Component

Human isolated-mitochondrial acetyl-CoA uptake

Human isolated-mitochondrial acetyl-CoA uptake

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.

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 acts on it

  1. Isolated K562 mitochondria showed negligible uptake of acetyl-labeled acetyl-CoA under the tested assay.

    Experimental context and source evidence
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_model
    Fig. 7d–e; 10 micromolar 13C2-acetyl-CoA, 6 min, 20–25 C.
    interpretation_status
    Source-derived curation with stated access limits; ungraded, not independent replication.
    limitations
    Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation.
    nutrient_topic
    Acetyl-L-carnitine collection; exact intervention and molecular form govern interpretation. · Acetyl-L-carnitine
    plain_language
    Isolated K562 mitochondria showed negligible uptake of acetyl-labeled acetyl-CoA under the tested assay.
    primary_references
    Cellular pan-chain acyl-CoA profiling reveals SLC25A42/SLC25A16 in mitochondrial CoA import and metabolism. | https://pubmed.ncbi.nlm.nih.gov/40925986/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC12460162/ | https://doi.org/10.1038/s42255-025-01358-y
    source_locator
    Reviewed reference coa-import-acetyl-null; CoA-backbone labeling after free CoASH uptake must not be mistaken for direct import of intact acetyl-CoA. A small residual signal could reflect membrane binding or minimal import.

    Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 76–82

    AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · Fig. 7d–e; 10 micromolar 13C2-acetyl-CoA, 6 min, 20–25 C. · Recorded from source · Recorded from source

    ### coa-import-acetyl-null Isolated K562 mitochondria showed negligible uptake of acetyl-labeled acetyl-CoA under the tested assay. CoA-backbone labeling after free CoASH uptake must not be mistaken for direct import of intact acetyl-CoA. A small residual signal could reflect membrane binding or minimal import. Model and exposure: Fig. 7d–e; 10 micromolar 13C2-acetyl-CoA, 6 min, 20–25 C. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Cellular pan-chain acyl-CoA profiling reveals SLC25A42/SLC25A16 in mitochondrial CoA import and metabolism. | 2025 | https://pubmed.ncbi.nlm.nih.gov/40925986/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC12460162/ | https://doi.org/10.1038/s42255-025-01358-y | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    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.