Component
Mouse colonic epithelial oxygen consumption
Context-specific entity; species, compartment and exposure are stated on each claim.
2 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What acts on it
Microbiota-supported PPAR-gamma signaling drove mouse colonocytes toward beta-oxidation, limiting oxygen available to bacteria in the colonic lumen.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse antibiotic, epithelial Pparg and microbial respiration experiments.
- limitations
- Pathway dependence does not establish direct binding of butyrate to PPAR-gamma.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- Colon-cell fuel use helped keep the neighboring microbial environment low in oxygen.
- primary_references
- Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28798125/ · DOI 10.1126/science.aam9949
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 214–220
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse antibiotic, epithelial Pparg and microbial respiration experiments. · source_derived_draft · unverified_draft
## butyrate-pparg-oxygen Colon-cell fuel use helped keep the neighboring microbial environment low in oxygen. Microbiota-supported PPAR-gamma signaling drove mouse colonocytes toward beta-oxidation, limiting oxygen available to bacteria in the colonic lumen. Model: Mouse antibiotic, epithelial Pparg and microbial respiration experiments. Limitations: Pathway dependence does not establish direct binding of butyrate to PPAR-gamma. Evidence access: Primary abstract Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28798125/ · DOI 10.1126/science.aam9949
Complete structured claim and evidence
Where it participates (unsigned role)
The mouse experiments linked increased luminal respiratory electron acceptors to expansion of Escherichia and Salmonella when the PPAR-gamma homeostatic pathway was disrupted.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse microbiota perturbation and bacterial respiration experiments.
- limitations
- The pathway is not a universal explanation for every case of dysbiosis.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- Host metabolism changed which bacteria could expand.
- primary_references
- Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28798125/ · DOI 10.1126/science.aam9949
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 230–236
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse microbiota perturbation and bacterial respiration experiments. · source_derived_draft · unverified_draft
## butyrate-electron-acceptor-growth Host metabolism changed which bacteria could expand. The mouse experiments linked increased luminal respiratory electron acceptors to expansion of Escherichia and Salmonella when the PPAR-gamma homeostatic pathway was disrupted. Model: Mouse microbiota perturbation and bacterial respiration experiments. Limitations: The pathway is not a universal explanation for every case of dysbiosis. Evidence access: Primary abstract Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28798125/ · DOI 10.1126/science.aam9949
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.