Component

Calcitriol production

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

4 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 acts on it

  1. Magnesium depletion did not impair measured calcifediol-to-calcitriol conversion in these rats; isolated renal activity persisted without added Mg.

    Magnesium → Calcitriol production source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Magnesium/vitamin D: qualify a universal CYP27B1 shutdown claim.
    experimental_model
    In-vivo tracer and isolated mitochondrial assays.
    limitations
    No-added-Mg buffer does not prove a metal-free preparation. This result cannot be generalized to every species or illness.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Rattus norvegicus
    plain_language
    Low magnesium did not switch off vitamin D activation in this rat experiment.
    primary_references
    [mg-carpenter1987] Effect of magnesium depletion on metabolism of 25-hydroxyvitamin D in rats (1987). https://pubmed.ncbi.nlm.nih.gov/3605332/ DOI: 10.1152/ajpendo.1987.253.1.e106
    tissue_or_cell_type
    Rat circulation and isolated kidney mitochondria
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1370–1380

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · In-vivo tracer and isolated mitochondrial assays. · source_derived_draft · unverified_draft

    ### mg-rat-calcitriol-conversion-preserved Magnesium depletion did not impair measured calcifediol-to-calcitriol conversion in these rats; isolated renal activity persisted without added Mg. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Low magnesium did not switch off vitamin D activation in this rat experiment. organism: Rattus norvegicus tissue_or_cell_type: Rat circulation and isolated kidney mitochondria experimental_model: In-vivo tracer and isolated mitochondrial assays. limitations: No-added-Mg buffer does not prove a metal-free preparation. This result cannot be generalized to every species or illness. cross_nutrient: Magnesium/vitamin D: qualify a universal CYP27B1 shutdown claim. [mg-carpenter1987] Effect of magnesium depletion on metabolism of 25-hydroxyvitamin D in rats (1987). https://pubmed.ncbi.nlm.nih.gov/3605332/ DOI: 10.1152/ajpendo.1987.253.1.e106
    Complete structured claim and evidence

  2. All four homozygous CYP27B1 missense variants identified in four unrelated rickets patients abolished measured 1alpha-hydroxylase activity when expressed in COS-1 cells.

    Human CYP27B1 gene → Calcitriol production source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    false
    evidence_location
    Primary abstract, Methods and Results.
    experimental_model
    Patient sequencing and heterologous functional assays
    exposure
    Four patient-derived variants versus normal enzyme; dose/time not specified in abstract.
    limitations
    Functional loss is experimentally supported; clinical severity cannot be predicted solely from this assay.
    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 proteins in COS-1 cells
    plain_language
    An inherited enzyme defect can block the final activation step.
    primary_references
    [kitanaka1998] Inactivating mutations in the 25-hydroxyvitamin D3 1alpha-hydroxylase gene in patients with pseudovitamin D-deficiency rickets. (1998). https://pubmed.ncbi.nlm.nih.gov/9486994/ DOI: 10.1056/NEJM199803053381004
    tissue_or_cell_type
    renal activation machinery modeled in cultured cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 482–495

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Patient sequencing and heterologous functional assays · source_derived_draft · unverified_draft

    ### vd-act-cyp27b1-mutations All four homozygous CYP27B1 missense variants identified in four unrelated rickets patients abolished measured 1alpha-hydroxylase activity when expressed in COS-1 cells. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: An inherited enzyme defect can block the final activation step. organism: Homo sapiens proteins in COS-1 cells tissue_or_cell_type: renal activation machinery modeled in cultured cells experimental_model: Patient sequencing and heterologous functional assays limitations: Functional loss is experimentally supported; clinical severity cannot be predicted solely from this assay. exposure: Four patient-derived variants versus normal enzyme; dose/time not specified in abstract. cross_nutrient: false evidence_location: Primary abstract, Methods and Results. nutrient: Vitamin D2 and D3 [kitanaka1998] Inactivating mutations in the 25-hydroxyvitamin D3 1alpha-hydroxylase gene in patients with pseudovitamin D-deficiency rickets. (1998). https://pubmed.ncbi.nlm.nih.gov/9486994/ DOI: 10.1056/NEJM199803053381004
    Complete structured claim and evidence

  3. Thyroparathyroidectomy nearly abolished calcitriol production in low-calcium-fed rats; parathyroid extract restored it.

    Parathyroid hormone / PTH → Calcitriol production source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    experimental_model
    Low-calcium-fed rats; thyroparathyroidectomy and parathyroid-extract replacement
    limitations
    Surgical removal plus extract replacement; not a purified-enzyme assay.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Rattus norvegicus
    plain_language
    Hormonal support helps activate vitamin D during calcium restriction.
    primary_references
    [garabedian1972] Control of 25-hydroxycholecalciferol metabolism by parathyroid glands (1972). https://pubmed.ncbi.nlm.nih.gov/4340153/ DOI: 10.1073/pnas.69.7.1673
    tissue_or_cell_type
    Systemic vitamin D metabolism
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Calcium: mechanism-first literature curation (2026-09-17) · lines 69–78

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Low-calcium-fed rats; thyroparathyroidectomy and parathyroid-extract replacement · source_derived_draft · unverified_draft

    ### parathyroid-loss-calcitriol-production Thyroparathyroidectomy nearly abolished calcitriol production in low-calcium-fed rats; parathyroid extract restored it. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Hormonal support helps activate vitamin D during calcium restriction. organism: Rattus norvegicus tissue_or_cell_type: Systemic vitamin D metabolism experimental_model: Low-calcium-fed rats; thyroparathyroidectomy and parathyroid-extract replacement limitations: Surgical removal plus extract replacement; not a purified-enzyme assay. [garabedian1972] Control of 25-hydroxycholecalciferol metabolism by parathyroid glands (1972). https://pubmed.ncbi.nlm.nih.gov/4340153/ DOI: 10.1073/pnas.69.7.1673
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The rise in circulating calcitriol during a six-hour human PTH(1-34) infusion was smaller after dietary Mg depletion.

    Parathyroid hormone / PTH → Calcitriol source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    magnesium -> PTH response -> vitamin D/calcium
    experimental_model
    26 initially normal adults before/after three-week low-Mg diet
    limitations
    Circulating metabolite response does not identify CYP27B1 as a directly Mg-dependent enzyme or distinguish all production/clearance effects.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Homo sapiens
    plain_language
    Even when PTH was supplied directly, the downstream vitamin-D response was reduced, supporting a target-organ component beyond reduced hormone release.
    primary_references
    [fatemi-1991-selective-depletion] Effect of experimental human magnesium depletion on parathyroid hormone secretion and 1,25-dihydroxyvitamin D metabolism. (1991). https://pubmed.ncbi.nlm.nih.gov/1939521/ DOI: 10.1210/jcem-73-5-1067
    tissue_or_cell_type
    Blood; parathyroid and renal mineral axis
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 385–395

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 26 initially normal adults before/after three-week low-Mg diet · source_derived_draft · unverified_draft

    ### selective-mg-depletion-blunts-pth-calcitriol-response The rise in circulating calcitriol during a six-hour human PTH(1-34) infusion was smaller after dietary Mg depletion. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Even when PTH was supplied directly, the downstream vitamin-D response was reduced, supporting a target-organ component beyond reduced hormone release. organism: Homo sapiens tissue_or_cell_type: Blood; parathyroid and renal mineral axis experimental_model: 26 initially normal adults before/after three-week low-Mg diet limitations: Circulating metabolite response does not identify CYP27B1 as a directly Mg-dependent enzyme or distinguish all production/clearance effects. cross_nutrient: magnesium -> PTH response -> vitamin D/calcium [fatemi-1991-selective-depletion] Effect of experimental human magnesium depletion on parathyroid hormone secretion and 1,25-dihydroxyvitamin D metabolism. (1991). https://pubmed.ncbi.nlm.nih.gov/1939521/ DOI: 10.1210/jcem-73-5-1067
    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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