Vitamin D receptor / VDR

cross_nutrient

false

experimental_model

Human cell lines and bone-marrow-derived cells; promoter studies and mouse comparison

exposure

Promoter binding and functional response-element experiments.

limitations

Human cell and promoter experiments; no oral D2/D3 efficacy or infection-incidence trial.

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

The receptor connects the active hormone to a specific DNA control element.

primary_references

[gombart2005] Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3. (2005). https://pubmed.ncbi.nlm.nih.gov/15985530/ DOI: 10.1096/fj.04-3284com

tissue_or_cell_type

Human CAMP promoter

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 918–929

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cell lines and bone-marrow-derived cells; promoter studies and mouse comparison · source_derived_draft · unverified_draft

### vd-camp-vdre VDR bound a consensus vitamin D response element in the human CAMP promoter; this element mediated the observed induction. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor connects the active hormone to a specific DNA control element. organism: Homo sapiens tissue_or_cell_type: Human CAMP promoter experimental_model: Human cell lines and bone-marrow-derived cells; promoter studies and mouse comparison limitations: Human cell and promoter experiments; no oral D2/D3 efficacy or infection-incidence trial. exposure: Promoter binding and functional response-element experiments. cross_nutrient: false [gombart2005] Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3. (2005). https://pubmed.ncbi.nlm.nih.gov/15985530/ DOI: 10.1096/fj.04-3284com

availability_state

machinery_impairment Imported condition classification; unverified.

experimental_model

Mice with targeted disruption of the VDR DNA-binding domain

limitations

Global receptor deletion; not isolated dietary calcium shortage.

nutrient_topic

Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium

organism

Mus musculus

plain_language

Vitamin D receptor failure disrupts calcium regulation.

primary_references

[li1997] Targeted ablation of the vitamin D receptor: an animal model of vitamin D-dependent rickets type II with alopecia (1997). https://pmc.ncbi.nlm.nih.gov/articles/PMC23277/ DOI: 10.1073/pnas.94.18.9831

tissue_or_cell_type

Systemic mineral metabolism

trigger_kind

machinery_impairment Imported condition classification; unverified.

Calcium: mechanism-first literature curation (2026-09-17) · lines 135–144

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mice with targeted disruption of the VDR DNA-binding domain · source_derived_draft · unverified_draft

### vdr-loss-hypocalcemia VDR-ablated mice develop hypocalcemia around postnatal day 21 with rising PTH. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Vitamin D receptor failure disrupts calcium regulation. organism: Mus musculus tissue_or_cell_type: Systemic mineral metabolism experimental_model: Mice with targeted disruption of the VDR DNA-binding domain limitations: Global receptor deletion; not isolated dietary calcium shortage. [li1997] Targeted ablation of the vitamin D receptor: an animal model of vitamin D-dependent rickets type II with alopecia (1997). https://pmc.ncbi.nlm.nih.gov/articles/PMC23277/ DOI: 10.1073/pnas.94.18.9831

cross_nutrient

false

experimental_model

Keratinocyte-targeted mutant VDR transgenes in VDR-null mice; binding/repression assays

exposure

VDR-Hairless interaction/repression assays accompanying transgenic studies.

limitations

Engineered mouse VDR system; does not establish a vitamin D supplement as treatment for human hair loss.

nutrient_topic

Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin D2 and D3

organism

Mouse-model-associated molecular assays

plain_language

The receptor also interacts with a gene-silencing partner, independently of normal hormone binding.

primary_references

[skorija2005] Ligand-independent actions of the vitamin D receptor maintain hair follicle homeostasis. (2005). https://pubmed.ncbi.nlm.nih.gov/15591533/ DOI: 10.1210/me.2004-0415

tissue_or_cell_type

Experimental receptor/corepressor system

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1210–1221

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Keratinocyte-targeted mutant VDR transgenes in VDR-null mice; binding/repression assays · source_derived_draft · unverified_draft

### vd-hairless-vdr Hairless bound VDR and supported transcriptional repression; the tested ligand-binding and AF2 mutations did not abolish those interactions. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor also interacts with a gene-silencing partner, independently of normal hormone binding. organism: Mouse-model-associated molecular assays tissue_or_cell_type: Experimental receptor/corepressor system experimental_model: Keratinocyte-targeted mutant VDR transgenes in VDR-null mice; binding/repression assays limitations: Engineered mouse VDR system; does not establish a vitamin D supplement as treatment for human hair loss. exposure: VDR-Hairless interaction/repression assays accompanying transgenic studies. cross_nutrient: false [skorija2005] Ligand-independent actions of the vitamin D receptor maintain hair follicle homeostasis. (2005). https://pubmed.ncbi.nlm.nih.gov/15591533/ DOI: 10.1210/me.2004-0415

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

cross_nutrient

magnesium -> calcium sensing

experimental_model

Six-hour ex-vivo gland incubation with receptor expression assays

limitations

Receptor abundance alone does not prove altered clinical calcium balance; VDR, FGFR1 and Klotho also rose in this experiment.

nutrient_topic

Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium

organism

Rattus norvegicus

plain_language

Mg exposure can change the amount of the calcium-sensing receptor, adding a slower response to immediate ion sensing.

primary_references

[rodriguez-ortiz-2014-pth-context] Magnesium modulates parathyroid hormone secretion and upregulates parathyroid receptor expression at moderately low calcium concentration (2014). https://pubmed.ncbi.nlm.nih.gov/24103811/ DOI: 10.1093/ndt/gft400

tissue_or_cell_type

Parathyroid gland

Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 289–299

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Six-hour ex-vivo gland incubation with receptor expression assays · source_derived_draft · unverified_draft

### mg-increases-parathyroid-casr-expression At 1.0 mM Ca, six-hour exposure to 2.0 versus 0.5 mM Mg increased CaSR mRNA and protein in intact rat glands. Condition category: normal nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Mg exposure can change the amount of the calcium-sensing receptor, adding a slower response to immediate ion sensing. organism: Rattus norvegicus tissue_or_cell_type: Parathyroid gland experimental_model: Six-hour ex-vivo gland incubation with receptor expression assays limitations: Receptor abundance alone does not prove altered clinical calcium balance; VDR, FGFR1 and Klotho also rose in this experiment. cross_nutrient: magnesium -> calcium sensing [rodriguez-ortiz-2014-pth-context] Magnesium modulates parathyroid hormone secretion and upregulates parathyroid receptor expression at moderately low calcium concentration (2014). https://pubmed.ncbi.nlm.nih.gov/24103811/ DOI: 10.1093/ndt/gft400

cross_nutrient

false

experimental_model

Human cell lines and bone-marrow-derived cells; promoter studies and mouse comparison

exposure

Calcitriol-treated primary cells and cell lines; concentrations not recovered from the abstract.

limitations

Human cell and promoter experiments; no oral D2/D3 efficacy or infection-incidence trial.

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

The active D3 hormone increased the instructions for an antimicrobial protein.

primary_references

[gombart2005] Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3. (2005). https://pubmed.ncbi.nlm.nih.gov/15985530/ DOI: 10.1096/fj.04-3284com

tissue_or_cell_type

Human myeloid and epithelial cells

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 905–916

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cell lines and bone-marrow-derived cells; promoter studies and mouse comparison · source_derived_draft · unverified_draft

### vd-camp-transcription Calcitriol induced CAMP expression in tested human myeloid, keratinocyte and colon cell models and bone-marrow-derived cells. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The active D3 hormone increased the instructions for an antimicrobial protein. organism: Homo sapiens tissue_or_cell_type: Human myeloid and epithelial cells experimental_model: Human cell lines and bone-marrow-derived cells; promoter studies and mouse comparison limitations: Human cell and promoter experiments; no oral D2/D3 efficacy or infection-incidence trial. exposure: Calcitriol-treated primary cells and cell lines; concentrations not recovered from the abstract. cross_nutrient: false [gombart2005] Human cathelicidin antimicrobial peptide (CAMP) gene is a direct target of the vitamin D receptor and is strongly up-regulated in myeloid cells by 1,25-dihydroxyvitamin D3. (2005). https://pubmed.ncbi.nlm.nih.gov/15985530/ DOI: 10.1096/fj.04-3284com

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Human macrophage IFN-gamma experiments with sera of differing 25OHD content

exposure

IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract.

limitations

Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred.

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

The cells recovered a recycling and defense process called autophagy.

primary_references

[fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045

tissue_or_cell_type

Human macrophages

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1048–1059

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human macrophage IFN-gamma experiments with sera of differing 25OHD content · source_derived_draft · unverified_draft

### vd-fabri-autophagy Adding 25(OH)D3 to low-vitamin-D serum restored IFN-gamma -induced macrophage autophagy. Condition category: nutrient_deficiency nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells recovered a recycling and defense process called autophagy. organism: Homo sapiens tissue_or_cell_type: Human macrophages experimental_model: Human macrophage IFN-gamma experiments with sera of differing 25OHD content limitations: Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred. exposure: IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract. cross_nutrient: false [fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Human macrophage IFN-gamma experiments with sera of differing 25OHD content

exposure

IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract.

limitations

Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred.

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

Adding precursor restored the antimicrobial gene response.

primary_references

[fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045

tissue_or_cell_type

Human macrophages

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1035–1046

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human macrophage IFN-gamma experiments with sera of differing 25OHD content · source_derived_draft · unverified_draft

### vd-fabri-camp Adding 25(OH)D3 to low-vitamin-D serum restored IFN-gamma -induced antimicrobial peptide expression. Condition category: nutrient_deficiency nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding precursor restored the antimicrobial gene response. organism: Homo sapiens tissue_or_cell_type: Human macrophages experimental_model: Human macrophage IFN-gamma experiments with sera of differing 25OHD content limitations: Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred. exposure: IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract. cross_nutrient: false [fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Human macrophage IFN-gamma experiments with sera of differing 25OHD content

exposure

IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract.

limitations

Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred.

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

The compartment holding the pathogen could fuse with a degradative compartment.

primary_references

[fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045

tissue_or_cell_type

Human macrophages

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1061–1072

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human macrophage IFN-gamma experiments with sera of differing 25OHD content · source_derived_draft · unverified_draft

### vd-fabri-fusion Adding 25(OH)D3 to low-vitamin-D serum restored IFN-gamma -induced phagosome-lysosome fusion. Condition category: nutrient_deficiency nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The compartment holding the pathogen could fuse with a degradative compartment. organism: Homo sapiens tissue_or_cell_type: Human macrophages experimental_model: Human macrophage IFN-gamma experiments with sera of differing 25OHD content limitations: Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred. exposure: IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract. cross_nutrient: false [fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

false

experimental_model

Human macrophage IFN-gamma experiments with sera of differing 25OHD content

exposure

IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract.

limitations

Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred.

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

The cell experiment also recovered antimicrobial activity.

primary_references

[fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045

tissue_or_cell_type

Human macrophages

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1074–1085

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human macrophage IFN-gamma experiments with sera of differing 25OHD content · source_derived_draft · unverified_draft

### vd-fabri-killing Adding 25(OH)D3 to low-vitamin-D serum restored IFN-gamma -induced antimicrobial activity against intracellularM. tuberculosis. Condition category: nutrient_deficiency nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cell experiment also recovered antimicrobial activity. organism: Homo sapiens tissue_or_cell_type: Human macrophages experimental_model: Human macrophage IFN-gamma experiments with sera of differing 25OHD content limitations: Cultured human macrophages and selected serum pools; no universal serum threshold or clinical tuberculosis cure inferred. exposure: IFN-gamma -stimulated human macrophages; low-vitamin-D serum with 25(OH)D3 add-back; dose/time not recovered from abstract. cross_nutrient: false [fabri2011] Vitamin D is required for IFN-gamma-mediated antimicrobial activity of human macrophages. (2011). https://pubmed.ncbi.nlm.nih.gov/21998409/ DOI: 10.1126/scitranslmed.3003045

cross_nutrient

false

experimental_model

Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay

exposure

TLR activation in cultured human monocytes/macrophages.

limitations

Gene-expression result; does not mean any dietary D dose reproduces pathogen-triggered signaling.

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

A pathogen-sensing signal increased part of the local vitamin D machinery.

primary_references

[liu2006] Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. (2006). https://pubmed.ncbi.nlm.nih.gov/16497887/ DOI: 10.1126/science.1123933

tissue_or_cell_type

Human monocytes/macrophages

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 957–968

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay · source_derived_draft · unverified_draft

### vd-tlr-cyp27b1 TLR activation increased vitamin D1-alpha-hydroxylase gene expression in human macrophages. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A pathogen-sensing signal increased part of the local vitamin D machinery. organism: Homo sapiens tissue_or_cell_type: Human monocytes/macrophages experimental_model: Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay limitations: Gene-expression result; does not mean any dietary D dose reproduces pathogen-triggered signaling. exposure: TLR activation in cultured human monocytes/macrophages. cross_nutrient: false [liu2006] Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. (2006). https://pubmed.ncbi.nlm.nih.gov/16497887/ DOI: 10.1126/science.1123933

cross_nutrient

false

experimental_model

Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay

exposure

TLR activation in cultured human monocytes/macrophages.

limitations

Gene-expression result; does not mean any dietary D dose reproduces pathogen-triggered signaling.

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

A pathogen-sensing signal increased part of the local vitamin D machinery.

primary_references

[liu2006] Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. (2006). https://pubmed.ncbi.nlm.nih.gov/16497887/ DOI: 10.1126/science.1123933

tissue_or_cell_type

Human monocytes/macrophages

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 944–955

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay · source_derived_draft · unverified_draft

### vd-tlr-vdr TLR activation increased VDR gene expression in human macrophages. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: A pathogen-sensing signal increased part of the local vitamin D machinery. organism: Homo sapiens tissue_or_cell_type: Human monocytes/macrophages experimental_model: Human monocyte/macrophage TLR stimulation and intracellular mycobacterial assay limitations: Gene-expression result; does not mean any dietary D dose reproduces pathogen-triggered signaling. exposure: TLR activation in cultured human monocytes/macrophages. cross_nutrient: false [liu2006] Toll-like receptor triggering of a vitamin D-mediated human antimicrobial response. (2006). https://pubmed.ncbi.nlm.nih.gov/16497887/ DOI: 10.1126/science.1123933

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Abstract: reported experimental results

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Calcitriol-injected mice; bone Fgf23 transcript assay and circulating FGF23 measurement

exposure

Calcitriol administration; circulating FGF23 rose by 8 hours. Dose and transcript collection time not specified in the retrieved abstract.

limitations

The mRNA result is distinguished from circulating hormone and renal action; the separate cell reporter experiment supports receptor dependence but is not inferred to prove every bone enhancer.

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

Mus musculus

plain_language

Active vitamin D induced a bone hormone that feeds back on vitamin D activation and phosphate handling.

primary_references

[vdm-liu2006] Fibroblast growth factor 23 is a counter-regulatory phosphaturic hormone for vitamin D. (2006). https://pubmed.ncbi.nlm.nih.gov/16597685/ DOI: 10.1681/asn.2005111185

tissue_or_cell_type

Bone

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 729–743

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Calcitriol-injected mice; bone Fgf23 transcript assay and circulating FGF23 measurement · source_derived_draft · unverified_draft

### vdm-calcitriol-increases-bone-fgf23-transcripts Calcitriol administration produced about a fourfold increase in bone Fgf23 transcripts in the Liu mouse study. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Active vitamin D induced a bone hormone that feeds back on vitamin D activation and phosphate handling. organism: Mus musculus tissue_or_cell_type: Bone experimental_model: Calcitriol-injected mice; bone Fgf23 transcript assay and circulating FGF23 measurement limitations: The mRNA result is distinguished from circulating hormone and renal action; the separate cell reporter experiment supports receptor dependence but is not inferred to prove every bone enhancer. exposure: Calcitriol administration; circulating FGF23 rose by 8 hours. Dose and transcript collection time not specified in the retrieved abstract. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-liu2006] Fibroblast growth factor 23 is a counter-regulatory phosphaturic hormone for vitamin D. (2006). https://pubmed.ncbi.nlm.nih.gov/16597685/ DOI: 10.1681/asn.2005111185

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Figure 6; Results: Increased circulating 1,25(OH)2D levels impair mineralization by upregulating mineralization inhibitors

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Differentiated primary Vdr-intact mouse osteoblasts; conditioned-medium pyrophosphate normalized to DNA

exposure

10^-8 M calcitriol for 4 days after osteogenic differentiation.

limitations

Direct culture result does not imply that usual dietary vitamin D damages bone; physiological outcome also depends on intestinal mineral delivery.

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

Mus musculus

plain_language

In this model, active vitamin D increased a molecule that restrains mineral deposition.

primary_references

[vdm-lieben2012] Normocalcemia is maintained in mice under conditions of calcium malabsorption by vitamin D-induced inhibition of bone mineralization. (2012). https://pubmed.ncbi.nlm.nih.gov/22523068/ DOI: 10.1172/jci45890

tissue_or_cell_type

Osteoblast culture

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 809–823

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Differentiated primary Vdr-intact mouse osteoblasts; conditioned-medium pyrophosphate normalized to DNA · source_derived_draft · unverified_draft

### vdm-calcitriol-increases-extracellular-ppi Calcitriol treatment increased extracellular pyrophosphate in differentiated Vdr-intact mouse osteoblast cultures. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: In this model, active vitamin D increased a molecule that restrains mineral deposition. organism: Mus musculus tissue_or_cell_type: Osteoblast culture experimental_model: Differentiated primary Vdr-intact mouse osteoblasts; conditioned-medium pyrophosphate normalized to DNA limitations: Direct culture result does not imply that usual dietary vitamin D damages bone; physiological outcome also depends on intestinal mineral delivery. exposure: 10^-8 M calcitriol for 4 days after osteogenic differentiation. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Figure 6; Results: Increased circulating 1,25(OH)2D levels impair mineralization by upregulating mineralization inhibitors nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-lieben2012] Normocalcemia is maintained in mice under conditions of calcium malabsorption by vitamin D-induced inhibition of bone mineralization. (2012). https://pubmed.ncbi.nlm.nih.gov/22523068/ DOI: 10.1172/jci45890

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Primary abstract and Results/Discussion on calcitriol-induced claudin expression; cached web-primary-excerpts.json

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Human Caco-2 cells; RT-PCR, immunoblotting and junctional localization

exposure

Calcitriol-treated versus vehicle Caco-2 cultures; exact hormone dose/time not recovered in the primary passages used.

limitations

Cell-line expression response; the separately reused permeability experiments support function, but neither establishes a universal fraction of human dietary calcium absorption.

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

Active vitamin D can increase a tight-junction protein involved in calcium movement between intestinal cells.

primary_references

[vdm-fujita2008] Tight junction proteins claudin-2 and -12 are critical for vitamin D-dependent Ca2+ absorption between enterocytes. (2008). https://pubmed.ncbi.nlm.nih.gov/18287530/ DOI: 10.1091/mbc.e07-09-0973

tissue_or_cell_type

Intestinal epithelial cell model

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 633–647

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human Caco-2 cells; RT-PCR, immunoblotting and junctional localization · source_derived_draft · unverified_draft

### vdm-calcitriol-induces-cldn12 Calcitriol increased Claudin-12 expression in human Caco-2 intestinal epithelial cells. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Active vitamin D can increase a tight-junction protein involved in calcium movement between intestinal cells. organism: Homo sapiens tissue_or_cell_type: Intestinal epithelial cell model experimental_model: Human Caco-2 cells; RT-PCR, immunoblotting and junctional localization limitations: Cell-line expression response; the separately reused permeability experiments support function, but neither establishes a universal fraction of human dietary calcium absorption. exposure: Calcitriol-treated versus vehicle Caco-2 cultures; exact hormone dose/time not recovered in the primary passages used. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Primary abstract and Results/Discussion on calcitriol-induced claudin expression; cached web-primary-excerpts.json nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-fujita2008] Tight junction proteins claudin-2 and -12 are critical for vitamin D-dependent Ca2+ absorption between enterocytes. (2008). https://pubmed.ncbi.nlm.nih.gov/18287530/ DOI: 10.1091/mbc.e07-09-0973

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Primary abstract and Results/Discussion on calcitriol-induced claudin expression; cached web-primary-excerpts.json

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Human Caco-2 cells; RT-PCR, immunoblotting and junctional localization

exposure

Calcitriol-treated versus vehicle Caco-2 cultures; exact hormone dose/time not recovered in the primary passages used.

limitations

Cell-line expression response; the separately reused permeability experiments support function, but neither establishes a universal fraction of human dietary calcium absorption.

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

Active vitamin D can increase a tight-junction protein involved in calcium movement between intestinal cells.

primary_references

[vdm-fujita2008] Tight junction proteins claudin-2 and -12 are critical for vitamin D-dependent Ca2+ absorption between enterocytes. (2008). https://pubmed.ncbi.nlm.nih.gov/18287530/ DOI: 10.1091/mbc.e07-09-0973

tissue_or_cell_type

Intestinal epithelial cell model

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 617–631

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human Caco-2 cells; RT-PCR, immunoblotting and junctional localization · source_derived_draft · unverified_draft

### vdm-calcitriol-induces-cldn2 Calcitriol increased Claudin-2 expression in human Caco-2 intestinal epithelial cells. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Active vitamin D can increase a tight-junction protein involved in calcium movement between intestinal cells. organism: Homo sapiens tissue_or_cell_type: Intestinal epithelial cell model experimental_model: Human Caco-2 cells; RT-PCR, immunoblotting and junctional localization limitations: Cell-line expression response; the separately reused permeability experiments support function, but neither establishes a universal fraction of human dietary calcium absorption. exposure: Calcitriol-treated versus vehicle Caco-2 cultures; exact hormone dose/time not recovered in the primary passages used. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Primary abstract and Results/Discussion on calcitriol-induced claudin expression; cached web-primary-excerpts.json nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-fujita2008] Tight junction proteins claudin-2 and -12 are critical for vitamin D-dependent Ca2+ absorption between enterocytes. (2008). https://pubmed.ncbi.nlm.nih.gov/18287530/ DOI: 10.1091/mbc.e07-09-0973

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Abstract: reported experimental results

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Mouse osteoblastic cells; VDR/RXR ChIP-chip, reporter mutagenesis and transcriptional assays

exposure

Calcitriol-treated cell and reporter systems; dose and time vary by experiment and are not specified in the retrieved abstract.

limitations

Enhancer activation is distinct from a fracture outcome. The human and mouse regulatory landscapes are not asserted to be identical.

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

Mus musculus

plain_language

Active vitamin D can induce the osteoclast-development signal RANKL through distant DNA control regions.

primary_references

[vdm-meyer2006rankl] Activation of receptor activator of NF-kappaB ligand gene expression by 1,25-dihydroxyvitamin D3 is mediated through multiple long-range enhancers. (2006). https://pubmed.ncbi.nlm.nih.gov/16914732/ DOI: 10.1128/mcb.00353-06

tissue_or_cell_type

Osteoblastic cell chromatin

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 841–855

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse osteoblastic cells; VDR/RXR ChIP-chip, reporter mutagenesis and transcriptional assays · source_derived_draft · unverified_draft

### vdm-calcitriol-rankl-distal-enhancer Calcitriol activated mouse Rankl transcription through distal VDR/RXR-associated regulatory regions, including a functional element about 76 kb upstream. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Active vitamin D can induce the osteoclast-development signal RANKL through distant DNA control regions. organism: Mus musculus tissue_or_cell_type: Osteoblastic cell chromatin experimental_model: Mouse osteoblastic cells; VDR/RXR ChIP-chip, reporter mutagenesis and transcriptional assays limitations: Enhancer activation is distinct from a fracture outcome. The human and mouse regulatory landscapes are not asserted to be identical. exposure: Calcitriol-treated cell and reporter systems; dose and time vary by experiment and are not specified in the retrieved abstract. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-meyer2006rankl] Activation of receptor activator of NF-kappaB ligand gene expression by 1,25-dihydroxyvitamin D3 is mediated through multiple long-range enhancers. (2006). https://pubmed.ncbi.nlm.nih.gov/16914732/ DOI: 10.1128/mcb.00353-06

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Abstract: reported experimental results

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Vitamin-D-deficient wild-type mice; everted duodenal gut-sac calcium transport

exposure

Diet-induced vitamin D deficiency followed by calcitriol administration; exact replacement dose/time not reported in the retrieved abstract.

limitations

Wild-type arm is separated from the knockout arms; this is active-hormone replacement, not a D2/D3 oral-dose equivalence test.

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

Mus musculus

plain_language

Providing the active hormone restored part of the intestinal calcium-transport response after vitamin D deprivation.

primary_references

[vdm-benn2008] Active intestinal calcium transport in the absence of transient receptor potential vanilloid type 6 and calbindin-D9k. (2008). https://pubmed.ncbi.nlm.nih.gov/18325990/ DOI: 10.1210/en.2007-1655

tissue_or_cell_type

Duodenum

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 649–663

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Vitamin-D-deficient wild-type mice; everted duodenal gut-sac calcium transport · source_derived_draft · unverified_draft

### vdm-calcitriol-restores-transport-after-d-deficiency Calcitriol administration increased active duodenal calcium transport in vitamin-D-deficient wild-type mice in the Benn study. Condition category: nutrient_deficiency nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Providing the active hormone restored part of the intestinal calcium-transport response after vitamin D deprivation. organism: Mus musculus tissue_or_cell_type: Duodenum experimental_model: Vitamin-D-deficient wild-type mice; everted duodenal gut-sac calcium transport limitations: Wild-type arm is separated from the knockout arms; this is active-hormone replacement, not a D2/D3 oral-dose equivalence test. exposure: Diet-induced vitamin D deficiency followed by calcitriol administration; exact replacement dose/time not reported in the retrieved abstract. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-benn2008] Active intestinal calcium transport in the absence of transient receptor potential vanilloid type 6 and calbindin-D9k. (2008). https://pubmed.ncbi.nlm.nih.gov/18325990/ DOI: 10.1210/en.2007-1655

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Abstract: reported experimental results

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

Vdr-null and wild-type mice; intestinal brush-border transporter immunodetection

exposure

Vdr deletion plus dietary phosphate restriction; exact dietary percentage and duration not given in the retrieved abstract.

limitations

Baseline NaPi-IIb protein and sodium-dependent phosphate transport were lower in knockout mice; preserved adaptation does not imply normal baseline transport.

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

Mus musculus

plain_language

The intestine retained a phosphate-conservation response despite loss of vitamin D receptor signaling.

primary_references

[vdm-segawa2004] Intestinal Na-P(i) cotransporter adaptation to dietary P(i) content in vitamin D receptor null mice. (2004). https://pubmed.ncbi.nlm.nih.gov/14996670/ DOI: 10.1152/ajprenal.00375.2003

tissue_or_cell_type

Intestinal brush-border membrane

trigger_kind

machinery_impairment Imported condition classification; unverified.

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 713–727

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Vdr-null and wild-type mice; intestinal brush-border transporter immunodetection · source_derived_draft · unverified_draft

### vdm-low-phosphate-adaptation-persists-without-vdr A low-phosphate diet increased intestinal NaPi-IIb protein expression even in Vdr-null mice. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The intestine retained a phosphate-conservation response despite loss of vitamin D receptor signaling. organism: Mus musculus tissue_or_cell_type: Intestinal brush-border membrane experimental_model: Vdr-null and wild-type mice; intestinal brush-border transporter immunodetection limitations: Baseline NaPi-IIb protein and sodium-dependent phosphate transport were lower in knockout mice; preserved adaptation does not imply normal baseline transport. exposure: Vdr deletion plus dietary phosphate restriction; exact dietary percentage and duration not given in the retrieved abstract. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-segawa2004] Intestinal Na-P(i) cotransporter adaptation to dietary P(i) content in vitamin D receptor null mice. (2004). https://pubmed.ncbi.nlm.nih.gov/14996670/ DOI: 10.1152/ajprenal.00375.2003

availability_state

machinery_impairment Imported condition classification; unverified.

cross_nutrient

Vitamin D–calcium–phosphate regulation.

evidence_locator

Abstract: reported experimental results

evidence_scope

D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison.

experimental_model

VDR-ablated mice and control littermates receiving a mineral/lactose rescue diet

exposure

Combined mineral/lactose rescue diet; individual ingredient contributions and exact formulation are not resolved by the retrieved abstract.

limitations

This is a combined dietary rescue of receptor-deficient mice, not phosphate monotherapy, not a D2/D3 trial, and not evidence that VDR has no direct skeletal functions.

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

Mus musculus

plain_language

Improving mineral delivery protected the skeleton even when the vitamin D receptor was missing.

primary_references

[vdm-li1998] Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice. (1998). https://pubmed.ncbi.nlm.nih.gov/9751523/ DOI: 10.1210/endo.139.10.6262

tissue_or_cell_type

Skeleton

trigger_kind

machinery_impairment Imported condition classification; unverified.

Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 761–775

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · VDR-ablated mice and control littermates receiving a mineral/lactose rescue diet · source_derived_draft · unverified_draft

### vdm-mineral-rescue-prevents-vdr-null-skeletal-defects The combined mineral/lactose rescue diet prevented rickets and osteomalacia in VDR-ablated mice. Condition category: machinery_impairment nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: Improving mineral delivery protected the skeleton even when the vitamin D receptor was missing. organism: Mus musculus tissue_or_cell_type: Skeleton experimental_model: VDR-ablated mice and control littermates receiving a mineral/lactose rescue diet limitations: This is a combined dietary rescue of receptor-deficient mice, not phosphate monotherapy, not a D2/D3 trial, and not evidence that VDR has no direct skeletal functions. exposure: Combined mineral/lactose rescue diet; individual ingredient contributions and exact formulation are not resolved by the retrieved abstract. cross_nutrient: Vitamin D–calcium–phosphate regulation. evidence_locator: Abstract: reported experimental results nutrient: Vitamin D2 and D3 evidence_scope: D3 active metabolite or VDR machinery experiment; not a direct D2-versus-D3 comparison. [vdm-li1998] Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice. (1998). https://pubmed.ncbi.nlm.nih.gov/9751523/ DOI: 10.1210/endo.139.10.6262

experimental_model

Human intestinal cell lines; chromatin immunoprecipitation, promoter reporters and regulatory-element mutagenesis

limitations

Promoter activity and receptor occupancy do not establish an exclusive transport route or whole-body calcium flux.

nutrient_topic

Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium

organism

Homo sapiens cell lines

plain_language

Active vitamin D increases a calcium-entry channel.

primary_references

[meyer2006] The human transient receptor potential vanilloid type 6 distal promoter contains multiple vitamin D receptor binding sites that mediate activation by 1,25-dihydroxyvitamin D3 in intestinal cells (2006). https://pubmed.ncbi.nlm.nih.gov/16574738/ DOI: 10.1210/me.2006-0031

tissue_or_cell_type

Intestinal cell transcriptional regulation

Calcium: mechanism-first literature curation (2026-09-17) · lines 181–190

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human intestinal cell lines; chromatin immunoprecipitation, promoter reporters and regulatory-element mutagenesis · source_derived_draft · unverified_draft

### calcitriol-vdr-induces-trpv6 Calcitriol induces human TRPV6 transcription through VDR/RXR-associated regulatory elements in intestinal cell models. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Active vitamin D increases a calcium-entry channel. organism: Homo sapiens cell lines tissue_or_cell_type: Intestinal cell transcriptional regulation experimental_model: Human intestinal cell lines; chromatin immunoprecipitation, promoter reporters and regulatory-element mutagenesis limitations: Promoter activity and receptor occupancy do not establish an exclusive transport route or whole-body calcium flux. [meyer2006] The human transient receptor potential vanilloid type 6 distal promoter contains multiple vitamin D receptor binding sites that mediate activation by 1,25-dihydroxyvitamin D3 in intestinal cells (2006). https://pubmed.ncbi.nlm.nih.gov/16574738/ DOI: 10.1210/me.2006-0031

availability_state

biomarker_context Imported condition classification; unverified.

experimental_model

Intestinal and osteoblast Vdr deletion, low-calcium diets, and skeletal assays in growing mice

limitations

Growing-mouse genetic model; not a validated human dietary diagnostic.

nutrient_topic

Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium

organism

Mus musculus

plain_language

Normal blood calcium can coexist with inadequate skeletal supply.

primary_references

[lieben2012] Normocalcemia is maintained in mice under conditions of calcium malabsorption by vitamin D-induced inhibition of bone mineralization (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3336970/ DOI: 10.1172/JCI45890

research_relationship_category

biomarker

tissue_or_cell_type

Blood, intestine and skeleton

trigger_kind

biomarker_context Imported condition classification; unverified.

Calcium: mechanism-first literature curation (2026-09-17) · lines 337–347

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Intestinal and osteoblast Vdr deletion, low-calcium diets, and skeletal assays in growing mice · source_derived_draft · unverified_draft

### normal-serum-calcium-does-not-establish-sufficiency Mice with intestinal Vdr deletion maintained serum calcium despite calcium malabsorption and impaired skeletal mineral storage. Condition category: biomarker_context nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Normal blood calcium can coexist with inadequate skeletal supply. organism: Mus musculus tissue_or_cell_type: Blood, intestine and skeleton experimental_model: Intestinal and osteoblast Vdr deletion, low-calcium diets, and skeletal assays in growing mice limitations: Growing-mouse genetic model; not a validated human dietary diagnostic. research_relationship_category: biomarker [lieben2012] Normocalcemia is maintained in mice under conditions of calcium malabsorption by vitamin D-induced inhibition of bone mineralization (2012). https://pmc.ncbi.nlm.nih.gov/articles/PMC3336970/ DOI: 10.1172/JCI45890

availability_state

machinery_impairment Imported condition classification; unverified.

experimental_model

VDR-ablated mice and controls fed a mineral/lactose rescue diet

limitations

Combined dietary intervention; cannot attribute rescue to calcium alone.

nutrient_topic

Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium

organism

Mus musculus

plain_language

Dietary mineral delivery can bypass part of receptor failure.

primary_references

[li1998] Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice (1998). https://pubmed.ncbi.nlm.nih.gov/9751523/ DOI: 10.1210/endo.139.10.6262

reported_effect

normalizing

tissue_or_cell_type

Intestine and blood

trigger_kind

machinery_impairment Imported condition classification; unverified.

Calcium: mechanism-first literature curation (2026-09-17) · lines 146–156

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · VDR-ablated mice and controls fed a mineral/lactose rescue diet · source_derived_draft · unverified_draft

### vdr-null-mineral-diet-rescue A mineral/lactose rescue diet normalizes ionized calcium in VDR-ablated mice. Condition category: machinery_impairment nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Dietary mineral delivery can bypass part of receptor failure. organism: Mus musculus tissue_or_cell_type: Intestine and blood experimental_model: VDR-ablated mice and controls fed a mineral/lactose rescue diet limitations: Combined dietary intervention; cannot attribute rescue to calcium alone. reported_effect: normalizing [li1998] Normalization of mineral ion homeostasis by dietary means prevents hyperparathyroidism, rickets, and osteomalacia, but not alopecia in vitamin D receptor-ablated mice (1998). https://pubmed.ncbi.nlm.nih.gov/9751523/ DOI: 10.1210/endo.139.10.6262