Component

Human plasma acetylcarnitine concentration

Human plasma acetylcarnitine concentration

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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. Higher serum ALCAR was associated with shorter progression-free survival in the reported ovarian-cancer cohort.

    Human plasma acetylcarnitine concentration → Ovarian-cancer progression-free survival associated with serum ALCAR Recorded from sourceungraded
    Experimental context and source evidence
    availability_state
    biomarker_context Imported condition classification; unverified.
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_model
    Patient serum upper-versus-lower quartile analysis; Fig. 5h; log-rank HR 2.439, P=0.0364.
    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
    Higher serum ALCAR was associated with shorter progression-free survival in the reported ovarian-cancer cohort.
    primary_references
    αKG-mediated carnitine synthesis drives DNA repair via histone acetylation. | https://pubmed.ncbi.nlm.nih.gov/42203879/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13307467/ | https://doi.org/10.1038/s41586-026-10584-7
    source_locator
    Reviewed reference cancer-serum-association; Observational association, not an ALCAR supplementation trial. Tumor metabolism, disease burden and other factors may influence circulating ALCAR. No causal direction from the blood measurement is established.
    trigger_kind
    biomarker_context Imported condition classification; unverified.

    Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 352–358

    AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · Patient serum upper-versus-lower quartile analysis; Fig. 5h; log-rank HR 2.439, P=0.0364. · Recorded from source · Recorded from source

    ### cancer-serum-association Higher serum ALCAR was associated with shorter progression-free survival in the reported ovarian-cancer cohort. Observational association, not an ALCAR supplementation trial. Tumor metabolism, disease burden and other factors may influence circulating ALCAR. No causal direction from the blood measurement is established. Model and exposure: Patient serum upper-versus-lower quartile analysis; Fig. 5h; log-rank HR 2.439, P=0.0364. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: αKG-mediated carnitine synthesis drives DNA repair via histone acetylation. | 2026 | https://pubmed.ncbi.nlm.nih.gov/42203879/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC13307467/ | https://doi.org/10.1038/s41586-026-10584-7 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    Complete structured claim and evidence

What acts on it

  1. A nominal 1.5-g oral ALCAR dose produced a nonsignificant plasma ALCAR increase in a small healthy-volunteer study.

    Acetyl-L-carnitine → Human plasma acetylcarnitine concentration Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_contrast
    {"intervention": "Single nominal 1.5-g ALCAR dose", "comparator": "Predose baseline", "endpoint": "A nominal 1.5-g oral ALCAR dose produced a nonsignificant plasma ALCAR increase in a small healthy-volunteer study.", "effect_direction": "no_detected_change", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Open-label pharmacokinetics; ALCAR 1.5-g group n=11; Results/Fig. 2, 2025.
    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
    A nominal 1.5-g oral ALCAR dose produced a nonsignificant plasma ALCAR increase in a small healthy-volunteer study.
    primary_references
    Low Bioavailability and High TMAO Production: Novel Insights Into Acetylcarnitine and Carnitine Metabolism. | https://pubmed.ncbi.nlm.nih.gov/41243468/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC12700042/ | https://doi.org/10.1002/mnfr.70316
    source_locator
    Reviewed reference pk-alcar-null; Median 9.4 to 12.5 micromolar, peak around 4 h. The study had no IV ALCAR reference or isotope-resolved mass balance; endogenous-pool change cannot measure absolute intact-drug bioavailability.

    Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 112–118

    AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · Open-label pharmacokinetics; ALCAR 1.5-g group n=11; Results/Fig. 2, 2025. · Recorded from source · Recorded from source

    ### pk-alcar-null A nominal 1.5-g oral ALCAR dose produced a nonsignificant plasma ALCAR increase in a small healthy-volunteer study. Median 9.4 to 12.5 micromolar, peak around 4 h. The study had no IV ALCAR reference or isotope-resolved mass balance; endogenous-pool change cannot measure absolute intact-drug bioavailability. Model and exposure: Open-label pharmacokinetics; ALCAR 1.5-g group n=11; Results/Fig. 2, 2025. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Low Bioavailability and High TMAO Production: Novel Insights Into Acetylcarnitine and Carnitine Metabolism. | 2025 | https://pubmed.ncbi.nlm.nih.gov/41243468/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC12700042/ | https://doi.org/10.1002/mnfr.70316 | Access: Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    Complete structured claim and evidence

  2. Oral L-carnitine also increased the circulating ALCAR pool in the 2025 study.

    L-Carnitine → Human plasma acetylcarnitine concentration Recorded from sourceungraded
    Experimental context and source evidence
    evidence_access
    Primary full text: relevant Results/Methods and figure descriptions reviewed; supplements only where explicitly stated.
    experimental_contrast
    {"intervention": "Single nominal 1.5-g L-carnitine dose", "comparator": "Predose baseline", "endpoint": "Oral L-carnitine also increased the circulating ALCAR pool in the 2025 study.", "effect_direction": "increase", "combination": "single", "conditions": []} Explicit extracted experimental comparison; source-derived draft.
    experimental_model
    Healthy-volunteer open-label pharmacokinetics; carnitine 1.5-g group n=12.
    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
    Oral L-carnitine also increased the circulating ALCAR pool in the 2025 study.
    primary_references
    Low Bioavailability and High TMAO Production: Novel Insights Into Acetylcarnitine and Carnitine Metabolism. | https://pubmed.ncbi.nlm.nih.gov/41243468/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC12700042/ | https://doi.org/10.1002/mnfr.70316
    source_locator
    Reviewed reference pk-carnitine-alcar; Median ALCAR 12.1 to 20.9 micromolar at 4 h after 1.5 g carnitine. Baselines differed among groups; this is not a matched tissue-efficacy comparison.

    Acetyl-L-carnitine: detailed mechanisms of action (reviewed 6 October 2026) · lines 120–126

    AI-assisted original review of primary studies and clearly identified official records. Exact primary access is stated; no independent replication is claimed. · supports · Healthy-volunteer open-label pharmacokinetics; carnitine 1.5-g group n=12. · Recorded from source · Recorded from source

    ### pk-carnitine-alcar Oral L-carnitine also increased the circulating ALCAR pool in the 2025 study. Median ALCAR 12.1 to 20.9 micromolar at 4 h after 1.5 g carnitine. Baselines differed among groups; this is not a matched tissue-efficacy comparison. Model and exposure: Healthy-volunteer open-label pharmacokinetics; carnitine 1.5-g group n=12. Limitations: Limited to the recorded preparation, model, exposure and endpoint. Does not establish a human dietary deficiency, clinical benefit or unique molecular mediation. Reference: Low Bioavailability and High TMAO Production: Novel Insights Into Acetylcarnitine and Carnitine Metabolism. | 2025 | https://pubmed.ncbi.nlm.nih.gov/41243468/ | https://pmc.ncbi.nlm.nih.gov/articles/PMC12700042/ | https://doi.org/10.1002/mnfr.70316 | 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.