Component
Mouse skeletal-muscle kynurenine aminotransferases; multiple enzymes
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.
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
Carbidopa inhibition of kynurenine aminotransferase activity impaired aspartate synthesis and mitochondrial respiration and reduced mouse exercise performance and muscle force.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary abstract
- experimental_model
- Mouse muscle/exercise experiments within a PGC-1alpha1 and malate–aspartate-shuttle study.
- limitations
- Carbidopa is not specific to a single KAT isoform; mouse exposures do not establish the same effect at a clinical human dose.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- The branch can support muscle energy handling as well as alter circulating metabolites.
- primary_references
- Skeletal muscle PGC-1α1 reroutes kynurenine metabolism to increase energy efficiency and fatigue-resistance. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31235694/ · DOI 10.1038/s41467-019-10712-0
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 626–632
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse muscle/exercise experiments within a PGC-1alpha1 and malate–aspartate-shuttle study. · source_derived_draft · unverified_draft
## tryptophan-muscle-kat-inhibition The branch can support muscle energy handling as well as alter circulating metabolites. Carbidopa inhibition of kynurenine aminotransferase activity impaired aspartate synthesis and mitochondrial respiration and reduced mouse exercise performance and muscle force. Model: Mouse muscle/exercise experiments within a PGC-1alpha1 and malate–aspartate-shuttle study. Limitations: Carbidopa is not specific to a single KAT isoform; mouse exposures do not establish the same effect at a clinical human dose. Evidence access: Primary abstract Skeletal muscle PGC-1α1 reroutes kynurenine metabolism to increase energy efficiency and fatigue-resistance. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31235694/ · DOI 10.1038/s41467-019-10712-0
Complete structured claim and evidence
What acts on it
The PGC-1alpha1–PPAR-alpha/delta program increased muscle kynurenine aminotransferases and conversion of kynurenine to kynurenic acid.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse skeletal-muscle transgenic and stress experiments.
- limitations
- Multiple aminotransferases are involved; do not assign the entire effect to human AADAT alone.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- Muscle metabolism can change which tryptophan products remain in circulation.
- primary_references
- Skeletal muscle PGC-1α1 modulates kynurenine metabolism and mediates resilience to stress-induced depression. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25259918/ · DOI 10.1016/j.cell.2014.07.051
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 610–616
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse skeletal-muscle transgenic and stress experiments. · source_derived_draft · unverified_draft
## tryptophan-muscle-kat-program Muscle metabolism can change which tryptophan products remain in circulation. The PGC-1alpha1–PPAR-alpha/delta program increased muscle kynurenine aminotransferases and conversion of kynurenine to kynurenic acid. Model: Mouse skeletal-muscle transgenic and stress experiments. Limitations: Multiple aminotransferases are involved; do not assign the entire effect to human AADAT alone. Evidence access: Primary abstract Skeletal muscle PGC-1α1 modulates kynurenine metabolism and mediates resilience to stress-induced depression. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25259918/ · DOI 10.1016/j.cell.2014.07.051
Complete structured claim and evidence
Where it participates (unsigned role)
Muscle-specific PGC-1alpha1 transgenic mice resisted depression-like changes induced by chronic mild stress or kynurenine administration as peripheral kynurenine handling shifted.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Mouse genetic overexpression and behavioral challenges.
- limitations
- Not proof that this is the sole human exercise–mood mechanism or that kynurenic acid freely enters the brain.
- nutrient_topic
- Tryptophan collection; molecular form, preparation, species, exposure and manipulation remain explicit. · L-Tryptophan
- plain_language
- A peripheral metabolic change altered a brain-related behavioral response.
- primary_references
- Skeletal muscle PGC-1α1 modulates kynurenine metabolism and mediates resilience to stress-induced depression. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25259918/ · DOI 10.1016/j.cell.2014.07.051
Tryptophan: transport, protein synthesis, neuroactive metabolites, NAD and microbial pathways (2026-09-19) · lines 618–624
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse genetic overexpression and behavioral challenges. · source_derived_draft · unverified_draft
## tryptophan-muscle-brain-context A peripheral metabolic change altered a brain-related behavioral response. Muscle-specific PGC-1alpha1 transgenic mice resisted depression-like changes induced by chronic mild stress or kynurenine administration as peripheral kynurenine handling shifted. Model: Mouse genetic overexpression and behavioral challenges. Limitations: Not proof that this is the sole human exercise–mood mechanism or that kynurenic acid freely enters the brain. Evidence access: Primary abstract Skeletal muscle PGC-1α1 modulates kynurenine metabolism and mediates resilience to stress-induced depression. · 2014 · https://pubmed.ncbi.nlm.nih.gov/25259918/ · DOI 10.1016/j.cell.2014.07.051
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.