Component
Mouse colonic luminal nitrate availability
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 it acts on
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
Where it participates (unsigned role)
Loss of epithelial PPAR-gamma signaling increased Nos2 expression and colonic nitrate availability in the mouse study.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Mouse epithelial signaling and luminal metabolite experiments.
- limitations
- Nitrate is a downstream electron acceptor; butyrate is not being claimed to chemically remove nitrate.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- Changing host signaling supplied a different bacterial respiratory fuel.
- primary_references
- Microbiota-activated PPAR-γ signaling inhibits dysbiotic Enterobacteriaceae expansion. · 2017 · https://pubmed.ncbi.nlm.nih.gov/28798125/ · DOI 10.1126/science.aam9949
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 222–228
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse epithelial signaling and luminal metabolite experiments. · source_derived_draft · unverified_draft
## butyrate-pparg-nos2 Changing host signaling supplied a different bacterial respiratory fuel. Loss of epithelial PPAR-gamma signaling increased Nos2 expression and colonic nitrate availability in the mouse study. Model: Mouse epithelial signaling and luminal metabolite experiments. Limitations: Nitrate is a downstream electron acceptor; butyrate is not being claimed to chemically remove nitrate. 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.