Component

Mouse mitochondrial BCAA carrier / Slc25a44

Context-specific entity; species, compartment and exposure are stated on each claim.

5 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. BAT-specific Slc25a44 knockout impaired BCAA clearance and insulin tolerance without a significant difference in energy expenditure or body weight in this study.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Conditional mouse knockout under defined temperature and diet conditions.
    limitations
    Different perturbations and conditions from prior Bckdha-loss thermogenesis work; no universal requirement for a weight change.
    nutrient_topic
    L-Isoleucine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Isoleucine
    plain_language
    The metabolic effect was separable from measured heat production and weight.
    primary_references
    BCAA-nitrogen flux in brown fat controls metabolic health independent of thermogenesis. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38653240/ · DOI 10.1016/j.cell.2024.03.030
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Isoleucine: transport, translation, catabolism and cross-nutrient mechanisms (2026-09-19) · lines 98–104

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Conditional mouse knockout under defined temperature and diet conditions. · source_derived_draft · unverified_draft

    ## isoleucine-bat-insulin-beyond-heat The metabolic effect was separable from measured heat production and weight. BAT-specific Slc25a44 knockout impaired BCAA clearance and insulin tolerance without a significant difference in energy expenditure or body weight in this study. Model: Conditional mouse knockout under defined temperature and diet conditions. Limitations: Different perturbations and conditions from prior Bckdha-loss thermogenesis work; no universal requirement for a weight change. Evidence access: Primary full text BCAA-nitrogen flux in brown fat controls metabolic health independent of thermogenesis. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38653240/ · DOI 10.1016/j.cell.2024.03.030
    Complete structured claim and evidence
  2. Impaired mitochondrial BCAA nitrogen flux reduced synthesis of downstream metabolites including glutathione and increased oxidative stress in the tested BAT system.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse BAT carrier-loss and isotope/metabolite experiments.
    limitations
    Does not establish isoleucine supplementation as a glutathione intervention; the traced amino acids and cell context remain explicit.
    nutrient_topic
    L-Isoleucine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Isoleucine
    plain_language
    Transport and nitrogen handling can affect antioxidant production.
    primary_references
    BCAA-nitrogen flux in brown fat controls metabolic health independent of thermogenesis. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38653240/ · DOI 10.1016/j.cell.2024.03.030
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Isoleucine: transport, translation, catabolism and cross-nutrient mechanisms (2026-09-19) · lines 90–96

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse BAT carrier-loss and isotope/metabolite experiments. · source_derived_draft · unverified_draft

    ## isoleucine-bcaa-glutathione Transport and nitrogen handling can affect antioxidant production. Impaired mitochondrial BCAA nitrogen flux reduced synthesis of downstream metabolites including glutathione and increased oxidative stress in the tested BAT system. Model: Mouse BAT carrier-loss and isotope/metabolite experiments. Limitations: Does not establish isoleucine supplementation as a glutathione intervention; the traced amino acids and cell context remain explicit. Evidence access: Primary full text BCAA-nitrogen flux in brown fat controls metabolic health independent of thermogenesis. · 2024 · https://pubmed.ncbi.nlm.nih.gov/38653240/ · DOI 10.1016/j.cell.2024.03.030
    Complete structured claim and evidence
  3. BAT-specific Slc25a44 deletion blunted BCAA oxidation and non-shivering thermogenesis following intracerebroventricular PGE2.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse conditional knockout; PGE2 1.4 micrograms per mouse; valine oxidation readout.
    limitations
    Not an isoleucine-specific tracer result or a supplement treatment for fever.
    nutrient_topic
    L-Isoleucine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Isoleucine
    plain_language
    The shared mitochondrial gate mattered during a defined fever response.
    primary_references
    Metabolic flexibility via mitochondrial BCAA carrier SLC25A44 is required for optimal fever. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33944778/ · DOI 10.7554/eLife.66865
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Isoleucine: transport, translation, catabolism and cross-nutrient mechanisms (2026-09-19) · lines 74–80

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse conditional knockout; PGE2 1.4 micrograms per mouse; valine oxidation readout. · source_derived_draft · unverified_draft

    ## isoleucine-fever-carrier The shared mitochondrial gate mattered during a defined fever response. BAT-specific Slc25a44 deletion blunted BCAA oxidation and non-shivering thermogenesis following intracerebroventricular PGE2. Model: Mouse conditional knockout; PGE2 1.4 micrograms per mouse; valine oxidation readout. Limitations: Not an isoleucine-specific tracer result or a supplement treatment for fever. Evidence access: Primary full text Metabolic flexibility via mitochondrial BCAA carrier SLC25A44 is required for optimal fever. · 2021 · https://pubmed.ncbi.nlm.nih.gov/33944778/ · DOI 10.7554/eLife.66865
    Complete structured claim and evidence
  4. Slc25a44 loss reduced mitochondrial valine and leucine uptake; ectopic expression and reconstituted liposomes supported transporter function.

    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse brown adipocytes/Neuro2a and membrane/proteoliposome assays.
    limitations
    Direct transport tracers highlighted here were valine and leucine; do not relabel them as an isolated isoleucine transport assay.
    nutrient_topic
    L-Isoleucine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Isoleucine
    plain_language
    Access to mitochondria is a separate gate from entry into the cell.
    primary_references
    BCAA catabolism in brown fat controls energy homeostasis through SLC25A44. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31435015/ · DOI 10.1038/s41586-019-1503-x
    transport_effect
    raises The object already names mitochondrial BCAA uptake.
    transport_pool
    the mitochondrial matrix The object already names mitochondrial BCAA uptake.

    L-Isoleucine: transport, translation, catabolism and cross-nutrient mechanisms (2026-09-19) · lines 50–56

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse brown adipocytes/Neuro2a and membrane/proteoliposome assays. · source_derived_draft · unverified_draft

    ## isoleucine-mitochondrial-carrier Access to mitochondria is a separate gate from entry into the cell. Slc25a44 loss reduced mitochondrial valine and leucine uptake; ectopic expression and reconstituted liposomes supported transporter function. Model: Mouse brown adipocytes/Neuro2a and membrane/proteoliposome assays. Limitations: Direct transport tracers highlighted here were valine and leucine; do not relabel them as an isolated isoleucine transport assay. Evidence access: Primary full text BCAA catabolism in brown fat controls energy homeostasis through SLC25A44. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31435015/ · DOI 10.1038/s41586-019-1503-x
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. BAT-specific BCAA catabolic impairment reduced BCAA clearance and thermogenic fuel oxidation and promoted glucose intolerance in the tested mice.

    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse BAT-targeted Bckdha manipulation and metabolic assays.
    limitations
    Mixed BCAA pathway; not a claim that isolated isoleucine intake causes obesity.
    nutrient_topic
    L-Isoleucine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Isoleucine
    plain_language
    Loss of a tissue processing route changed whole-body amino-acid handling.
    primary_references
    BCAA catabolism in brown fat controls energy homeostasis through SLC25A44. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31435015/ · DOI 10.1038/s41586-019-1503-x
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Isoleucine: transport, translation, catabolism and cross-nutrient mechanisms (2026-09-19) · lines 66–72

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse BAT-targeted Bckdha manipulation and metabolic assays. · source_derived_draft · unverified_draft

    ## isoleucine-brown-fat-catabolic-loss Loss of a tissue processing route changed whole-body amino-acid handling. BAT-specific BCAA catabolic impairment reduced BCAA clearance and thermogenic fuel oxidation and promoted glucose intolerance in the tested mice. Model: Mouse BAT-targeted Bckdha manipulation and metabolic assays. Limitations: Mixed BCAA pathway; not a claim that isolated isoleucine intake causes obesity. Evidence access: Primary full text BCAA catabolism in brown fat controls energy homeostasis through SLC25A44. · 2019 · https://pubmed.ncbi.nlm.nih.gov/31435015/ · DOI 10.1038/s41586-019-1503-x
    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