Component

Mouse colonic stem/progenitor-cell proliferation

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

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What acts on it

  1. Direct butyrate exposure suppressed mouse colonic stem/progenitor-cell proliferation; mature colonocytes normally consumed butyrate and limited its access to the crypt base.

    Butyrate → Mouse colonic stem/progenitor-cell proliferation source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Mouse stem-cell culture, crypt architecture and injury experiments.
    limitations
    Anatomical access matters; this does not mean butyrate uniformly damages the intact colon. Correction record: A published erratum is confirmed by PubMed and publisher/Crossref metadata: Cell 167(4):1137, 2016. The notice body was not available through the accessed publisher endpoints. The main article's Acads/Foxo3 and crypt experiments were read, but the specific effect of the correction remains unassessed. https://pubmed.ncbi.nlm.nih.gov/27814510/
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    The normal tissue layout protected dividing cells from excessive local exposure.
    primary_references
    The Colonic Crypt Protects Stem Cells from Microbiota-Derived Metabolites. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27264604/ · DOI 10.1016/j.cell.2016.05.018

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 310–316

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse stem-cell culture, crypt architecture and injury experiments. · source_derived_draft · unverified_draft

    ## butyrate-crypt-exposure The normal tissue layout protected dividing cells from excessive local exposure. Direct butyrate exposure suppressed mouse colonic stem/progenitor-cell proliferation; mature colonocytes normally consumed butyrate and limited its access to the crypt base. Model: Mouse stem-cell culture, crypt architecture and injury experiments. Limitations: Anatomical access matters; this does not mean butyrate uniformly damages the intact colon. Correction record: A published erratum is confirmed by PubMed and publisher/Crossref metadata: Cell 167(4):1137, 2016. The notice body was not available through the accessed publisher endpoints. The main article's Acads/Foxo3 and crypt experiments were read, but the specific effect of the correction remains unassessed. https://pubmed.ncbi.nlm.nih.gov/27814510/ Evidence access: Primary abstract The Colonic Crypt Protects Stem Cells from Microbiota-Derived Metabolites. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27264604/ · DOI 10.1016/j.cell.2016.05.018
    Complete structured claim and evidence

  2. Foxo3 deletion, unlike Foxo1 deletion, made mouse stem/progenitor cells resistant to butyrate-mediated proliferation suppression.

    Mouse forkhead transcription factor Foxo3 → Mouse colonic stem/progenitor-cell proliferation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, Figure 7
    experimental_model
    Mouse genetic stem-cell experiments.
    limitations
    Loss of a response is not rescue of a nutrient deficiency. Correction record: A published erratum is confirmed by PubMed and publisher/Crossref metadata: Cell 167(4):1137, 2016. The notice body was not available through the accessed publisher endpoints. The main article's Acads/Foxo3 and crypt experiments were read, but the specific effect of the correction remains unassessed. https://pubmed.ncbi.nlm.nih.gov/27814510/
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    The growth-suppressing response depended on a specific transcription factor.
    primary_references
    The Colonic Crypt Protects Stem Cells from Microbiota-Derived Metabolites. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27264604/ · DOI 10.1016/j.cell.2016.05.018
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 326–332

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

    ## butyrate-foxo3-loss The growth-suppressing response depended on a specific transcription factor. Foxo3 deletion, unlike Foxo1 deletion, made mouse stem/progenitor cells resistant to butyrate-mediated proliferation suppression. Model: Mouse genetic stem-cell experiments. Limitations: Loss of a response is not rescue of a nutrient deficiency. Correction record: A published erratum is confirmed by PubMed and publisher/Crossref metadata: Cell 167(4):1137, 2016. The notice body was not available through the accessed publisher endpoints. The main article's Acads/Foxo3 and crypt experiments were read, but the specific effect of the correction remains unassessed. https://pubmed.ncbi.nlm.nih.gov/27814510/ Evidence access: Primary full text, Figure 7 The Colonic Crypt Protects Stem Cells from Microbiota-Derived Metabolites. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27264604/ · DOI 10.1016/j.cell.2016.05.018
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Acads-deficient colonocytes oxidized less butyrate; knockout mice had a smaller crypt proliferative zone that exogenous butyrate further suppressed.

    Mouse short-chain acyl-CoA dehydrogenase / Acads → Mouse colonocyte butyrate oxidation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text, Figure 6
    experimental_model
    Mouse Acads knockout, colonocyte metabolism and crypt measurements.
    limitations
    ACADS participates in oxidation; it does not perform the entire butyrate-to-acetyl-CoA pathway alone. Correction record: A published erratum is confirmed by PubMed and publisher/Crossref metadata: Cell 167(4):1137, 2016. The notice body was not available through the accessed publisher endpoints. The main article's Acads/Foxo3 and crypt experiments were read, but the specific effect of the correction remains unassessed. https://pubmed.ncbi.nlm.nih.gov/27814510/
    nutrient_topic
    Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
    plain_language
    Weakening fuel oxidation let butyrate affect cells normally protected from it.
    primary_references
    The Colonic Crypt Protects Stem Cells from Microbiota-Derived Metabolites. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27264604/ · DOI 10.1016/j.cell.2016.05.018
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 206–212

    AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse Acads knockout, colonocyte metabolism and crypt measurements. · source_derived_draft · unverified_draft

    ## butyrate-acads-loss Weakening fuel oxidation let butyrate affect cells normally protected from it. Acads-deficient colonocytes oxidized less butyrate; knockout mice had a smaller crypt proliferative zone that exogenous butyrate further suppressed. Model: Mouse Acads knockout, colonocyte metabolism and crypt measurements. Limitations: ACADS participates in oxidation; it does not perform the entire butyrate-to-acetyl-CoA pathway alone. Correction record: A published erratum is confirmed by PubMed and publisher/Crossref metadata: Cell 167(4):1137, 2016. The notice body was not available through the accessed publisher endpoints. The main article's Acads/Foxo3 and crypt experiments were read, but the specific effect of the correction remains unassessed. https://pubmed.ncbi.nlm.nih.gov/27814510/ Evidence access: Primary full text, Figure 6 The Colonic Crypt Protects Stem Cells from Microbiota-Derived Metabolites. · 2016 · https://pubmed.ncbi.nlm.nih.gov/27264604/ · DOI 10.1016/j.cell.2016.05.018
    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