Component
Rodent intestinal gluconeogenic response to butyrate; species unresolved in accessed abstract
Context-specific entity; species, compartment and exposure are stated on each claim.
1 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
Butyrate activated intestinal gluconeogenic gene expression through a cAMP-dependent mechanism in the rodent study.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Rodent intestinal metabolism and signaling experiments.
- limitations
- The paper assigned propionate, not butyrate, the distinct FFAR3-dependent gut-brain route; butyrate is not being labeled a net glucose carbon source.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- A gut glucose-producing pathway contributed to metabolic signaling.
- primary_references
- Microbiota-generated metabolites promote metabolic benefits via gut-brain neural circuits. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24412651/ · DOI 10.1016/j.cell.2013.12.016
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 518–524
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Rodent intestinal metabolism and signaling experiments. · source_derived_draft · unverified_draft
## butyrate-ign-camp A gut glucose-producing pathway contributed to metabolic signaling. Butyrate activated intestinal gluconeogenic gene expression through a cAMP-dependent mechanism in the rodent study. Model: Rodent intestinal metabolism and signaling experiments. Limitations: The paper assigned propionate, not butyrate, the distinct FFAR3-dependent gut-brain route; butyrate is not being labeled a net glucose carbon source. Evidence access: Primary abstract Microbiota-generated metabolites promote metabolic benefits via gut-brain neural circuits. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24412651/ · DOI 10.1016/j.cell.2013.12.016
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.