Component
Mouse carnitine acetyltransferase / Crat
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
Muscle Crat deletion reduced short-chain acyltransferase activity and acetylcarnitine pools, supporting transfer of acetyl groups from acetyl-CoA to carnitine.
Experimental context and source evidence
- evidence_access
- Primary abstract and full-text Figures 1-4
- experimental_model
- Muscle-specific mouse knockout, enzyme assays and metabolomics.
- limitations
- Crat buffer function depends on tissue and substrate conditions.
- nutrient_topic
- L-Carnitine collection; isomer, preparation, species, exposure and manipulation remain explicit. · L-Carnitine
- plain_language
- Carnitine can carry excess acetyl groups as well as long fatty-acid groups.
- primary_references
- Muscle-specific deletion of carnitine acetyltransferase compromises glucose tolerance and metabolic flexibility. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22560225/ · DOI 10.1016/j.cmet.2012.04.005
L-Carnitine: synthesis, acyl-group transport, fuel selection and nutrient interactions (2026-09-19) · lines 154–160
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Muscle-specific mouse knockout, enzyme assays and metabolomics. · source_derived_draft · unverified_draft
## l-carnitine-crat-buffer Carnitine can carry excess acetyl groups as well as long fatty-acid groups. Muscle Crat deletion reduced short-chain acyltransferase activity and acetylcarnitine pools, supporting transfer of acetyl groups from acetyl-CoA to carnitine. Model: Muscle-specific mouse knockout, enzyme assays and metabolomics. Limitations: Crat buffer function depends on tissue and substrate conditions. Evidence access: Primary abstract and full-text Figures 1-4 Muscle-specific deletion of carnitine acetyltransferase compromises glucose tolerance and metabolic flexibility. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22560225/ · DOI 10.1016/j.cmet.2012.04.005
Complete structured claim and evidenceRemoving Crat impaired glucose-derived lipid synthesis in ACLY-deficient mouse HCC cells.
Experimental context and source evidence
- evidence_access
- Primary full text and cell-line methods
- experimental_model
- Mouse HCC cell genetic perturbation and carbon tracing.
- limitations
- Dependence arises in the specified metabolic background.
- nutrient_topic
- L-Carnitine collection; isomer, preparation, species, exposure and manipulation remain explicit. · L-Carnitine
- plain_language
- The acetyl shuttle can supply lipid synthesis when a usual route is missing.
- primary_references
- Acetylcarnitine shuttling links mitochondrial metabolism to histone acetylation and lipogenesis. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37134161/ · DOI 10.1126/sciadv.adf0115
L-Carnitine: synthesis, acyl-group transport, fuel selection and nutrient interactions (2026-09-19) · lines 242–248
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Mouse HCC cell genetic perturbation and carbon tracing. · source_derived_draft · unverified_draft
## l-carnitine-crat-lipogenesis The acetyl shuttle can supply lipid synthesis when a usual route is missing. Removing Crat impaired glucose-derived lipid synthesis in ACLY-deficient mouse HCC cells. Model: Mouse HCC cell genetic perturbation and carbon tracing. Limitations: Dependence arises in the specified metabolic background. Evidence access: Primary full text and cell-line methods Acetylcarnitine shuttling links mitochondrial metabolism to histone acetylation and lipogenesis. · 2023 · https://pubmed.ncbi.nlm.nih.gov/37134161/ · DOI 10.1126/sciadv.adf0115
Complete structured claim and evidence
Where it participates (unsigned role)
Adding carnitine stimulated PDH activity 1.8-fold in control muscle mitochondria but did not stimulate it in Crat-null mitochondria.
Experimental context and source evidence
- evidence_access
- Primary full-text Figure 4
- experimental_model
- Isolated mouse muscle mitochondria; pyruvate-only respiratory context and direct PDH assay.
- limitations
- The effect is context-dependent; liver mitochondria also lacked the stimulation.
- nutrient_topic
- L-Carnitine collection; isomer, preparation, species, exposure and manipulation remain explicit. · L-Carnitine
- plain_language
- Carnitine needs the acetyl-transfer enzyme to relieve this brake on glucose oxidation.
- primary_references
- Muscle-specific deletion of carnitine acetyltransferase compromises glucose tolerance and metabolic flexibility. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22560225/ · DOI 10.1016/j.cmet.2012.04.005
L-Carnitine: synthesis, acyl-group transport, fuel selection and nutrient interactions (2026-09-19) · lines 162–168
AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Isolated mouse muscle mitochondria; pyruvate-only respiratory context and direct PDH assay. · source_derived_draft · unverified_draft
## l-carnitine-crat-pdh Carnitine needs the acetyl-transfer enzyme to relieve this brake on glucose oxidation. Adding carnitine stimulated PDH activity 1.8-fold in control muscle mitochondria but did not stimulate it in Crat-null mitochondria. Model: Isolated mouse muscle mitochondria; pyruvate-only respiratory context and direct PDH assay. Limitations: The effect is context-dependent; liver mitochondria also lacked the stimulation. Evidence access: Primary full-text Figure 4 Muscle-specific deletion of carnitine acetyltransferase compromises glucose tolerance and metabolic flexibility. · 2012 · https://pubmed.ncbi.nlm.nih.gov/22560225/ · DOI 10.1016/j.cmet.2012.04.005
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.