Component

Calcitriol catabolism

Enzymatic oxidation and subsequent metabolism of 1alpha,25-dihydroxyvitamin D3.

1 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 acts on it

  1. 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

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.

    Evidence, AI assistance and curation standards