Component
Mouse podocyte injury and proteinuria after butyrate
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
Hcar2-deficient mice lost the reported protective response to butyrate in Adriamycin nephropathy.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Mouse receptor knockout during induced nephropathy.
- limitations
- Does not establish the same dependency for human IBD monocytes or all kidney injury.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- The kidney response required a receptor in this model.
- primary_references
- Gut microbial metabolite butyrate protects against proteinuric kidney disease through epigenetic- and GPR109a-mediated mechanisms. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31366236/ · DOI 10.1096/fj.201901080R
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 614–620
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse receptor knockout during induced nephropathy. · source_derived_draft · unverified_draft
## butyrate-kidney-hcar2-loss The kidney response required a receptor in this model. Hcar2-deficient mice lost the reported protective response to butyrate in Adriamycin nephropathy. Model: Mouse receptor knockout during induced nephropathy. Limitations: Does not establish the same dependency for human IBD monocytes or all kidney injury. Evidence access: Primary abstract Gut microbial metabolite butyrate protects against proteinuric kidney disease through epigenetic- and GPR109a-mediated mechanisms. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31366236/ · DOI 10.1096/fj.201901080R
Complete structured claim and evidenceSodium butyrate reduced proteinuria, podocyte loss and renal injury in the mouse Adriamycin-nephropathy study.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse induced-nephropathy intervention, with a separate butyrate-releasing starch arm.
- limitations
- Not evidence of efficacy in all human kidney diseases.
- nutrient_topic
- Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate
- plain_language
- The experimental benefit extended beyond the gut to the kidney.
- primary_references
- Gut microbial metabolite butyrate protects against proteinuric kidney disease through epigenetic- and GPR109a-mediated mechanisms. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31366236/ · DOI 10.1096/fj.201901080R
Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 606–612
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse induced-nephropathy intervention, with a separate butyrate-releasing starch arm. · source_derived_draft · unverified_draft
## butyrate-kidney-protection The experimental benefit extended beyond the gut to the kidney. Sodium butyrate reduced proteinuria, podocyte loss and renal injury in the mouse Adriamycin-nephropathy study. Model: Mouse induced-nephropathy intervention, with a separate butyrate-releasing starch arm. Limitations: Not evidence of efficacy in all human kidney diseases. Evidence access: Primary abstract Gut microbial metabolite butyrate protects against proteinuric kidney disease through epigenetic- and GPR109a-mediated mechanisms. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31366236/ · DOI 10.1096/fj.201901080R
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.