Component

Vitamin D 24-hydroxylase / CYP24A1

Independent biological entity. Read linked claims for experimental scope and context.

10 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. Human CYP24A1 initiated 25-hydroxyvitamin D2 oxidation by hydroxylation at C24R in the vesicle-reconstituted enzyme system.

    Vitamin D 24-hydroxylase / CYP24A1 → 24R,25-Dihydroxyvitamin D2 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_location
    Primary abstract: identified C24R products and comparative initial-rate kinetics.
    experimental_model
    Partially purified human CYP24A1 product analysis
    exposure
    25(OH)D2 substrate; concentration/time not specified in retrieved primary abstract.
    limitations
    Additional oxidation sites and products were not all fully identified; this is one identified initial route.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens protein
    plain_language
    CYP24A1 begins one breakdown route for the D2 precursor.
    primary_references
    [li2023] Inactivation of vitamin D2 metabolites by human CYP24A1. (2023). https://pubmed.ncbi.nlm.nih.gov/37495192/ DOI: 10.1016/j.jsbmb.2023.106368
    tissue_or_cell_type
    phospholipid-vesicle membrane

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 512–525

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Partially purified human CYP24A1 product analysis · source_derived_draft · unverified_draft

    ### vd-act-cyp24a1-25d2 Human CYP24A1 initiated 25-hydroxyvitamin D2 oxidation by hydroxylation at C24R in the vesicle-reconstituted enzyme system. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: CYP24A1 begins one breakdown route for the D2 precursor. organism: Homo sapiens protein tissue_or_cell_type: phospholipid-vesicle membrane experimental_model: Partially purified human CYP24A1 product analysis limitations: Additional oxidation sites and products were not all fully identified; this is one identified initial route. exposure: 25(OH)D2 substrate; concentration/time not specified in retrieved primary abstract. cross_nutrient: false evidence_location: Primary abstract: identified C24R products and comparative initial-rate kinetics. nutrient: Vitamin D2 and D3 [li2023] Inactivation of vitamin D2 metabolites by human CYP24A1. (2023). https://pubmed.ncbi.nlm.nih.gov/37495192/ DOI: 10.1016/j.jsbmb.2023.106368
    Complete structured claim and evidence

  2. Human CYP24A1 initiated active 1alpha,25-dihydroxyvitamin D2 oxidation through C24R hydroxylation.

    Vitamin D 24-hydroxylase / CYP24A1 → 1-alpha,24R,25-Trihydroxyvitamin D2 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_location
    Primary abstract: identified C24R products and comparative initial-rate kinetics.
    experimental_model
    Partially purified human CYP24A1 product analysis
    exposure
    1,25(OH)2D2 substrate; concentration/time not specified in abstract.
    limitations
    Product profile is human enzyme-specific; active D2 is not calcitriol.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens protein
    plain_language
    CYP24A1 also starts breaking down the active D2 hormone.
    primary_references
    [li2023] Inactivation of vitamin D2 metabolites by human CYP24A1. (2023). https://pubmed.ncbi.nlm.nih.gov/37495192/ DOI: 10.1016/j.jsbmb.2023.106368
    tissue_or_cell_type
    phospholipid-vesicle membrane

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 527–540

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Partially purified human CYP24A1 product analysis · source_derived_draft · unverified_draft

    ### vd-act-cyp24a1-active-d2 Human CYP24A1 initiated active 1alpha,25-dihydroxyvitamin D2 oxidation through C24R hydroxylation. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: CYP24A1 also starts breaking down the active D2 hormone. organism: Homo sapiens protein tissue_or_cell_type: phospholipid-vesicle membrane experimental_model: Partially purified human CYP24A1 product analysis limitations: Product profile is human enzyme-specific; active D2 is not calcitriol. exposure: 1,25(OH)2D2 substrate; concentration/time not specified in abstract. cross_nutrient: false evidence_location: Primary abstract: identified C24R products and comparative initial-rate kinetics. nutrient: Vitamin D2 and D3 [li2023] Inactivation of vitamin D2 metabolites by human CYP24A1. (2023). https://pubmed.ncbi.nlm.nih.gov/37495192/ DOI: 10.1016/j.jsbmb.2023.106368
    Complete structured claim and evidence

  3. Wild-type human CYP24A1 expressed in V79-4 cells metabolized calcitriol through C24-pathway intermediates to a water-soluble fraction assigned to calcitroic acid.

    Vitamin D 24-hydroxylase / CYP24A1 → Calcitroic acid source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_location
    Primary Results, in-vitro analysis and Figure 4; clinical cohorts and Discussion.
    experimental_model
    Human CYP24A1 expressed in V79-4 cells
    exposure
    Calcitriol 0.003-9 micromolar across transient/stable systems; Figure 4.
    limitations
    Aqueous radioactivity measures the terminal catabolic fraction; not every oxidation intermediate is individually isolated in this record.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens protein in hamster-derived cells
    plain_language
    CYP24A1 carries active D3 through a multistep breakdown pathway.
    primary_references
    [schlingmann2011] Mutations in CYP24A1 and idiopathic infantile hypercalcemia. (2011). https://pubmed.ncbi.nlm.nih.gov/21675912/ DOI: 10.1056/NEJMoa1103864
    tissue_or_cell_type
    cellular vitamin D catabolic assay

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 497–510

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CYP24A1 expressed in V79-4 cells · source_derived_draft · unverified_draft

    ### vd-act-cyp24a1-calcitroic Wild-type human CYP24A1 expressed in V79-4 cells metabolized calcitriol through C24-pathway intermediates to a water-soluble fraction assigned to calcitroic acid. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: CYP24A1 carries active D3 through a multistep breakdown pathway. organism: Homo sapiens protein in hamster-derived cells tissue_or_cell_type: cellular vitamin D catabolic assay experimental_model: Human CYP24A1 expressed in V79-4 cells limitations: Aqueous radioactivity measures the terminal catabolic fraction; not every oxidation intermediate is individually isolated in this record. exposure: Calcitriol 0.003-9 micromolar across transient/stable systems; Figure 4. cross_nutrient: false evidence_location: Primary Results, in-vitro analysis and Figure 4; clinical cohorts and Discussion. nutrient: Vitamin D2 and D3 [schlingmann2011] Mutations in CYP24A1 and idiopathic infantile hypercalcemia. (2011). https://pubmed.ncbi.nlm.nih.gov/21675912/ DOI: 10.1056/NEJMoa1103864
    Complete structured claim and evidence

  4. Human CYP24A1 hydroxylates calcitriol to 1-alpha,24,25-trihydroxyvitamin D3 in the first C24-oxidation step.

    Vitamin D 24-hydroxylase / CYP24A1 → 1-alpha,24,25-Trihydroxyvitamin D3 source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Human CYP24A1 expressed in E. coli, partially purified and reconstituted in phospholipid vesicles
    limitations
    This is a C24-pathway intermediate, not a final inactive product. Further oxidation and the distinct C23 route are not represented by this single edge.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Homo sapiens enzyme
    plain_language
    CYP24A1 begins a defined calcitriol breakdown route.
    primary_references
    [tieu2014] Kinetic analysis of human CYP24A1 metabolism of vitamin D via the C24-oxidation pathway (2014). https://pubmed.ncbi.nlm.nih.gov/24893882/ DOI: 10.1111/febs.12862
    research_relationship_category
    biochemical_reaction
    tissue_or_cell_type
    Reconstituted enzyme/membrane system
    transport_or_reaction_direction
    forward

    Calcium: mechanism-first literature curation (2026-09-17) · lines 362–373

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human CYP24A1 expressed in E. coli, partially purified and reconstituted in phospholipid vesicles · source_derived_draft · unverified_draft

    ### cyp24a1-calcitriol-c24-hydroxylation Human CYP24A1 hydroxylates calcitriol to 1-alpha,24,25-trihydroxyvitamin D3 in the first C24-oxidation step. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: CYP24A1 begins a defined calcitriol breakdown route. organism: Homo sapiens enzyme tissue_or_cell_type: Reconstituted enzyme/membrane system experimental_model: Human CYP24A1 expressed in E. coli, partially purified and reconstituted in phospholipid vesicles limitations: This is a C24-pathway intermediate, not a final inactive product. Further oxidation and the distinct C23 route are not represented by this single edge. research_relationship_category: biochemical_reaction transport_or_reaction_direction: forward [tieu2014] Kinetic analysis of human CYP24A1 metabolism of vitamin D via the C24-oxidation pathway (2014). https://pubmed.ncbi.nlm.nih.gov/24893882/ DOI: 10.1111/febs.12862
    Complete structured claim and evidence

What acts on it

  1. Recombinant FGF23 raises renal CYP24A1 mRNA as circulating calcitriol declines.

    Fibroblast growth factor 23 / FGF23 → Vitamin D 24-hydroxylase / CYP24A1 source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Recombinant FGF23 injections in normal and parathyroidectomized rodents
    limitations
    Acute rodent transcript response; does not quantify human calcium balance.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mus musculus; Rattus norvegicus
    plain_language
    FGF23 increases vitamin D inactivation machinery.
    primary_references
    [shimada2004injection] FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis (2004). https://pubmed.ncbi.nlm.nih.gov/15040831/ DOI: 10.1359/JBMR.0301264
    tissue_or_cell_type
    Kidney

    Calcium: mechanism-first literature curation (2026-09-17) · lines 102–111

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant FGF23 injections in normal and parathyroidectomized rodents · source_derived_draft · unverified_draft

    ### fgf23-increases-cyp24a1-expression Recombinant FGF23 raises renal CYP24A1 mRNA as circulating calcitriol declines. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: FGF23 increases vitamin D inactivation machinery. organism: Mus musculus; Rattus norvegicus tissue_or_cell_type: Kidney experimental_model: Recombinant FGF23 injections in normal and parathyroidectomized rodents limitations: Acute rodent transcript response; does not quantify human calcium balance. [shimada2004injection] FGF-23 is a potent regulator of vitamin D metabolism and phosphate homeostasis (2004). https://pubmed.ncbi.nlm.nih.gov/15040831/ DOI: 10.1359/JBMR.0301264
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Magnesium deprivation increased renal cyp24a1-mrna abundance in the 21-day rat experiment.

    Magnesium → CYP24A1 mRNA source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Magnesium -> vitamin D/phosphate handling; transcript-level evidence.
    experimental_model
    Mg-free versus 0.05% Mg diet.
    limitations
    mRNA endpoint; no transporter flux or obligatory enzyme-bound Mg inference.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Rattus norvegicus
    plain_language
    The message for a vitamin D breakdown enzyme rose.
    primary_references
    [mg-matsuzaki2013] Magnesium deficiency regulates vitamin D metabolizing enzymes and type II sodium-phosphate cotransporter mRNA expression in rats (2013). https://pubmed.ncbi.nlm.nih.gov/23816829/ DOI: 10.1684/mrh.2013.0341
    tissue_or_cell_type
    Rat kidney
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1394–1404

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mg-free versus 0.05% Mg diet. · source_derived_draft · unverified_draft

    ### mg-deficiency-cyp24a1-transcript Magnesium deprivation increased renal cyp24a1-mrna abundance in the 21-day rat experiment. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The message for a vitamin D breakdown enzyme rose. organism: Rattus norvegicus tissue_or_cell_type: Rat kidney experimental_model: Mg-free versus 0.05% Mg diet. limitations: mRNA endpoint; no transporter flux or obligatory enzyme-bound Mg inference. cross_nutrient: Magnesium -> vitamin D/phosphate handling; transcript-level evidence. [mg-matsuzaki2013] Magnesium deficiency regulates vitamin D metabolizing enzymes and type II sodium-phosphate cotransporter mRNA expression in rats (2013). https://pubmed.ncbi.nlm.nih.gov/23816829/ DOI: 10.1684/mrh.2013.0341
    Complete structured claim and evidence

  2. Human CYP24A1 initial catalytic efficiency for calcitriol was almost twice that for the active D2 hormone in the matched vesicle experiment.

    1-alpha,25-Dihydroxyvitamin D2 → Calcitriol source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_location
    Primary abstract: identified C24R products and comparative initial-rate kinetics.
    experimental_model
    Matched recombinant human CYP24A1 kinetics
    exposure
    Comparison of kcat/Km; low-substrate limit.
    limitations
    This observation does not establish longer in-vivo D2 hormone exposure or negate clinical differences between parent vitamin dosing regimens.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens protein
    plain_language
    Active D2 was initially oxidized more slowly than active D3 in this assay.
    primary_references
    [li2023] Inactivation of vitamin D2 metabolites by human CYP24A1. (2023). https://pubmed.ncbi.nlm.nih.gov/37495192/ DOI: 10.1016/j.jsbmb.2023.106368
    tissue_or_cell_type
    phospholipid-vesicle membrane

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 557–570

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Matched recombinant human CYP24A1 kinetics · source_derived_draft · unverified_draft

    ### vd-act-cyp24a1-hormone-selectivity Human CYP24A1 initial catalytic efficiency for calcitriol was almost twice that for the active D2 hormone in the matched vesicle experiment. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Active D2 was initially oxidized more slowly than active D3 in this assay. organism: Homo sapiens protein tissue_or_cell_type: phospholipid-vesicle membrane experimental_model: Matched recombinant human CYP24A1 kinetics limitations: This observation does not establish longer in-vivo D2 hormone exposure or negate clinical differences between parent vitamin dosing regimens. exposure: Comparison of kcat/Km; low-substrate limit. cross_nutrient: false evidence_location: Primary abstract: identified C24R products and comparative initial-rate kinetics. nutrient: Vitamin D2 and D3 [li2023] Inactivation of vitamin D2 metabolites by human CYP24A1. (2023). https://pubmed.ncbi.nlm.nih.gov/37495192/ DOI: 10.1016/j.jsbmb.2023.106368
    Complete structured claim and evidence

  3. Recessive CYP24A1 variants were identified in infants with hypercalcemia, including a second group whose illness followed high-dose vitamin D prophylaxis.

    Human CYP24A1 gene → Serum calcium concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    true
    evidence_location
    Primary Results, in-vitro analysis and Figure 4; clinical cohorts and Discussion.
    experimental_model
    Human candidate-gene study with supporting enzyme assays
    exposure
    First cohort received 500 IU/day; second cohort became symptomatic 2-3 weeks after intermittent high-dose prophylaxis.
    limitations
    Selected families do not estimate population risk. Genotype, dose and penetrance matter; this is not a universal safe/unsafe serum or dose threshold.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens
    plain_language
    Defective vitamin D breakdown can make infants unusually sensitive to supplementation.
    primary_references
    [schlingmann2011] Mutations in CYP24A1 and idiopathic infantile hypercalcemia. (2011). https://pubmed.ncbi.nlm.nih.gov/21675912/ DOI: 10.1056/NEJMoa1103864
    tissue_or_cell_type
    systemic calcium handling
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 602–615

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human candidate-gene study with supporting enzyme assays · source_derived_draft · unverified_draft

    ### vd-act-cyp24a1-hypercalcemia Recessive CYP24A1 variants were identified in infants with hypercalcemia, including a second group whose illness followed high-dose vitamin D prophylaxis. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Defective vitamin D breakdown can make infants unusually sensitive to supplementation. organism: Homo sapiens tissue_or_cell_type: systemic calcium handling experimental_model: Human candidate-gene study with supporting enzyme assays limitations: Selected families do not estimate population risk. Genotype, dose and penetrance matter; this is not a universal safe/unsafe serum or dose threshold. exposure: First cohort received 500 IU/day; second cohort became symptomatic 2-3 weeks after intermittent high-dose prophylaxis. cross_nutrient: true evidence_location: Primary Results, in-vitro analysis and Figure 4; clinical cohorts and Discussion. nutrient: Vitamin D2 and D3 [schlingmann2011] Mutations in CYP24A1 and idiopathic infantile hypercalcemia. (2011). https://pubmed.ncbi.nlm.nih.gov/21675912/ DOI: 10.1056/NEJMoa1103864
    Complete structured claim and evidence

  4. Patient-derived CYP24A1 variants severely impaired calcitriol catabolism in expression assays; L409S retained 5.3% of wild-type activity in the detailed results.

    Human CYP24A1 gene → Calcitriol catabolism source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Primary Results, in-vitro analysis and Figure 4; clinical cohorts and Discussion.
    experimental_model
    Patient variants expressed in V79-4 cells
    exposure
    Transient/stable transfection; calcitriol 0.003-9 micromolar depending on system.
    limitations
    The full text qualifies its abstract: L409S retained small measurable activity, so not all variants were absolutely inactive.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens protein in hamster-derived cells
    plain_language
    Some inherited defects prevent normal removal of active vitamin D.
    primary_references
    [schlingmann2011] Mutations in CYP24A1 and idiopathic infantile hypercalcemia. (2011). https://pubmed.ncbi.nlm.nih.gov/21675912/ DOI: 10.1056/NEJMoa1103864
    tissue_or_cell_type
    cellular catabolic assay
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 587–600

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient variants expressed in V79-4 cells · source_derived_draft · unverified_draft

    ### vd-act-cyp24a1-loss Patient-derived CYP24A1 variants severely impaired calcitriol catabolism in expression assays; L409S retained 5.3% of wild-type activity in the detailed results. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Some inherited defects prevent normal removal of active vitamin D. organism: Homo sapiens protein in hamster-derived cells tissue_or_cell_type: cellular catabolic assay experimental_model: Patient variants expressed in V79-4 cells limitations: The full text qualifies its abstract: L409S retained small measurable activity, so not all variants were absolutely inactive. exposure: Transient/stable transfection; calcitriol 0.003-9 micromolar depending on system. cross_nutrient: false evidence_location: Primary Results, in-vitro analysis and Figure 4; clinical cohorts and Discussion. nutrient: Vitamin D2 and D3 [schlingmann2011] Mutations in CYP24A1 and idiopathic infantile hypercalcemia. (2011). https://pubmed.ncbi.nlm.nih.gov/21675912/ DOI: 10.1056/NEJMoa1103864
    Complete structured claim and evidence

  5. Human CYP24A1 had similar initial hydroxylation catalytic efficiencies for 25-hydroxyvitamin D2 and calcifediol in the matched vesicle assay.

    25-Hydroxyvitamin D2 → Calcifediol / 25-hydroxyvitamin D3 source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    false
    evidence_location
    Primary abstract: identified C24R products and comparative initial-rate kinetics.
    experimental_model
    Matched recombinant human CYP24A1 initial-rate kinetics
    exposure
    Comparative kcat/Km at low substrate availability; exact substrate range not reported in abstract.
    limitations
    This is an enzyme comparison; it does not measure binding-protein clearance, repeated dosing, or whole-person serum responses.
    nutrient
    Vitamin D2 and D3 · Vitamin D2 and D3
    nutrient_topic
    Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3
    organism
    Homo sapiens protein
    plain_language
    The two 25-hydroxy precursors were initially oxidized with similar enzyme efficiency.
    primary_references
    [li2023] Inactivation of vitamin D2 metabolites by human CYP24A1. (2023). https://pubmed.ncbi.nlm.nih.gov/37495192/ DOI: 10.1016/j.jsbmb.2023.106368
    tissue_or_cell_type
    phospholipid-vesicle membrane

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 542–555

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Matched recombinant human CYP24A1 initial-rate kinetics · source_derived_draft · unverified_draft

    ### vd-act-cyp24a1-precursor-selectivity Human CYP24A1 had similar initial hydroxylation catalytic efficiencies for 25-hydroxyvitamin D2 and calcifediol in the matched vesicle assay. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The two 25-hydroxy precursors were initially oxidized with similar enzyme efficiency. organism: Homo sapiens protein tissue_or_cell_type: phospholipid-vesicle membrane experimental_model: Matched recombinant human CYP24A1 initial-rate kinetics limitations: This is an enzyme comparison; it does not measure binding-protein clearance, repeated dosing, or whole-person serum responses. exposure: Comparative kcat/Km at low substrate availability; exact substrate range not reported in abstract. cross_nutrient: false evidence_location: Primary abstract: identified C24R products and comparative initial-rate kinetics. nutrient: Vitamin D2 and D3 [li2023] Inactivation of vitamin D2 metabolites by human CYP24A1. (2023). https://pubmed.ncbi.nlm.nih.gov/37495192/ DOI: 10.1016/j.jsbmb.2023.106368
    Complete structured claim and evidence

In the sources

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

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