    Mouse MODE-K cells and intestinal epithelial Rarb deletion.
    exposure
    Epithelial Rarb deletion
    limitations
    Does not establish a complete retinol-transfer chain.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    A receptor in epithelial cells helps neighboring immune cells function.
    primary_references
    [va-gattu-2019] Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6561173/ DOI: 10.1073/pnas.1812069116
    tissue_or_cell_type
    Intestinal lamina propria
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1331–1342

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse MODE-K cells and intestinal epithelial Rarb deletion. · source_derived_draft · unverified_draft

    ### va-sig-rarb-th17-effector Epithelial Rarb deletion reduced intestinal Th17 IL-17A production without reducing overall Th17 frequency. Condition category: machinery_impairment nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: A receptor in epithelial cells helps neighboring immune cells function. organism: Mus musculus tissue_or_cell_type: Intestinal lamina propria experimental_model: Mouse MODE-K cells and intestinal epithelial Rarb deletion. limitations: Does not establish a complete retinol-transfer chain. evidence_locator: Figure 4A-D exposure: Epithelial Rarb deletion [va-gattu-2019] Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6561173/ DOI: 10.1073/pnas.1812069116
    Complete structured claim and evidence
  30. An RXR-selective agonist alone failed to induce mucin transcripts but enhanced a suboptimal RAR agonist response.

    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Normal human tracheobronchial epithelial cultures with receptor-selective agonists/antagonists.
    exposure
    Selective receptor agonists
    limitations
    No inference that 9-cis RA improves airway disease.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    plain_language
    Both partners can cooperate, with RAR activation required in this assay.
    primary_references
    [va-koo-1999] Role of retinoid receptors in the regulation of mucin gene expression by retinoic acid in human tracheobronchial epithelial cells (1999). https://pubmed.ncbi.nlm.nih.gov/10024510/ DOI: 10.1042/bj3380351
    tissue_or_cell_type
    Normal tracheobronchial epithelial cells

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1370–1381

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Normal human tracheobronchial epithelial cultures with receptor-selective agonists/antagonists. · source_derived_draft · unverified_draft

    ### va-sig-rxr-airway-cooperation An RXR-selective agonist alone failed to induce mucin transcripts but enhanced a suboptimal RAR agonist response. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Both partners can cooperate, with RAR activation required in this assay. organism: Homo sapiens tissue_or_cell_type: Normal tracheobronchial epithelial cells experimental_model: Normal human tracheobronchial epithelial cultures with receptor-selective agonists/antagonists. limitations: No inference that 9-cis RA improves airway disease. evidence_locator: Abstract exposure: Selective receptor agonists [va-koo-1999] Role of retinoid receptors in the regulation of mucin gene expression by retinoic acid in human tracheobronchial epithelial cells (1999). https://pubmed.ncbi.nlm.nih.gov/10024510/ DOI: 10.1042/bj3380351
    Complete structured claim and evidence
  31. RXRA enhanced RAR-mediated transcription at RA concentrations insufficient to substantially activate RXRA itself.

    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Receptor interaction, DNA binding and transfection experiments.
    exposure
    Receptor cotransfection and RA
    limitations
    Reporter-system dependence; no nutrient dose response.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Engineered cellular receptor system
    plain_language
    RXRA can assist RAR signaling without equivalent activation of both partners.
    primary_references
    [va-zhang-1992] Retinoid X receptor is an auxiliary protein for thyroid hormone and retinoic acid receptors (1992). https://pubmed.ncbi.nlm.nih.gov/1310350/ DOI: 10.1038/355441a0
    tissue_or_cell_type
    Transfection reporters

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1123–1134

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Receptor interaction, DNA binding and transfection experiments. · source_derived_draft · unverified_draft

    ### va-sig-rxra-rar-transactivation RXRA enhanced RAR-mediated transcription at RA concentrations insufficient to substantially activate RXRA itself. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: RXRA can assist RAR signaling without equivalent activation of both partners. organism: Engineered cellular receptor system tissue_or_cell_type: Transfection reporters experimental_model: Receptor interaction, DNA binding and transfection experiments. limitations: Reporter-system dependence; no nutrient dose response. evidence_locator: Abstract exposure: Receptor cotransfection and RA [va-zhang-1992] Retinoid X receptor is an auxiliary protein for thyroid hormone and retinoic acid receptors (1992). https://pubmed.ncbi.nlm.nih.gov/1310350/ DOI: 10.1038/355441a0
    Complete structured claim and evidence
  32. RXRA complexed with TR beta and enhanced thyroid-response-element binding.

    Experimental context and source evidence
    cross_nutrient
    Vitamin A-iodine: shared receptor machinery for an iodine-containing hormone; not evidence of iodine repletion.
    evidence_locator
    Figure 3
    experimental_model
    Recombinant receptors, gel shifts, coimmunoprecipitation and CV-1 reporters.
    exposure
    Reconstituted TR beta/RXRA
    limitations
    No iodine nutritional manipulation.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Recombinant receptors
    plain_language
    A receptor used by retinoids also supports thyroid-hormone DNA recognition.
    primary_references
    [va-kliewer-1992] Retinoid X receptor interacts with nuclear receptors in retinoic acid, thyroid hormone and vitamin D3 signalling (1992). https://pubmed.ncbi.nlm.nih.gov/1310351/ DOI: 10.1038/355446a0
    tissue_or_cell_type
    Cell-free DNA-binding assay

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1109–1121

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant receptors, gel shifts, coimmunoprecipitation and CV-1 reporters. · source_derived_draft · unverified_draft

    ### va-sig-rxra-thrb-partnership RXRA complexed with TR beta and enhanced thyroid-response-element binding. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: A receptor used by retinoids also supports thyroid-hormone DNA recognition. organism: Recombinant receptors tissue_or_cell_type: Cell-free DNA-binding assay experimental_model: Recombinant receptors, gel shifts, coimmunoprecipitation and CV-1 reporters. limitations: No iodine nutritional manipulation. evidence_locator: Figure 3 cross_nutrient: Vitamin A-iodine: shared receptor machinery for an iodine-containing hormone; not evidence of iodine repletion. exposure: Reconstituted TR beta/RXRA [va-kliewer-1992] Retinoid X receptor interacts with nuclear receptors in retinoic acid, thyroid hormone and vitamin D3 signalling (1992). https://pubmed.ncbi.nlm.nih.gov/1310351/ DOI: 10.1038/355446a0
    Complete structured claim and evidence
  33. RXRA formed a VDR complex and enhanced binding to the osteopontin vitamin D response element.

    Retinoid X receptor alpha → Vitamin D receptor / VDR source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Vitamin A-vitamin D: shared receptor partner; no supplementation or deficiency rescue tested.
    evidence_locator
    Figure 3
    experimental_model
    Recombinant receptors, gel shifts, coimmunoprecipitation and CV-1 reporters.
    exposure
    Reconstituted VDR/RXRA
    limitations
    Does not prove vitamin A intake enhances calcium absorption.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Recombinant receptors
    plain_language
    Vitamin D signaling shares RXRA receptor machinery with retinoid pathways.
    primary_references
    [va-kliewer-1992] Retinoid X receptor interacts with nuclear receptors in retinoic acid, thyroid hormone and vitamin D3 signalling (1992). https://pubmed.ncbi.nlm.nih.gov/1310351/ DOI: 10.1038/355446a0
    tissue_or_cell_type
    Cell-free DNA-binding assay

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1095–1107

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant receptors, gel shifts, coimmunoprecipitation and CV-1 reporters. · source_derived_draft · unverified_draft

    ### va-sig-rxra-vdr-partnership RXRA formed a VDR complex and enhanced binding to the osteopontin vitamin D response element. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin D signaling shares RXRA receptor machinery with retinoid pathways. organism: Recombinant receptors tissue_or_cell_type: Cell-free DNA-binding assay experimental_model: Recombinant receptors, gel shifts, coimmunoprecipitation and CV-1 reporters. limitations: Does not prove vitamin A intake enhances calcium absorption. evidence_locator: Figure 3 cross_nutrient: Vitamin A-vitamin D: shared receptor partner; no supplementation or deficiency rescue tested. exposure: Reconstituted VDR/RXRA [va-kliewer-1992] Retinoid X receptor interacts with nuclear receptors in retinoic acid, thyroid hormone and vitamin D3 signalling (1992). https://pubmed.ncbi.nlm.nih.gov/1310351/ DOI: 10.1038/355446a0
    Complete structured claim and evidence
  34. Recombinant SAA1 restored impaired Th17 cytokine output in cultured lamina propria cells from epithelial Rarb mutants.

    Serum amyloid A1 → Interleukin 17A source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_locator
    Figure 4E
    experimental_model
    Mouse MODE-K cells and intestinal epithelial Rarb deletion.
    exposure
    rSAA1 during 4-hour stimulation
    limitations
    Rescue does not establish delivery of retinol to Th17 cells.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Adding an epithelial-associated mediator rescued the measured immune output.
    primary_references
    [va-gattu-2019] Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6561173/ DOI: 10.1073/pnas.1812069116
    tissue_or_cell_type
    Ex vivo intestinal lamina propria cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1344–1355

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse MODE-K cells and intestinal epithelial Rarb deletion. · source_derived_draft · unverified_draft

    ### va-sig-saa1-rescue-th17 Recombinant SAA1 restored impaired Th17 cytokine output in cultured lamina propria cells from epithelial Rarb mutants. Condition category: machinery_impairment nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding an epithelial-associated mediator rescued the measured immune output. organism: Mus musculus tissue_or_cell_type: Ex vivo intestinal lamina propria cells experimental_model: Mouse MODE-K cells and intestinal epithelial Rarb deletion. limitations: Rescue does not establish delivery of retinol to Th17 cells. evidence_locator: Figure 4E exposure: rSAA1 during 4-hour stimulation [va-gattu-2019] Epithelial retinoic acid receptor beta regulates serum amyloid A expression and vitamin A-dependent intestinal immunity (2019). https://pmc.ncbi.nlm.nih.gov/articles/PMC6561173/ DOI: 10.1073/pnas.1812069116
    Complete structured claim and evidence
  35. SMRT associated with retinoid receptors and mediated transcriptional silencing in engineered assays.

    Experimental context and source evidence
    evidence_locator
    Abstract
    experimental_model
    Biochemical interactions and engineered cellular transcription reporters.
    exposure
    Unliganded receptor and SMRT
    limitations
    Not a claim that all unliganded RAR targets are repressed.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Biochemical and cellular reporter systems
    plain_language
    Corepressor proteins help keep selected receptor-controlled genes quiet.
    primary_references
    [va-chen-1995] A transcriptional co-repressor that interacts with nuclear hormone receptors (1995). https://pubmed.ncbi.nlm.nih.gov/7566127/ DOI: 10.1038/377454a0
    tissue_or_cell_type
    Receptor complexes

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1136–1147

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Biochemical interactions and engineered cellular transcription reporters. · source_derived_draft · unverified_draft

    ### va-sig-smrt-repression SMRT associated with retinoid receptors and mediated transcriptional silencing in engineered assays. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Corepressor proteins help keep selected receptor-controlled genes quiet. organism: Biochemical and cellular reporter systems tissue_or_cell_type: Receptor complexes experimental_model: Biochemical interactions and engineered cellular transcription reporters. limitations: Not a claim that all unliganded RAR targets are repressed. evidence_locator: Abstract exposure: Unliganded receptor and SMRT [va-chen-1995] A transcriptional co-repressor that interacts with nuclear hormone receptors (1995). https://pubmed.ncbi.nlm.nih.gov/7566127/ DOI: 10.1038/377454a0
    Complete structured claim and evidence
  36. In women with low initial zinc, vitamin A plus zinc improved night-vision recovery versus double placebo; zinc alone did not.

    Zinc → Night vision source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Zinc/vitamin A -> dark-adaptation response.
    experimental_model
    Three-week zinc randomization, existing vitamin A allocation.
    limitations
    Not a universal zinc requirement; relative estimate had a wide confidence interval.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens
    plain_language
    An additional shortage may limit the response, but this result was subgroup-specific.
    primary_references
    [va-christian2001] Zinc supplementation might potentiate the effect of vitamin A in restoring night vision in pregnant Nepalese women (2001). https://pubmed.ncbi.nlm.nih.gov/11382658/ DOI: 10.1093/ajcn/73.6.1045
    tissue_or_cell_type
    Human visual function
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1507–1517

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Three-week zinc randomization, existing vitamin A allocation. · source_derived_draft · unverified_draft

    ### va-zinc-night-vision-subgroup In women with low initial zinc, vitamin A plus zinc improved night-vision recovery versus double placebo; zinc alone did not. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: An additional shortage may limit the response, but this result was subgroup-specific. organism: Homo sapiens tissue_or_cell_type: Human visual function experimental_model: Three-week zinc randomization, existing vitamin A allocation. limitations: Not a universal zinc requirement; relative estimate had a wide confidence interval. cross_nutrient: Zinc/vitamin A -> dark-adaptation response. [va-christian2001] Zinc supplementation might potentiate the effect of vitamin A in restoring night vision in pregnant Nepalese women (2001). https://pubmed.ncbi.nlm.nih.gov/11382658/ DOI: 10.1093/ajcn/73.6.1045
    Complete structured claim and evidence
  37. Despite combined vitamin A and E treatment, 11 of 13 ABL/HBL patients had subnormal mixed cone-rod electroretinogram amplitudes at long-term follow-up.

    Vitamin E → Retinal function in abetalipoproteinemia source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    true
    experimental_model
    Longitudinal treated cohort; 10 abetalipoproteinemia and 3 homozygous hypobetalipoproteinemia patients
    exposure
    Combined oral vitamins A and E; mean 11.7 years follow-up, range 4–20; exact doses unavailable in abstract.
    limitations
    No randomized A-only, E-only or untreated comparator. Residual retinal disease is compatible with partial benefit; it is not proof that supplementation has no effect.
    nutrient_topic
    Vitamin E research collection; topical membership is not evidence of a direct dietary effect. · Vitamin E
    organism
    Homo sapiens
    plain_language
    Combined treatment did not fully prevent retinal abnormalities in every patient.
    primary_references
    [e-clin-retina2001] Long-term assessment of combined vitamin A and E treatment for the prevention of retinal degeneration in abetalipoproteinaemia and hypobetalipoproteinaemia patients. (2001). https://pubmed.ncbi.nlm.nih.gov/11767031/ DOI: 10.1038/eye.2001.167
    tissue_or_cell_type
    Retina
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin E: transport, membrane protection and nutrient interactions (2026-09-17) · lines 1466–1477

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Longitudinal treated cohort; 10 abetalipoproteinemia and 3 homozygous hypobetalipoproteinemia patients · source_derived_draft · unverified_draft

    ### e-clin-abetalipo-residual-retinopathy Despite combined vitamin A and E treatment, 11 of 13 ABL/HBL patients had subnormal mixed cone-rod electroretinogram amplitudes at long-term follow-up. Condition category: machinery_impairment nutrient_topic: Vitamin E research collection; topical membership is not evidence of a direct dietary effect. plain_language: Combined treatment did not fully prevent retinal abnormalities in every patient. organism: Homo sapiens tissue_or_cell_type: Retina experimental_model: Longitudinal treated cohort; 10 abetalipoproteinemia and 3 homozygous hypobetalipoproteinemia patients limitations: No randomized A-only, E-only or untreated comparator. Residual retinal disease is compatible with partial benefit; it is not proof that supplementation has no effect. exposure: Combined oral vitamins A and E; mean 11.7 years follow-up, range 4–20; exact doses unavailable in abstract. cross_nutrient: true [e-clin-retina2001] Long-term assessment of combined vitamin A and E treatment for the prevention of retinal degeneration in abetalipoproteinaemia and hypobetalipoproteinaemia patients. (2001). https://pubmed.ncbi.nlm.nih.gov/11767031/ DOI: 10.1038/eye.2001.167
    Complete structured claim and evidence
  38. Retinoic acid production following retinol administration was reduced 8.5-fold in Adh4-null mice and 4.8-fold in Adh1-null mice, showing overlapping roles for Adh1 and Adh4 in both ethanol and retinol metabolism.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/alcohol-research/10358022.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1e4e6f0703d814d36609e71a38be53f7c36bebcfdcd3a60c52ea49625369305", "start_char": 0, "end_char": 1272, "text_sha256": "c1e4e6f0703d814d36609e71a38be53f7c36bebcfdcd3a60c52ea49625369305"}
    experimental_model
    Adh1, Adh3 and Adh4 null mutant mice with ethanol, formaldehyde and retinol challenges
    exposure
    Intoxicating ethanol dose, formaldehyde LD50, and retinol administration
    limitations
    A clean three-gene dissection showing which enzyme does which job. It is a mouse gene family that does not map one-to-one onto the human one.
    nutrient_topic
    Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
    organism
    Mouse
    plain_language
    The same enzymes that clear alcohol also turn vitamin A into its signalling form.
    primary_references
    [alcohol-p10358022] Metabolic deficiencies in alcohol dehydrogenase Adh1, Adh3, and Adh4 null mutant mice. Overlapping roles of Adh1 and Adh4 in ethanol clearance and metabolism of retinol to retinoic acid. (1999). https://pubmed.ncbi.nlm.nih.gov/10358022/ DOI: 10.1074/jbc.274.24.16796
    tissue_or_cell_type
    Liver and embryo
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 241–252

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Adh1, Adh3 and Adh4 null mutant mice with ethanol, formaldehyde and retinol challenges · source_derived_draft · unverified_draft

    ### alcohol-adh-retinoic-acid Retinoic acid production following retinol administration was reduced 8.5-fold in Adh4-null mice and 4.8-fold in Adh1-null mice, showing overlapping roles for Adh1 and Adh4 in both ethanol and retinol metabolism. Condition category: machinery_impairment nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: The same enzymes that clear alcohol also turn vitamin A into its signalling form. organism: Mouse tissue_or_cell_type: Liver and embryo experimental_model: Adh1, Adh3 and Adh4 null mutant mice with ethanol, formaldehyde and retinol challenges limitations: A clean three-gene dissection showing which enzyme does which job. It is a mouse gene family that does not map one-to-one onto the human one. exposure: Intoxicating ethanol dose, formaldehyde LD50, and retinol administration evidence_span: {"source_cache": "artifacts/alcohol-research/10358022.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1e4e6f0703d814d36609e71a38be53f7c36bebcfdcd3a60c52ea49625369305", "start_char": 0, "end_char": 1272, "text_sha256": "c1e4e6f0703d814d36609e71a38be53f7c36bebcfdcd3a60c52ea49625369305"} [alcohol-p10358022] Metabolic deficiencies in alcohol dehydrogenase Adh1, Adh3, and Adh4 null mutant mice. Overlapping roles of Adh1 and Adh4 in ethanol clearance and metabolism of retinol to retinoic acid. (1999). https://pubmed.ncbi.nlm.nih.gov/10358022/ DOI: 10.1074/jbc.274.24.16796
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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