Component

Lecithin:retinol acyltransferase / LRAT

Independent protein identity; organism and experimental state are specified on individual claims. Retinol esterification enzyme.

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

Read recorded mechanisms Open recursive mind map

How nutrients influence it

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

How nutrients reach it in more than one step

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

Tracing routes…

What it does

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

Recorded relationships

What it acts on

  1. Lrat-null mice still secreted chylomicron retinyl esters whose acyl composition reflected the gavage oil.

    Lecithin:retinol acyltransferase / LRAT → Chylomicron retinoid delivery source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_location
    Figure 3
    experimental_model
    Lrat-knockout mice; retinol gavage and one-month retinoid-deficient diet.
    exposure
    6 micrograms retinol in peanut oil; P-407 clearance blockade; sampling at three hours.
    limitations
    Clearance was pharmacologically blocked; remaining enzyme identity was not established here.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    outcome
    Lrat-null mice still secreted chylomicron retinyl esters whose acyl composition reflected the gavage oil.
    plain_language
    Alternative esterification partly handles absorbed retinol when LRAT is missing.
    primary_references
    [va-obyrne-2005] Retinoid Absorption and Storage Is Impaired in Mice Lacking Lecithin:Retinol Acyltransferase (LRAT) (2005). https://pmc.ncbi.nlm.nih.gov/articles/PMC1352312/ DOI: 10.1074/jbc.M507924200
    tissue_or_cell_type
    Intestine and isolated chylomicrons
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 346–358

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lrat-knockout mice; retinol gavage and one-month retinoid-deficient diet. · source_derived_draft · unverified_draft

    ### va-lrat-chylomicron-retinoids Lrat-null mice still secreted chylomicron retinyl esters whose acyl composition reflected the gavage oil. Condition category: machinery_impairment nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Alternative esterification partly handles absorbed retinol when LRAT is missing. organism: Mus musculus tissue_or_cell_type: Intestine and isolated chylomicrons experimental_model: Lrat-knockout mice; retinol gavage and one-month retinoid-deficient diet. limitations: Clearance was pharmacologically blocked; remaining enzyme identity was not established here. exposure: 6 micrograms retinol in peanut oil; P-407 clearance blockade; sampling at three hours. outcome: Lrat-null mice still secreted chylomicron retinyl esters whose acyl composition reflected the gavage oil. evidence_location: Figure 3 [va-obyrne-2005] Retinoid Absorption and Storage Is Impaired in Mice Lacking Lecithin:Retinol Acyltransferase (LRAT) (2005). https://pmc.ncbi.nlm.nih.gov/articles/PMC1352312/ DOI: 10.1074/jbc.M507924200
    Complete structured claim and evidence

  2. Coexpression of LRAT enhanced STRA6-mediated retinol uptake by coupling transport to ester storage.

    Lecithin:retinol acyltransferase / LRAT → STRA6-mediated retinol uptake source_derived_draftungraded
    Experimental context and source evidence
    evidence_location
    Figure 1
    experimental_model
    Transfected-cell radioretinol uptake and real-time retinol-release assays.
    exposure
    STRA6 with or without LRAT; radiolabeled holo-RBP uptake.
    limitations
    No single intracellular protein was absolutely required for STRA6 activity. Cell-line species were not resolved in the retrieved abstract/figure evidence; no species-specific extension is asserted.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mammalian transfected cells
    outcome
    Coexpression of LRAT enhanced STRA6-mediated retinol uptake by coupling transport to ester storage.
    plain_language
    Retinol esterification helps keep inward uptake moving.
    primary_references
    [va-kawaguchi-2011] Receptor-mediated cellular uptake mechanism that couples to intracellular storage (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3199320/ DOI: 10.1021/cb200178w
    tissue_or_cell_type
    Plasma membrane and intracellular retinoid compartment

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 459–471

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Transfected-cell radioretinol uptake and real-time retinol-release assays. · source_derived_draft · unverified_draft

    ### va-lrat-couples-stra6 Coexpression of LRAT enhanced STRA6-mediated retinol uptake by coupling transport to ester storage. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Retinol esterification helps keep inward uptake moving. organism: Mammalian transfected cells tissue_or_cell_type: Plasma membrane and intracellular retinoid compartment experimental_model: Transfected-cell radioretinol uptake and real-time retinol-release assays. limitations: No single intracellular protein was absolutely required for STRA6 activity. Cell-line species were not resolved in the retrieved abstract/figure evidence; no species-specific extension is asserted. exposure: STRA6 with or without LRAT; radiolabeled holo-RBP uptake. outcome: Coexpression of LRAT enhanced STRA6-mediated retinol uptake by coupling transport to ester storage. evidence_location: Figure 1 [va-kawaguchi-2011] Receptor-mediated cellular uptake mechanism that couples to intracellular storage (2011). https://pmc.ncbi.nlm.nih.gov/articles/PMC3199320/ DOI: 10.1021/cb200178w
    Complete structured claim and evidence

  3. One month of dietary retinoid withdrawal lowered serum retinol in Lrat-null mice, with no comparable fall in wild type.

    Lecithin:retinol acyltransferase / LRAT → Serum retinol concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_location
    Figure 6
    experimental_model
    Lrat-knockout mice; retinol gavage and one-month retinoid-deficient diet.
    exposure
    Three-month-old males and females; one month of retinoid-free diet.
    limitations
    Combined genetic and dietary perturbation; not a human depletion timetable.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    outcome
    One month of dietary retinoid withdrawal lowered serum retinol in Lrat-null mice, with no comparable fall in wild type.
    plain_language
    Poor storage made dietary vitamin A withdrawal affect blood retinol sooner.
    primary_references
    [va-obyrne-2005] Retinoid Absorption and Storage Is Impaired in Mice Lacking Lecithin:Retinol Acyltransferase (LRAT) (2005). https://pmc.ncbi.nlm.nih.gov/articles/PMC1352312/ DOI: 10.1074/jbc.M507924200
    tissue_or_cell_type
    Serum
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 360–372

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lrat-knockout mice; retinol gavage and one-month retinoid-deficient diet. · source_derived_draft · unverified_draft

    ### va-lrat-dietary-depletion-retinol One month of dietary retinoid withdrawal lowered serum retinol in Lrat-null mice, with no comparable fall in wild type. Condition category: nutrient_deficiency nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Poor storage made dietary vitamin A withdrawal affect blood retinol sooner. organism: Mus musculus tissue_or_cell_type: Serum experimental_model: Lrat-knockout mice; retinol gavage and one-month retinoid-deficient diet. limitations: Combined genetic and dietary perturbation; not a human depletion timetable. exposure: Three-month-old males and females; one month of retinoid-free diet. outcome: One month of dietary retinoid withdrawal lowered serum retinol in Lrat-null mice, with no comparable fall in wild type. evidence_location: Figure 6 [va-obyrne-2005] Retinoid Absorption and Storage Is Impaired in Mice Lacking Lecithin:Retinol Acyltransferase (LRAT) (2005). https://pmc.ncbi.nlm.nih.gov/articles/PMC1352312/ DOI: 10.1074/jbc.M507924200
    Complete structured claim and evidence

  4. Lrat-null mice retained only trace hepatic retinyl esters.

    Lecithin:retinol acyltransferase / LRAT → Hepatic retinyl ester storage source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_location
    Abstract
    experimental_model
    Lrat-knockout mice; retinol gavage and one-month retinoid-deficient diet.
    exposure
    Lrat deletion on a retinoid-sufficient control diet.
    limitations
    Adipose stores were preserved or increased; deficiency is not uniform across tissues.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    outcome
    Lrat-null mice retained only trace hepatic retinyl esters.
    plain_language
    Loss of LRAT removes most liver vitamin A storage.
    primary_references
    [va-obyrne-2005] Retinoid Absorption and Storage Is Impaired in Mice Lacking Lecithin:Retinol Acyltransferase (LRAT) (2005). https://pmc.ncbi.nlm.nih.gov/articles/PMC1352312/ DOI: 10.1074/jbc.M507924200
    tissue_or_cell_type
    Liver
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 332–344

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lrat-knockout mice; retinol gavage and one-month retinoid-deficient diet. · source_derived_draft · unverified_draft

    ### va-lrat-loss-stores Lrat-null mice retained only trace hepatic retinyl esters. Condition category: machinery_impairment nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Loss of LRAT removes most liver vitamin A storage. organism: Mus musculus tissue_or_cell_type: Liver experimental_model: Lrat-knockout mice; retinol gavage and one-month retinoid-deficient diet. limitations: Adipose stores were preserved or increased; deficiency is not uniform across tissues. exposure: Lrat deletion on a retinoid-sufficient control diet. outcome: Lrat-null mice retained only trace hepatic retinyl esters. evidence_location: Abstract [va-obyrne-2005] Retinoid Absorption and Storage Is Impaired in Mice Lacking Lecithin:Retinol Acyltransferase (LRAT) (2005). https://pmc.ncbi.nlm.nih.gov/articles/PMC1352312/ DOI: 10.1074/jbc.M507924200
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Maternal retinyl-palmitate supplementation rescued SYCP3-positive meiotic cells in vitamin A-depleted Lrat-null pups.

    All-trans-retinyl palmitate → Mouse germ-cell meiotic initiation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Dietary rescue experiment
    exposure
    100 U/day maternal retinyl palmitate from P5; assessment at P10.
    limitations
    Rescue of early markers is not proof of adult fertility or a human dose.
    nutrient_topic
    Vitamin A expansion research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Replacing the missing nutrient restored early meiotic development.
    primary_references
    [li2011] Vitamin A deficiency results in meiotic failure and accumulation of undifferentiated spermatogonia in prepubertal mouse testis. (2011). https://pubmed.ncbi.nlm.nih.gov/20881313/ DOI: 10.1095/biolreprod.110.086157
    tissue_or_cell_type
    neonatal testis
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A expansion: reproduction, light-driven vision and shared mechanisms (2026-09-17) · lines 278–289

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

    ### va-repro-retinyl-palmitate-rescue Maternal retinyl-palmitate supplementation rescued SYCP3-positive meiotic cells in vitamin A-depleted Lrat-null pups. Condition category: nutrient_deficiency nutrient_topic: Vitamin A expansion research collection; topical membership is not evidence of a direct dietary effect. plain_language: Replacing the missing nutrient restored early meiotic development. organism: Mus musculus tissue_or_cell_type: neonatal testis experimental_model: Dietary rescue experiment limitations: Rescue of early markers is not proof of adult fertility or a human dose. exposure: 100 U/day maternal retinyl palmitate from P5; assessment at P10. cross_nutrient: false [li2011] Vitamin A deficiency results in meiotic failure and accumulation of undifferentiated spermatogonia in prepubertal mouse testis. (2011). https://pubmed.ncbi.nlm.nih.gov/20881313/ DOI: 10.1095/biolreprod.110.086157
    Complete structured claim and evidence

  2. Dietary vitamin A depletion caused undifferentiated spermatogonia to accumulate in prepubertal Lrat-null testes.

    All-trans-retinol → Mouse spermatogonial differentiation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    false
    experimental_model
    Genotype-by-diet mouse comparison
    exposure
    Maternal vitamin A-free diet from E0.5 through lactation; neonatal endpoints through P18.
    limitations
    Storage-defective background accelerated depletion; this is not a knockout-only effect.
    nutrient_topic
    Vitamin A expansion research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Vitamin A shortage can stop early sperm-cell differentiation.
    primary_references
    [li2011] Vitamin A deficiency results in meiotic failure and accumulation of undifferentiated spermatogonia in prepubertal mouse testis. (2011). https://pubmed.ncbi.nlm.nih.gov/20881313/ DOI: 10.1095/biolreprod.110.086157
    tissue_or_cell_type
    prepubertal testis
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Vitamin A expansion: reproduction, light-driven vision and shared mechanisms (2026-09-17) · lines 265–276

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Genotype-by-diet mouse comparison · source_derived_draft · unverified_draft

    ### va-repro-vitamin-a-withdrawal Dietary vitamin A depletion caused undifferentiated spermatogonia to accumulate in prepubertal Lrat-null testes. Condition category: nutrient_deficiency nutrient_topic: Vitamin A expansion research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin A shortage can stop early sperm-cell differentiation. organism: Mus musculus tissue_or_cell_type: prepubertal testis experimental_model: Genotype-by-diet mouse comparison limitations: Storage-defective background accelerated depletion; this is not a knockout-only effect. exposure: Maternal vitamin A-free diet from E0.5 through lactation; neonatal endpoints through P18. cross_nutrient: false [li2011] Vitamin A deficiency results in meiotic failure and accumulation of undifferentiated spermatogonia in prepubertal mouse testis. (2011). https://pubmed.ncbi.nlm.nih.gov/20881313/ DOI: 10.1095/biolreprod.110.086157
    Complete structured claim and evidence

  3. Lrat deletion severely depleted the ocular all-trans-retinyl ester pool in mice.

    LRAT loss → All-trans-retinyl esters source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Lrat knockout versus controls
    limitations
    Other tissues and dietary deficiency are separate questions.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Mus musculus
    plain_language
    Without LRAT, the eye cannot maintain its normal ester reserve.
    primary_references
    [batten-2004] Lecithin-retinol acyltransferase is essential for accumulation of all-trans-retinyl esters in the eye and in the liver (2004). https://pubmed.ncbi.nlm.nih.gov/14684738/ DOI: 10.1074/jbc.M312410200
    tissue_or_cell_type
    Eye/RPE
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 701–710

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Lrat knockout versus controls · source_derived_draft · unverified_draft

    ### a-vision-lrat-esters Lrat deletion severely depleted the ocular all-trans-retinyl ester pool in mice. Condition category: machinery_impairment nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Without LRAT, the eye cannot maintain its normal ester reserve. organism: Mus musculus tissue_or_cell_type: Eye/RPE experimental_model: Lrat knockout versus controls limitations: Other tissues and dietary deficiency are separate questions. [batten-2004] Lecithin-retinol acyltransferase is essential for accumulation of all-trans-retinyl esters in the eye and in the liver (2004). https://pubmed.ncbi.nlm.nih.gov/14684738/ DOI: 10.1074/jbc.M312410200
    Complete structured claim and evidence

  4. Recombinant RPE65 catalyzed conversion of all-trans-retinyl esters to 11-cis-retinol in visual-cycle reconstitution.

    RPE65 retinoid isomerohydrolase → 11-cis-retinol source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Recombinant enzyme reconstitution
    limitations
    Production of the aldehyde requires a subsequent oxidation step.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    QBI-293A human cells and COS-1 monkey cells
    plain_language
    RPE65 converts the ester pool into the cis alcohol needed for chromophore renewal.
    primary_references
    [moiseyev-2005] RPE65 is the isomerohydrolase in the retinoid visual cycle (2005). https://pubmed.ncbi.nlm.nih.gov/16116091/ DOI: 10.1073/pnas.0503460102
    tissue_or_cell_type
    RPE visual-cycle biochemical model

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 666–675

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

    ### a-vision-rpe65-isomerization Recombinant RPE65 catalyzed conversion of all-trans-retinyl esters to 11-cis-retinol in visual-cycle reconstitution. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: RPE65 converts the ester pool into the cis alcohol needed for chromophore renewal. organism: QBI-293A human cells and COS-1 monkey cells tissue_or_cell_type: RPE visual-cycle biochemical model experimental_model: Recombinant enzyme reconstitution limitations: Production of the aldehyde requires a subsequent oxidation step. [moiseyev-2005] RPE65 is the isomerohydrolase in the retinoid visual cycle (2005). https://pubmed.ncbi.nlm.nih.gov/16116091/ DOI: 10.1073/pnas.0503460102
    Complete structured claim and evidence

  5. Human and rat liver LRAT activity transferred the sn-1 acyl group of phosphatidylcholine to CRBP-bound retinol.

    Phosphatidylcholine → Retinyl ester formation source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Phosphatidylcholine-dependent retinol storage links retinoid metabolism to choline-containing phospholipid availability.
    evidence_location
    Abstract
    experimental_model
    Human and rat liver microsomes supplied phosphatidylcholine and CRBP-bound retinol.
    exposure
    Exogenous phosphatidylcholine plus CRBP-bound retinol.
    limitations
    Biochemical donor requirement; dietary choline deficiency was not tested.
    nutrient_topic
    Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
    organism
    Homo sapiens and Rattus norvegicus
    outcome
    Human and rat liver LRAT activity transferred the sn-1 acyl group of phosphatidylcholine to CRBP-bound retinol.
    plain_language
    A membrane choline phospholipid supplies the fatty-acid group used to store vitamin A.
    primary_references
    [va-macdonald-1988] A lecithin:retinol acyltransferase activity in human and rat liver (1988). https://pubmed.ncbi.nlm.nih.gov/3178828/ DOI: 10.1016/S0006-291X(88)80818-0
    tissue_or_cell_type
    Liver microsomes

    Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 317–330

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human and rat liver microsomes supplied phosphatidylcholine and CRBP-bound retinol. · source_derived_draft · unverified_draft

    ### va-lrat-phosphatidylcholine-donor Human and rat liver LRAT activity transferred the sn-1 acyl group of phosphatidylcholine to CRBP-bound retinol. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: A membrane choline phospholipid supplies the fatty-acid group used to store vitamin A. organism: Homo sapiens and Rattus norvegicus tissue_or_cell_type: Liver microsomes experimental_model: Human and rat liver microsomes supplied phosphatidylcholine and CRBP-bound retinol. limitations: Biochemical donor requirement; dietary choline deficiency was not tested. exposure: Exogenous phosphatidylcholine plus CRBP-bound retinol. outcome: Human and rat liver LRAT activity transferred the sn-1 acyl group of phosphatidylcholine to CRBP-bound retinol. evidence_location: Abstract cross_nutrient: Phosphatidylcholine-dependent retinol storage links retinoid metabolism to choline-containing phospholipid availability. [va-macdonald-1988] A lecithin:retinol acyltransferase activity in human and rat liver (1988). https://pubmed.ncbi.nlm.nih.gov/3178828/ DOI: 10.1016/S0006-291X(88)80818-0
    Complete structured claim and evidence

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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