Component

Mouse Wnt family member 10B / Wnt10b

Context-specific entity; species, compartment and exposure are stated on each claim.

5 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. Reconstituting TCR-beta-deficient mice with Wnt10b-deficient CD8 T cells prevented butyrate-induced bone formation and mass acquisition; lowering Treg numbers also prevented the response.

    Mouse Wnt family member 10B / Wnt10b → Mouse bone formation after butyrate source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse cellular reconstitution and Treg reduction.
    limitations
    A genetic dependency is not evidence that a person needs more dietary calcium.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Butyrate could not replace the missing immune-cell signal.
    primary_references
    The Microbial Metabolite Butyrate Stimulates Bone Formation via T Regulatory Cell-Mediated Regulation of WNT10B Expression. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30446387/ · DOI 10.1016/j.immuni.2018.10.013
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 470–476

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse cellular reconstitution and Treg reduction. · source_derived_draft · unverified_draft

    ## butyrate-bone-wnt-loss Butyrate could not replace the missing immune-cell signal. Reconstituting TCR-beta-deficient mice with Wnt10b-deficient CD8 T cells prevented butyrate-induced bone formation and mass acquisition; lowering Treg numbers also prevented the response. Model: Mouse cellular reconstitution and Treg reduction. Limitations: A genetic dependency is not evidence that a person needs more dietary calcium. Evidence access: Primary abstract The Microbial Metabolite Butyrate Stimulates Bone Formation via T Regulatory Cell-Mediated Regulation of WNT10B Expression. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30446387/ · DOI 10.1016/j.immuni.2018.10.013
    Complete structured claim and evidence

What acts on it

  1. Tregs promoted NFAT1-SMAD3 complex assembly in mouse CD8 cells, driving Wnt10b expression in the butyrate-associated bone pathway.

    Mouse NFAT1 / Nfatc2 → Mouse Wnt family member 10B / Wnt10b source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse CD8/Treg mechanistic experiments.
    limitations
    NFAT1 is Nfatc2, not the osteoclast NFATc1 protein.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Two transcription factors linked the immune relay to a bone-building ligand.
    primary_references
    The Microbial Metabolite Butyrate Stimulates Bone Formation via T Regulatory Cell-Mediated Regulation of WNT10B Expression. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30446387/ · DOI 10.1016/j.immuni.2018.10.013

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 462–468

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse CD8/Treg mechanistic experiments. · source_derived_draft · unverified_draft

    ## butyrate-wnt-transcription-complex Two transcription factors linked the immune relay to a bone-building ligand. Tregs promoted NFAT1-SMAD3 complex assembly in mouse CD8 cells, driving Wnt10b expression in the butyrate-associated bone pathway. Model: Mouse CD8/Treg mechanistic experiments. Limitations: NFAT1 is Nfatc2, not the osteoclast NFATc1 protein. Evidence access: Primary abstract The Microbial Metabolite Butyrate Stimulates Bone Formation via T Regulatory Cell-Mediated Regulation of WNT10B Expression. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30446387/ · DOI 10.1016/j.immuni.2018.10.013
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Butyrate expanded gut and bone-marrow Tregs; their interaction with CD8 T cells increased Wnt10b production and bone formation in young mice.

    Butyrate → Mouse bone formation after butyrate source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Young eugonadic mice; butyrate and separate probiotic interventions.
    limitations
    No human fracture-prevention result; mineral substrate requirements were not tested.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    An immune-cell relay connected a gut metabolite to bone-building signals.
    primary_references
    The Microbial Metabolite Butyrate Stimulates Bone Formation via T Regulatory Cell-Mediated Regulation of WNT10B Expression. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30446387/ · DOI 10.1016/j.immuni.2018.10.013

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 454–460

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Young eugonadic mice; butyrate and separate probiotic interventions. · source_derived_draft · unverified_draft

    ## butyrate-bone-treg-wnt An immune-cell relay connected a gut metabolite to bone-building signals. Butyrate expanded gut and bone-marrow Tregs; their interaction with CD8 T cells increased Wnt10b production and bone formation in young mice. Model: Young eugonadic mice; butyrate and separate probiotic interventions. Limitations: No human fracture-prevention result; mineral substrate requirements were not tested. Evidence access: Primary abstract The Microbial Metabolite Butyrate Stimulates Bone Formation via T Regulatory Cell-Mediated Regulation of WNT10B Expression. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30446387/ · DOI 10.1016/j.immuni.2018.10.013
    Complete structured claim and evidence

  2. The permissive butyrate response involved GPR43 signaling in dendritic cells and GPR43-independent effects in T cells in the PTH study.

    Mouse free fatty acid receptor 2 / Ffar2 → Mouse bone-anabolic response to intermittent PTH source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse cell-specific receptor and PTH experiments.
    limitations
    Do not assign every T-cell butyrate response to FFAR2.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    The same pathway used different signaling routes in different immune cells.
    primary_references
    Parathyroid hormone-dependent bone formation requires butyrate production by intestinal microbiota. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31917685/ · DOI 10.1172/JCI133473

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 494–500

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse cell-specific receptor and PTH experiments. · source_derived_draft · unverified_draft

    ## butyrate-pth-ffar2 The same pathway used different signaling routes in different immune cells. The permissive butyrate response involved GPR43 signaling in dendritic cells and GPR43-independent effects in T cells in the PTH study. Model: Mouse cell-specific receptor and PTH experiments. Limitations: Do not assign every T-cell butyrate response to FFAR2. Evidence access: Primary abstract Parathyroid hormone-dependent bone formation requires butyrate production by intestinal microbiota. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31917685/ · DOI 10.1172/JCI133473
    Complete structured claim and evidence

  3. Antibiotic-depleted or germ-free female mice lost the bone-anabolic response to intermittent PTH; restoring physiological butyrate levels restored the response.

    Butyrate → Mouse bone-anabolic response to intermittent PTH source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    evidence_access
    Primary abstract and full-text intervention methods
    experimental_model
    Female mice; microbial depletion, daily subcutaneous human PTH(1-34) at 80 micrograms/kg for four weeks; 5 mM butyrate repletion in drinking water.
    limitations
    Not proof that human PTH treatment failure is usually butyrate deficiency, or that butyrate replaces PTH, calcium or vitamin D.
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    In this mouse model, the hormone response depended on a microbial metabolite.
    primary_references
    Parathyroid hormone-dependent bone formation requires butyrate production by intestinal microbiota. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31917685/ · DOI 10.1172/JCI133473
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 486–492

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Female mice; microbial depletion, daily subcutaneous human PTH(1-34) at 80 micrograms/kg for four weeks; 5 mM butyrate repletion in drinking water. · source_derived_draft · unverified_draft

    ## butyrate-pth-microbial-depletion In this mouse model, the hormone response depended on a microbial metabolite. Antibiotic-depleted or germ-free female mice lost the bone-anabolic response to intermittent PTH; restoring physiological butyrate levels restored the response. Model: Female mice; microbial depletion, daily subcutaneous human PTH(1-34) at 80 micrograms/kg for four weeks; 5 mM butyrate repletion in drinking water. Limitations: Not proof that human PTH treatment failure is usually butyrate deficiency, or that butyrate replaces PTH, calcium or vitamin D. Evidence access: Primary abstract and full-text intervention methods Parathyroid hormone-dependent bone formation requires butyrate production by intestinal microbiota. · 2020 · https://pubmed.ncbi.nlm.nih.gov/31917685/ · DOI 10.1172/JCI133473
    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