Component

Cellular fatty acid oxidation

Cellular fatty acid oxidation. Species, exposure and limitations are retained in each linked claim.

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 acts on it

  1. Dlat-overexpressing rat cardiomyocytes retained more labeled palmitoyl-CoA and showed less label in shorter acyl-CoAs and acetyl-CoA.

    Dlat overexpression in neonatal rat ventricular cardiomyocytes → Cellular fatty acid oxidation source_derived_draftungraded
    Experimental context and source evidence
    access_level
    full_text_and_supplement_review
    compartment
    Mitochondria or cell lysate, depending on assay
    dose
    Adenovirus MOI 50:1 where applicable; compound concentrations not specified in reviewed methods
    duration
    Adenovirus incubation 6–8 h; subsequent endpoint timing not consistently specified
    endpoint
    fatty-acid-oxidation
    evidence_location
    13C-palmitate tracing; Figure 6L
    experimental_model
    Adenoviral/cell perturbation study
    exposure
    rat-dlat-overexpression
    limitations
    Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Reported metabolite-labeling pattern supports impaired breakdown; it does not itself establish every kinetic step or isolate HADHA from other Dlat effects.
    organism
    Rattus norvegicus host cells; construct species may be unspecified
    plain_language
    Dlat-overexpressing rat cardiomyocytes retained more labeled palmitoyl-CoA and showed less label in shorter acyl-CoAs and acetyl-CoA.
    primary_locator
    [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 44, "text_sha256": "e0a92f47bc76c894816706ffb5158242c968928ac61e4561262c370035eda621", "xml_element_id": "Par19"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 46, "text_sha256": "d56a90702bdf004de1efc2e43103b1b771e15b38288dc01f3741676782b1f5ff", "xml_element_id": null}]
    primary_references
    https://doi.org/10.1038/s41467-026-70703-w
    sample_size
    4 per group
    tissue_or_cell_type
    Neonatal rat ventricular cardiomyocytes (NRVCMs)

    DLAT: cardiac fatty-acid oxidation and mitochondrial glutathione evidence · lines 214–229

    AI-assisted two-paper curation, 2026-09-20. Cardiac full-text/supplement review; CRC abstract only. No pulmonary endothelial validation. · supports · Adenoviral/cell perturbation study · source_derived_draft · unverified_draft

    Dlat-overexpressing rat cardiomyocytes retained more labeled palmitoyl-CoA and showed less label in shorter acyl-CoAs and acetyl-CoA. organism: Rattus norvegicus host cells; construct species may be unspecified tissue_or_cell_type: Neonatal rat ventricular cardiomyocytes (NRVCMs) experimental_model: Adenoviral/cell perturbation study compartment: Mitochondria or cell lysate, depending on assay dose: Adenovirus MOI 50:1 where applicable; compound concentrations not specified in reviewed methods duration: Adenovirus incubation 6–8 h; subsequent endpoint timing not consistently specified primary_references: https://doi.org/10.1038/s41467-026-70703-w access_level: full_text_and_supplement_review evidence_location: 13C-palmitate tracing; Figure 6L endpoint: fatty-acid-oxidation exposure: rat-dlat-overexpression limitations: Single primary study; not independently replicated here. Cardiac and recombinant findings do not establish pulmonary endothelial, viral-sepsis or ARDS effects. Reported metabolite-labeling pattern supports impaired breakdown; it does not itself establish every kinetic step or isolate HADHA from other Dlat effects. primary_locator: [{"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 44, "text_sha256": "e0a92f47bc76c894816706ffb5158242c968928ac61e4561262c370035eda621", "xml_element_id": "Par19"}, {"cache": "artifacts/dlat-curation/heart-blocks.json", "block_index": 46, "text_sha256": "d56a90702bdf004de1efc2e43103b1b771e15b38288dc01f3741676782b1f5ff", "xml_element_id": null}] plain_language: Dlat-overexpressing rat cardiomyocytes retained more labeled palmitoyl-CoA and showed less label in shorter acyl-CoAs and acetyl-CoA. sample_size: 4 per group
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Metformin activated AMPK in hepatocytes, reducing acetyl-CoA carboxylase activity, inducing fatty acid oxidation and suppressing expression of lipogenic enzymes.

    Metformin → AMP-activated protein kinase complexes source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/11602624.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "86e283289def8a6e3e3098d49f321dbcca9a6cd4677ba84f26daf17467179237", "start_char": 0, "end_char": 1390, "text_sha256": "86e283289def8a6e3e3098d49f321dbcca9a6cd4677ba84f26daf17467179237"}
    experimental_model
    Rat hepatocytes, isolated rat skeletal muscle and metformin-treated rats with an AMPK inhibitor
    exposure
    Metformin in hepatocytes and in vivo; compound C AMPK inhibition
    limitations
    The inhibitor experiment supports a requirement for AMPK in these hepatocytes; later work in AMPK-deficient mice reached a different conclusion, recorded separately.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Rat
    plain_language
    The cell reads the drug as an energy shortage and switches to burning rather than storing.
    primary_references
    [metformin-p11602624] Role of AMP-activated protein kinase in mechanism of metformin action. (2001). https://pubmed.ncbi.nlm.nih.gov/11602624/ DOI: 10.1172/jci13505
    tissue_or_cell_type
    Liver and skeletal muscle

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 528–539

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rat hepatocytes, isolated rat skeletal muscle and metformin-treated rats with an AMPK inhibitor · source_derived_draft · unverified_draft

    ### metformin-ampk-activation Metformin activated AMPK in hepatocytes, reducing acetyl-CoA carboxylase activity, inducing fatty acid oxidation and suppressing expression of lipogenic enzymes. Condition category: normal nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: The cell reads the drug as an energy shortage and switches to burning rather than storing. organism: Rat tissue_or_cell_type: Liver and skeletal muscle experimental_model: Rat hepatocytes, isolated rat skeletal muscle and metformin-treated rats with an AMPK inhibitor limitations: The inhibitor experiment supports a requirement for AMPK in these hepatocytes; later work in AMPK-deficient mice reached a different conclusion, recorded separately. exposure: Metformin in hepatocytes and in vivo; compound C AMPK inhibition evidence_span: {"source_cache": "artifacts/metformin-research/11602624.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "86e283289def8a6e3e3098d49f321dbcca9a6cd4677ba84f26daf17467179237", "start_char": 0, "end_char": 1390, "text_sha256": "86e283289def8a6e3e3098d49f321dbcca9a6cd4677ba84f26daf17467179237"} [metformin-p11602624] Role of AMP-activated protein kinase in mechanism of metformin action. (2001). https://pubmed.ncbi.nlm.nih.gov/11602624/ DOI: 10.1172/jci13505
    Complete structured claim and evidence

  2. At 4 hours after feeding, liver malonyl-CoA, an allosteric inhibitor of carnitine palmitoyl-transferase, was significantly lower in the acetic acid group than in the control group, along with a lower serum lactate concentration and a lower ratio of insulin to glucagon, indicating the possibility of a transient enhancement of fatty acid oxidation in liver.

    Acetic acid → Malonyl-CoA source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/acetate-research/16277773.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "305aa81aca9908a350132a7c7dcc42c86be0b6030c70f51b5fe0c8971e75bcfe", "start_char": 0, "end_char": 1594, "text_sha256": "305aa81aca9908a350132a7c7dcc42c86be0b6030c70f51b5fe0c8971e75bcfe"}
    experimental_model
    Rats meal-fed once daily for 10 days, then sampled 4, 8 or 24 hours after feeding
    exposure
    0.7 g/kg-diet acetic acid in a 9 g meal, with sampling across the daily cycle
    limitations
    Adds the time dimension that single-timepoint studies miss. The effects were present at 4 hours and the authors explicitly rule out supercompensation.
    nutrient_topic
    Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. · Acetic acid
    organism
    Rat
    plain_language
    The brake on fat burning came off for a few hours.
    primary_references
    [acetate-p16277773] Effect of acetic acid feeding on the circadian changes in glycogen and metabolites of glucose and lipid in liver and skeletal muscle of rats. (2005). https://pubmed.ncbi.nlm.nih.gov/16277773/ DOI: 10.1079/bjn20051545
    tissue_or_cell_type
    Liver and skeletal muscle

    Acetic acid: the ingested acid, the receptors acetate binds, the acetyl-CoA it becomes, and the acetyl groups that reach histones (2026-09-21) · lines 472–483

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Rats meal-fed once daily for 10 days, then sampled 4, 8 or 24 hours after feeding · source_derived_draft · unverified_draft

    ### acetate-malonyl-coa-fall At 4 hours after feeding, liver malonyl-CoA, an allosteric inhibitor of carnitine palmitoyl-transferase, was significantly lower in the acetic acid group than in the control group, along with a lower serum lactate concentration and a lower ratio of insulin to glucagon, indicating the possibility of a transient enhancement of fatty acid oxidation in liver. Condition category: normal nutrient_topic: Acetic acid research collection; topical membership is not evidence of a direct clinical effect, and the ingested acid is recorded separately from the circulating acetate anion. plain_language: The brake on fat burning came off for a few hours. organism: Rat tissue_or_cell_type: Liver and skeletal muscle experimental_model: Rats meal-fed once daily for 10 days, then sampled 4, 8 or 24 hours after feeding limitations: Adds the time dimension that single-timepoint studies miss. The effects were present at 4 hours and the authors explicitly rule out supercompensation. exposure: 0.7 g/kg-diet acetic acid in a 9 g meal, with sampling across the daily cycle evidence_span: {"source_cache": "artifacts/acetate-research/16277773.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "305aa81aca9908a350132a7c7dcc42c86be0b6030c70f51b5fe0c8971e75bcfe", "start_char": 0, "end_char": 1594, "text_sha256": "305aa81aca9908a350132a7c7dcc42c86be0b6030c70f51b5fe0c8971e75bcfe"} [acetate-p16277773] Effect of acetic acid feeding on the circadian changes in glycogen and metabolites of glucose and lipid in liver and skeletal muscle of rats. (2005). https://pubmed.ncbi.nlm.nih.gov/16277773/ DOI: 10.1079/bjn20051545
    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