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.

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.

Recorded relationships

What it acts on

  1. 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 evidence
  2. Removing 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)

  1. 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

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

    Evidence, AI assistance and curation standards