Component

Fibroblast growth factor 23 / FGF23

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

14 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. Recombinant FGF23 reduced renal NaPi-IIa mRNA and protein abundance in the acute rodent injection study.

    Fibroblast growth factor 23 / FGF23 → Sodium-phosphate cotransporter NaPi-IIa / SLC34A1 source_derived_draftungraded
    Experimental context and source evidence
    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
    Single recombinant FGF23 injection in rodents; renal transcript/protein and serum phosphate measurements
    exposure
    Single recombinant FGF23 injection; serum phosphate reduction was first observed at 9 hours; dose not recovered in the primary abstract.
    limitations
    Transporter abundance is not itself a flux measurement. Lack of a PTH rise and parathyroidectomized-rat responses support a PTH-independent action in this experiment.
    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; Rattus norvegicus
    plain_language
    FGF23 reduced a kidney transporter that normally helps retain phosphate.
    primary_references
    [vdm-shimada2004] 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

    Vitamin D2 and D3: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 745–759

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Single recombinant FGF23 injection in rodents; renal transcript/protein and serum phosphate measurements · source_derived_draft · unverified_draft

    ### vdm-fgf23-reduces-renal-napi2a Recombinant FGF23 reduced renal NaPi-IIa mRNA and protein abundance in the acute rodent injection study. Condition category: normal nutrient_topic: Vitamin D2 and D3 research collection; topical membership is not evidence of a direct dietary effect. plain_language: FGF23 reduced a kidney transporter that normally helps retain phosphate. organism: Mus musculus; Rattus norvegicus tissue_or_cell_type: Kidney experimental_model: Single recombinant FGF23 injection in rodents; renal transcript/protein and serum phosphate measurements limitations: Transporter abundance is not itself a flux measurement. Lack of a PTH rise and parathyroidectomized-rat responses support a PTH-independent action in this experiment. exposure: Single recombinant FGF23 injection; serum phosphate reduction was first observed at 9 hours; dose not recovered in the primary 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-shimada2004] 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

  2. 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

  3. FGF23 increases renal distal-tubular TRPV5 membrane abundance through FGFR/alpha-Klotho signaling involving ERK1/2, SGK1 and WNK4.

    Fibroblast growth factor 23 / FGF23 → TRPV5 source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Mouse Fgf23/Klotho/Vdr genetic models, recombinant FGF23, isolated tubules and kidney slices
    limitations
    Mouse genetic/pharmacological models; no claim of equivalent human effect magnitude.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mus musculus
    plain_language
    FGF23 can help kidneys retain calcium.
    primary_references
    [andrukhova2014] FGF23 promotes renal calcium reabsorption through the TRPV5 channel (2014). https://pmc.ncbi.nlm.nih.gov/articles/PMC3983685/ DOI: 10.1002/embj.201284188
    tissue_or_cell_type
    Renal distal tubules

    Calcium: mechanism-first literature curation (2026-09-17) · lines 124–133

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse Fgf23/Klotho/Vdr genetic models, recombinant FGF23, isolated tubules and kidney slices · source_derived_draft · unverified_draft

    ### fgf23-increases-trpv5-membrane-abundance FGF23 increases renal distal-tubular TRPV5 membrane abundance through FGFR/alpha-Klotho signaling involving ERK1/2, SGK1 and WNK4. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: FGF23 can help kidneys retain calcium. organism: Mus musculus tissue_or_cell_type: Renal distal tubules experimental_model: Mouse Fgf23/Klotho/Vdr genetic models, recombinant FGF23, isolated tubules and kidney slices limitations: Mouse genetic/pharmacological models; no claim of equivalent human effect magnitude. [andrukhova2014] FGF23 promotes renal calcium reabsorption through the TRPV5 channel (2014). https://pmc.ncbi.nlm.nih.gov/articles/PMC3983685/ DOI: 10.1002/embj.201284188
    Complete structured claim and evidence

  4. Recombinant FGF23 lowers renal CYP27B1 mRNA before the fall in serum phosphate.

    Fibroblast growth factor 23 / FGF23 → Vitamin D 1-alpha-hydroxylase / CYP27B1 source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Recombinant FGF23 injections in normal and parathyroidectomized rodents
    limitations
    Injection study; transcript change is not direct enzyme inhibition.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mus musculus; Rattus norvegicus
    plain_language
    FGF23 restrains a vitamin D activation enzyme.
    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 91–100

    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-reduces-cyp27b1-expression Recombinant FGF23 lowers renal CYP27B1 mRNA before the fall in serum phosphate. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: FGF23 restrains a vitamin D activation enzyme. organism: Mus musculus; Rattus norvegicus tissue_or_cell_type: Kidney experimental_model: Recombinant FGF23 injections in normal and parathyroidectomized rodents limitations: Injection study; transcript change is not direct enzyme inhibition. [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

What acts on it

  1. Burosumab binds and inhibits FGF23, the phosphate-wasting hormone targeted in the XLH trial.

    Burosumab anti-FGF23 antibody → Fibroblast growth factor 23 / FGF23 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/29947083.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1b305f00a7b9a569ccd197728d942ebbf55f9eaa164a95086d69a34608d3c4e", "start_char": 0, "end_char": 2327, "text_sha256": "c1b305f00a7b9a569ccd197728d942ebbf55f9eaa164a95086d69a34608d3c4e"}
    experimental_model
    Randomized double-blind placebo-controlled phase 3 trial
    exposure
    Burosumab 1 mg/kg or placebo every four weeks; week-24 analysis
    limitations
    FGF23-mediated inherited disease, not simple nutritional deficiency. Pain and function outcomes require multiplicity-adjusted interpretation.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Human
    plain_language
    The treatment targets the hormone driving phosphate loss, rather than only adding phosphate.
    primary_references
    [phosphorus-p29947083] A Randomized, Double-Blind, Placebo-Controlled, Phase 3 Trial Evaluating the Efficacy of Burosumab, an Anti-FGF23 Antibody, in Adults With X-Linked Hypophosphatemia: Week 24 Primary Analysis. (2018). https://pubmed.ncbi.nlm.nih.gov/29947083/ DOI: 10.1002/jbmr.3475
    tissue_or_cell_type
    134 symptomatic adults with X-linked hypophosphatemia

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 1180–1191

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled phase 3 trial · source_derived_draft · unverified_draft

    ### phosphorus-burosumab-target Burosumab binds and inhibits FGF23, the phosphate-wasting hormone targeted in the XLH trial. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: The treatment targets the hormone driving phosphate loss, rather than only adding phosphate. organism: Human tissue_or_cell_type: 134 symptomatic adults with X-linked hypophosphatemia experimental_model: Randomized double-blind placebo-controlled phase 3 trial limitations: FGF23-mediated inherited disease, not simple nutritional deficiency. Pain and function outcomes require multiplicity-adjusted interpretation. exposure: Burosumab 1 mg/kg or placebo every four weeks; week-24 analysis evidence_span: {"source_cache": "artifacts/phosphorus-research/29947083.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1b305f00a7b9a569ccd197728d942ebbf55f9eaa164a95086d69a34608d3c4e", "start_char": 0, "end_char": 2327, "text_sha256": "c1b305f00a7b9a569ccd197728d942ebbf55f9eaa164a95086d69a34608d3c4e"} [phosphorus-p29947083] A Randomized, Double-Blind, Placebo-Controlled, Phase 3 Trial Evaluating the Efficacy of Burosumab, an Anti-FGF23 Antibody, in Adults With X-Linked Hypophosphatemia: Week 24 Primary Analysis. (2018). https://pubmed.ncbi.nlm.nih.gov/29947083/ DOI: 10.1002/jbmr.3475
    Complete structured claim and evidence

  2. The vegetarian diet produced lower FGF23 than the meat diet after one week.

    Vegetarian diet in the 2011 CKD crossover trial → Fibroblast growth factor 23 / FGF23 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/21183586.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1361f250bd0c2febcef675ba888387b4f2ea0b81b171150734d8f148982a660", "start_char": 0, "end_char": 1667, "text_sha256": "c1361f250bd0c2febcef675ba888387b4f2ea0b81b171150734d8f148982a660"}
    experimental_model
    Randomized-order crossover feeding trial
    exposure
    Seven-day vegetarian and meat diets with equivalent nutrients prepared by research staff
    limitations
    Small short-term CKD study; food source/form matters, but the trial does not isolate one phytate mechanism or establish that all plant phosphate is unabsorbed.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Human
    plain_language
    The hormone response also depended on the food source.
    primary_references
    [phosphorus-p21183586] Vegetarian compared with meat dietary protein source and phosphorus homeostasis in chronic kidney disease. (2011). https://pubmed.ncbi.nlm.nih.gov/21183586/ DOI: 10.2215/cjn.05040610
    tissue_or_cell_type
    Nine people with CKD; mean eGFR 32 mL/min

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 998–1009

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized-order crossover feeding trial · source_derived_draft · unverified_draft

    ### phosphorus-plant-diet-fgf23 The vegetarian diet produced lower FGF23 than the meat diet after one week. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: The hormone response also depended on the food source. organism: Human tissue_or_cell_type: Nine people with CKD; mean eGFR 32 mL/min experimental_model: Randomized-order crossover feeding trial limitations: Small short-term CKD study; food source/form matters, but the trial does not isolate one phytate mechanism or establish that all plant phosphate is unabsorbed. exposure: Seven-day vegetarian and meat diets with equivalent nutrients prepared by research staff evidence_span: {"source_cache": "artifacts/phosphorus-research/21183586.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1361f250bd0c2febcef675ba888387b4f2ea0b81b171150734d8f148982a660", "start_char": 0, "end_char": 1667, "text_sha256": "c1361f250bd0c2febcef675ba888387b4f2ea0b81b171150734d8f148982a660"} [phosphorus-p21183586] Vegetarian compared with meat dietary protein source and phosphorus homeostasis in chronic kidney disease. (2011). https://pubmed.ncbi.nlm.nih.gov/21183586/ DOI: 10.2215/cjn.05040610
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. The HHRH phenotype included elevated circulating 1,25-dihydroxyvitamin D with normal or low-normal FGF23.

    Sodium-phosphate cotransporter NaPi-IIc / SLC34A3 → Circulating calcitriol concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"}
    experimental_model
    Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria
    exposure
    SLC34A3 disease-associated mutations in five families
    limitations
    Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention.
    nutrient_topic
    Sodium research collection; topical membership is not evidence of a direct dietary effect. · Sodium
    organism
    Human
    plain_language
    A phosphate-handling defect can change the vitamin D environment.
    primary_references
    [sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410
    tissue_or_cell_type
    Renal proximal tubule and systemic mineral phenotype
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Sodium: gradients, nutrient transport, fluid regulation and loss states (2026-09-17) · lines 681–692

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria · source_derived_draft · unverified_draft

    ### sodium-napi2c-calcitriol The HHRH phenotype included elevated circulating 1,25-dihydroxyvitamin D with normal or low-normal FGF23. Condition category: machinery_impairment nutrient_topic: Sodium research collection; topical membership is not evidence of a direct dietary effect. plain_language: A phosphate-handling defect can change the vitamin D environment. organism: Human tissue_or_cell_type: Renal proximal tubule and systemic mineral phenotype experimental_model: Mapping and sequencing in families with hereditary hypophosphatemic rickets with hypercalciuria limitations: Genotype–phenotype evidence supports a primary renal defect; downstream calcitriol/calcium pattern is observed, not a dietary sodium intervention. exposure: SLC34A3 disease-associated mutations in five families evidence_span: {"source_cache": "artifacts/sodium-research/16358215.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb", "start_char": 0, "end_char": 1515, "text_sha256": "876374dd0624cf69b89f3f5b17e5be423d7d9a0358f135add88f2493314d2ceb"} [sodium-p16358215] Hereditary hypophosphatemic rickets with hypercalciuria is caused by mutations in the sodium-phosphate cotransporter gene SLC34A3. (2006). https://pubmed.ncbi.nlm.nih.gov/16358215/ DOI: 10.1086/499410
    Complete structured claim and evidence

  2. Calcitriol administration produced about a fourfold increase in bone Fgf23 transcripts in the Liu mouse study.

    Calcitriol → FGF23 mRNA source_derived_draftungraded
    Experimental context and source evidence
    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
    Complete structured claim and evidence

  3. Alpha-Klotho cooperates with FGFR1(IIIc) to confer high-affinity binding and signaling by FGF23.

    Alpha-Klotho / KL → Fibroblast growth factor receptor 1 / FGFR1 source_derived_draftungraded
    Experimental context and source evidence
    experimental_model
    Renal homogenates, receptor-reconstitution cell assays and anti-Klotho antibody in mice
    limitations
    Specifically FGFR1(IIIc) reconstitution; not all FGFR1 splice forms are equivalent.
    nutrient_topic
    Calcium research collection; topical membership is not evidence of a direct dietary effect. · Calcium
    organism
    Mammalian cell systems; Mus musculus
    plain_language
    FGF23 needs a suitable receptor partnership.
    primary_references
    [urakawa2006] Klotho converts canonical FGF receptor into a specific receptor for FGF23 (2006). https://pubmed.ncbi.nlm.nih.gov/17086194/ DOI: 10.1038/nature05315
    tissue_or_cell_type
    Kidney receptor system

    Calcium: mechanism-first literature curation (2026-09-17) · lines 113–122

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Renal homogenates, receptor-reconstitution cell assays and anti-Klotho antibody in mice · source_derived_draft · unverified_draft

    ### klotho-fgfr1-fgf23-receptor Alpha-Klotho cooperates with FGFR1(IIIc) to confer high-affinity binding and signaling by FGF23. Condition category: normal nutrient_topic: Calcium research collection; topical membership is not evidence of a direct dietary effect. plain_language: FGF23 needs a suitable receptor partnership. organism: Mammalian cell systems; Mus musculus tissue_or_cell_type: Kidney receptor system experimental_model: Renal homogenates, receptor-reconstitution cell assays and anti-Klotho antibody in mice limitations: Specifically FGFR1(IIIc) reconstitution; not all FGFR1 splice forms are equivalent. [urakawa2006] Klotho converts canonical FGF receptor into a specific receptor for FGF23 (2006). https://pubmed.ncbi.nlm.nih.gov/17086194/ DOI: 10.1038/nature05315
    Complete structured claim and evidence

  4. Ferric carboxymaltose increased biologically active FGF23 in the substudy; the mean within-person increase at the week-two peak was approximately 303%, versus 10% with ferumoxytol.

    Ferric carboxymaltose → Circulating biologically active intact FGF23 source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/iron-research/30518682.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "489945718bb05c0630fd563dc5a6da0874e80685717ab06ceedfefc38d172257", "start_char": 0, "end_char": 2371, "text_sha256": "489945718bb05c0630fd563dc5a6da0874e80685717ab06ceedfefc38d172257"}
    experimental_model
    Double-blind randomized comparison with physiological substudy
    exposure
    One treatment course of ferric carboxymaltose versus ferumoxytol; five-week follow-up
    limitations
    Formulation-specific pharmacological effect, not dietary iron or all intravenous iron. Trial funded by ferumoxytol manufacturer; mineral associations support but do not individually prove every causal arrow.
    nutrient_topic
    Iron research collection; topical membership is not evidence of a direct dietary effect. · Iron
    organism
    1997 adults with iron-deficiency anemia; 185 in substudy
    plain_language
    The treatment changed a hormone that controls phosphate handling.
    primary_references
    [iron-p30518682] Randomized trial of intravenous iron-induced hypophosphatemia. (2018). https://pubmed.ncbi.nlm.nih.gov/30518682/ DOI: 10.1172/jci.insight.124486
    tissue_or_cell_type
    Blood and renal phosphate handling
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Iron: absorption, trafficking, iron-dependent enzymes and nutrient interactions (2026-09-17) · lines 953–964

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Double-blind randomized comparison with physiological substudy · source_derived_draft · unverified_draft

    ### iron-fcm-intact-fgf23 Ferric carboxymaltose increased biologically active FGF23 in the substudy; the mean within-person increase at the week-two peak was approximately 303%, versus 10% with ferumoxytol. Condition category: nutrient_deficiency nutrient_topic: Iron research collection; topical membership is not evidence of a direct dietary effect. plain_language: The treatment changed a hormone that controls phosphate handling. organism: 1997 adults with iron-deficiency anemia; 185 in substudy tissue_or_cell_type: Blood and renal phosphate handling experimental_model: Double-blind randomized comparison with physiological substudy limitations: Formulation-specific pharmacological effect, not dietary iron or all intravenous iron. Trial funded by ferumoxytol manufacturer; mineral associations support but do not individually prove every causal arrow. exposure: One treatment course of ferric carboxymaltose versus ferumoxytol; five-week follow-up evidence_span: {"source_cache": "artifacts/iron-research/30518682.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "489945718bb05c0630fd563dc5a6da0874e80685717ab06ceedfefc38d172257", "start_char": 0, "end_char": 2371, "text_sha256": "489945718bb05c0630fd563dc5a6da0874e80685717ab06ceedfefc38d172257"} [iron-p30518682] Randomized trial of intravenous iron-induced hypophosphatemia. (2018). https://pubmed.ncbi.nlm.nih.gov/30518682/ DOI: 10.1172/jci.insight.124486
    Complete structured claim and evidence

  5. Across dosing-interval midpoints, 94.1% on burosumab versus 7.6% on placebo attained mean serum phosphate above the lower limit of normal.

    Burosumab anti-FGF23 antibody → Serum inorganic phosphate concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/29947083.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1b305f00a7b9a569ccd197728d942ebbf55f9eaa164a95086d69a34608d3c4e", "start_char": 0, "end_char": 2327, "text_sha256": "c1b305f00a7b9a569ccd197728d942ebbf55f9eaa164a95086d69a34608d3c4e"}
    experimental_model
    Randomized double-blind placebo-controlled phase 3 trial
    exposure
    Burosumab 1 mg/kg or placebo every four weeks; week-24 analysis
    limitations
    FGF23-mediated inherited disease, not simple nutritional deficiency. Pain and function outcomes require multiplicity-adjusted interpretation.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Human
    plain_language
    Blocking the wasting signal substantially improved the phosphate measurement.
    primary_references
    [phosphorus-p29947083] A Randomized, Double-Blind, Placebo-Controlled, Phase 3 Trial Evaluating the Efficacy of Burosumab, an Anti-FGF23 Antibody, in Adults With X-Linked Hypophosphatemia: Week 24 Primary Analysis. (2018). https://pubmed.ncbi.nlm.nih.gov/29947083/ DOI: 10.1002/jbmr.3475
    tissue_or_cell_type
    134 symptomatic adults with X-linked hypophosphatemia
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 1193–1204

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Randomized double-blind placebo-controlled phase 3 trial · source_derived_draft · unverified_draft

    ### phosphorus-burosumab-phosphate Across dosing-interval midpoints, 94.1% on burosumab versus 7.6% on placebo attained mean serum phosphate above the lower limit of normal. Condition category: machinery_impairment nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking the wasting signal substantially improved the phosphate measurement. organism: Human tissue_or_cell_type: 134 symptomatic adults with X-linked hypophosphatemia experimental_model: Randomized double-blind placebo-controlled phase 3 trial limitations: FGF23-mediated inherited disease, not simple nutritional deficiency. Pain and function outcomes require multiplicity-adjusted interpretation. exposure: Burosumab 1 mg/kg or placebo every four weeks; week-24 analysis evidence_span: {"source_cache": "artifacts/phosphorus-research/29947083.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "c1b305f00a7b9a569ccd197728d942ebbf55f9eaa164a95086d69a34608d3c4e", "start_char": 0, "end_char": 2327, "text_sha256": "c1b305f00a7b9a569ccd197728d942ebbf55f9eaa164a95086d69a34608d3c4e"} [phosphorus-p29947083] A Randomized, Double-Blind, Placebo-Controlled, Phase 3 Trial Evaluating the Efficacy of Burosumab, an Anti-FGF23 Antibody, in Adults With X-Linked Hypophosphatemia: Week 24 Primary Analysis. (2018). https://pubmed.ncbi.nlm.nih.gov/29947083/ DOI: 10.1002/jbmr.3475
    Complete structured claim and evidence

  6. Diet-related FGF23 changes correlated inversely with maximal tubular phosphate reabsorption and calcitriol, and positively with urinary phosphate excretion.

    Phosphorus → Renal phosphate reabsorption source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/15613425.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4a8c4110b9c57e9f8f54305eb77abb80dd90253fc99e2f5aa21a4a3f129983c2", "start_char": 0, "end_char": 1563, "text_sha256": "4a8c4110b9c57e9f8f54305eb77abb80dd90253fc99e2f5aa21a4a3f129983c2"}
    experimental_model
    Controlled sequential dietary intervention
    exposure
    Five-day low-phosphate diet plus binder, then phosphate loading; calcium adjusted to minimize PTH changes
    limitations
    Phosphate intake and calcium/binder cointerventions are explicit; correlation of hormones with renal handling does not independently prove each mediator.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Human
    plain_language
    The hormone, kidney and vitamin D responses moved together during the intervention.
    primary_references
    [phosphorus-p15613425] Fibroblast growth factor-23 relationship to dietary phosphate and renal phosphate handling in healthy young men. (2005). https://pubmed.ncbi.nlm.nih.gov/15613425/ DOI: 10.1210/jc.2004-1039
    tissue_or_cell_type
    29 healthy young men; serum hormones and renal handling

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 920–931

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Controlled sequential dietary intervention · source_derived_draft · unverified_draft

    ### phosphorus-diet-renal-feedback Diet-related FGF23 changes correlated inversely with maximal tubular phosphate reabsorption and calcitriol, and positively with urinary phosphate excretion. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: The hormone, kidney and vitamin D responses moved together during the intervention. organism: Human tissue_or_cell_type: 29 healthy young men; serum hormones and renal handling experimental_model: Controlled sequential dietary intervention limitations: Phosphate intake and calcium/binder cointerventions are explicit; correlation of hormones with renal handling does not independently prove each mediator. exposure: Five-day low-phosphate diet plus binder, then phosphate loading; calcium adjusted to minimize PTH changes evidence_span: {"source_cache": "artifacts/phosphorus-research/15613425.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "4a8c4110b9c57e9f8f54305eb77abb80dd90253fc99e2f5aa21a4a3f129983c2", "start_char": 0, "end_char": 1563, "text_sha256": "4a8c4110b9c57e9f8f54305eb77abb80dd90253fc99e2f5aa21a4a3f129983c2"} [phosphorus-p15613425] Fibroblast growth factor-23 relationship to dietary phosphate and renal phosphate handling in healthy young men. (2005). https://pubmed.ncbi.nlm.nih.gov/15613425/ DOI: 10.1210/jc.2004-1039
    Complete structured claim and evidence

  7. FAM20C-dependent FGF23 phosphorylation promoted furin cleavage and hormone inactivation.

    FGF23 phosphorylated at Ser180 → Proteolytically cleaved FGF23 products source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/24706917.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7ccd1d1a23c74c980009e67ac6b0feafa3c30c28a99d8b240bef93bcc4cf29be", "start_char": 0, "end_char": 1346, "text_sha256": "7ccd1d1a23c74c980009e67ac6b0feafa3c30c28a99d8b240bef93bcc4cf29be"}
    experimental_model
    Recombinant processing and phosphorylation/glycosylation experiments
    exposure
    FAM20C, GalNAc-T3 and furin manipulation
    limitations
    Protein-modification control, not a claim that dietary phosphate directly phosphorylates FGF23. Construct scope is retained rather than assigning every result to intact human physiology.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Construct system; precise species not inferred from abstract
    plain_language
    Changing the hormone’s processing reduced the amount of intact active signal.
    primary_references
    [phosphorus-p24706917] Dynamic regulation of FGF23 by Fam20C phosphorylation, GalNAc-T3 glycosylation, and furin proteolysis. (2014). https://pubmed.ncbi.nlm.nih.gov/24706917/ DOI: 10.1073/pnas.1402218111
    tissue_or_cell_type
    Secretory protein processing

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 516–527

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant processing and phosphorylation/glycosylation experiments · source_derived_draft · unverified_draft

    ### phosphorus-fgf23-cleavage FAM20C-dependent FGF23 phosphorylation promoted furin cleavage and hormone inactivation. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: Changing the hormone’s processing reduced the amount of intact active signal. organism: Construct system; precise species not inferred from abstract tissue_or_cell_type: Secretory protein processing experimental_model: Recombinant processing and phosphorylation/glycosylation experiments limitations: Protein-modification control, not a claim that dietary phosphate directly phosphorylates FGF23. Construct scope is retained rather than assigning every result to intact human physiology. exposure: FAM20C, GalNAc-T3 and furin manipulation evidence_span: {"source_cache": "artifacts/phosphorus-research/24706917.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7ccd1d1a23c74c980009e67ac6b0feafa3c30c28a99d8b240bef93bcc4cf29be", "start_char": 0, "end_char": 1346, "text_sha256": "7ccd1d1a23c74c980009e67ac6b0feafa3c30c28a99d8b240bef93bcc4cf29be"} [phosphorus-p24706917] Dynamic regulation of FGF23 by Fam20C phosphorylation, GalNAc-T3 glycosylation, and furin proteolysis. (2014). https://pubmed.ncbi.nlm.nih.gov/24706917/ DOI: 10.1073/pnas.1402218111
    Complete structured claim and evidence

  8. FAM20C directly phosphorylated FGF23 at Ser180 within its proteolytic processing motif.

    FAM20C secretory-pathway kinase → FGF23 phosphorylated at Ser180 source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/phosphorus-research/24706917.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7ccd1d1a23c74c980009e67ac6b0feafa3c30c28a99d8b240bef93bcc4cf29be", "start_char": 0, "end_char": 1346, "text_sha256": "7ccd1d1a23c74c980009e67ac6b0feafa3c30c28a99d8b240bef93bcc4cf29be"}
    experimental_model
    Recombinant processing and phosphorylation/glycosylation experiments
    exposure
    FAM20C, GalNAc-T3 and furin manipulation
    limitations
    Protein-modification control, not a claim that dietary phosphate directly phosphorylates FGF23. Construct scope is retained rather than assigning every result to intact human physiology.
    nutrient_topic
    Phosphorus research collection; topical membership is not evidence of a direct dietary effect. · Phosphorus
    organism
    Construct system; precise species not inferred from abstract
    plain_language
    A phosphate mark controls how this phosphate-regulating hormone is processed.
    primary_references
    [phosphorus-p24706917] Dynamic regulation of FGF23 by Fam20C phosphorylation, GalNAc-T3 glycosylation, and furin proteolysis. (2014). https://pubmed.ncbi.nlm.nih.gov/24706917/ DOI: 10.1073/pnas.1402218111
    tissue_or_cell_type
    Secretory protein processing

    Phosphorus: metabolism, signaling and nutrient connections (2026-09-17) · lines 490–501

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant processing and phosphorylation/glycosylation experiments · source_derived_draft · unverified_draft

    ### phosphorus-fgf23-phosphorylation FAM20C directly phosphorylated FGF23 at Ser180 within its proteolytic processing motif. Condition category: normal nutrient_topic: Phosphorus research collection; topical membership is not evidence of a direct dietary effect. plain_language: A phosphate mark controls how this phosphate-regulating hormone is processed. organism: Construct system; precise species not inferred from abstract tissue_or_cell_type: Secretory protein processing experimental_model: Recombinant processing and phosphorylation/glycosylation experiments limitations: Protein-modification control, not a claim that dietary phosphate directly phosphorylates FGF23. Construct scope is retained rather than assigning every result to intact human physiology. exposure: FAM20C, GalNAc-T3 and furin manipulation evidence_span: {"source_cache": "artifacts/phosphorus-research/24706917.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "7ccd1d1a23c74c980009e67ac6b0feafa3c30c28a99d8b240bef93bcc4cf29be", "start_char": 0, "end_char": 1346, "text_sha256": "7ccd1d1a23c74c980009e67ac6b0feafa3c30c28a99d8b240bef93bcc4cf29be"} [phosphorus-p24706917] Dynamic regulation of FGF23 by Fam20C phosphorylation, GalNAc-T3 glycosylation, and furin proteolysis. (2014). https://pubmed.ncbi.nlm.nih.gov/24706917/ DOI: 10.1073/pnas.1402218111
    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