Component

Mouse aralar / Slc25a12

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

6 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. Aralar1 silencing in primary mouse brown adipocytes impaired norepinephrine-induced lipid mobilization and increased small lipid-droplet accumulation.

    Mouse aralar / Slc25a12 → Norepinephrine-stimulated lipolysis in mouse brown adipocytes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse primary brown adipocytes; approximately 80% knockdown in the reported experiment.
    limitations
    This does not establish human weight-loss effects or a nutrient-intake threshold.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    Disrupting the carrier changed fat handling in the cell.
    primary_references
    The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41704162/ · DOI 10.1111/febs.70461
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 330–336

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse primary brown adipocytes; approximately 80% knockdown in the reported experiment. · source_derived_draft · unverified_draft

    ## l-aspartate-brown-aralar-lipids Disrupting the carrier changed fat handling in the cell. Aralar1 silencing in primary mouse brown adipocytes impaired norepinephrine-induced lipid mobilization and increased small lipid-droplet accumulation. Model: Mouse primary brown adipocytes; approximately 80% knockdown in the reported experiment. Limitations: This does not establish human weight-loss effects or a nutrient-intake threshold. Evidence access: Primary full text The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41704162/ · DOI 10.1111/febs.70461
    Complete structured claim and evidence

  2. Exogenous aralar expression reversed the increased NADH/NAD+ ratio in hepatocytes from citrin-null mice.

    Mouse aralar / Slc25a12 → NADH/NAD+ balance in citrin-null mouse hepatocytes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse Slc25a13-null hepatocytes with exogenous aralar expression.
    limitations
    Gene-expression rescue is not proof that oral aspartate or calcium corrects human citrin deficiency.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    A related carrier can substitute for part of the missing transport function in this model.
    primary_references
    Exogenous aralar/slc25a12 can replace citrin/slc25a13 as malate aspartate shuttle component in liver. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36967723/ · DOI 10.1016/j.ymgmr.2023.100967
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 122–128

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse Slc25a13-null hepatocytes with exogenous aralar expression. · source_derived_draft · unverified_draft

    ## l-aspartate-citrin-aralar-rescue A related carrier can substitute for part of the missing transport function in this model. Exogenous aralar expression reversed the increased NADH/NAD+ ratio in hepatocytes from citrin-null mice. Model: Mouse Slc25a13-null hepatocytes with exogenous aralar expression. Limitations: Gene-expression rescue is not proof that oral aspartate or calcium corrects human citrin deficiency. Evidence access: Primary full text Exogenous aralar/slc25a12 can replace citrin/slc25a13 as malate aspartate shuttle component in liver. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36967723/ · DOI 10.1016/j.ymgmr.2023.100967
    Complete structured claim and evidence

  3. Liver-specific transgenic aralar expression increased residual shuttle activity in citrin-null mouse mitochondria by approximately 4–6 nmol per mg protein per minute.

    Mouse aralar / Slc25a12 → Malate–aspartate shuttle activity in citrin-null mouse liver source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Isolated liver mitochondria from genetically modified mice.
    limitations
    Small ex vivo flux increment; not human therapeutic efficacy.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    A measurable transport rescue did not amount to proof of complete disease correction.
    primary_references
    Exogenous aralar/slc25a12 can replace citrin/slc25a13 as malate aspartate shuttle component in liver. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36967723/ · DOI 10.1016/j.ymgmr.2023.100967
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 130–136

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Isolated liver mitochondria from genetically modified mice. · source_derived_draft · unverified_draft

    ## l-aspartate-citrin-shuttle-rescue A measurable transport rescue did not amount to proof of complete disease correction. Liver-specific transgenic aralar expression increased residual shuttle activity in citrin-null mouse mitochondria by approximately 4–6 nmol per mg protein per minute. Model: Isolated liver mitochondria from genetically modified mice. Limitations: Small ex vivo flux increment; not human therapeutic efficacy. Evidence access: Primary full text Exogenous aralar/slc25a12 can replace citrin/slc25a13 as malate aspartate shuttle component in liver. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36967723/ · DOI 10.1016/j.ymgmr.2023.100967
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Silencing either carrier had no apparent effect on the measured respiratory rates despite changes in lipid handling.

    Aralar1 or OGC silencing in mouse brown adipocytes → Respiratory rate in mouse brown adipocyte carrier-knockdown experiments source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Same mouse primary-cell experiments; respiration measurements.
    limitations
    The null result is limited to the tested conditions and does not establish that the shuttle never contributes to respiration.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    A lipid-storage phenotype did not imply that mitochondrial oxygen consumption had collapsed.
    primary_references
    The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41704162/ · DOI 10.1111/febs.70461
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 346–352

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Same mouse primary-cell experiments; respiration measurements. · source_derived_draft · unverified_draft

    ## l-aspartate-brown-respiration-limit A lipid-storage phenotype did not imply that mitochondrial oxygen consumption had collapsed. Silencing either carrier had no apparent effect on the measured respiratory rates despite changes in lipid handling. Model: Same mouse primary-cell experiments; respiration measurements. Limitations: The null result is limited to the tested conditions and does not establish that the shuttle never contributes to respiration. Evidence access: Primary full text The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41704162/ · DOI 10.1111/febs.70461
    Complete structured claim and evidence

  2. Isolated mouse brown-fat mitochondria reconstituted with cytosolic shuttle enzymes oxidized extramitochondrial NADH in a glutamate-dependent manner.

    L-Glutamate → Extramitochondrial NADH oxidation in a mouse brown-fat shuttle assay source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse C57BL/6J brown-fat mitochondria and reconstituted enzyme system.
    limitations
    An isolated-organelle assay does not prove that oral aspartate increases thermogenesis.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    The transport cycle linked a cytosolic redox pool to mitochondrial machinery.
    primary_references
    The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41704162/ · DOI 10.1111/febs.70461

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 322–328

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse C57BL/6J brown-fat mitochondria and reconstituted enzyme system. · source_derived_draft · unverified_draft

    ## l-aspartate-brown-shuttle-redox The transport cycle linked a cytosolic redox pool to mitochondrial machinery. Isolated mouse brown-fat mitochondria reconstituted with cytosolic shuttle enzymes oxidized extramitochondrial NADH in a glutamate-dependent manner. Model: Mouse C57BL/6J brown-fat mitochondria and reconstituted enzyme system. Limitations: An isolated-organelle assay does not prove that oral aspartate increases thermogenesis. Evidence access: Primary full text The malate-aspartate shuttle supports thermogenic lipid mobilization in brown adipocytes. · 2026 · https://pubmed.ncbi.nlm.nih.gov/41704162/ · DOI 10.1111/febs.70461
    Complete structured claim and evidence

  3. Absolute proteomics found citrin/aralar molar ratios of about 7.8 in mouse liver and 397 in human liver, indicating much less endogenous aralar relative to citrin in humans.

    Species-dependent liver aspartate-carrier expression → Human aralar / SLC25A12 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse and human liver quantitative proteomics.
    limitations
    Sampled expression ratios are not universal constants or proof of a clinical rescue strategy.
    nutrient_topic
    L-Aspartate collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Aspartate
    plain_language
    A mouse may compensate for a missing carrier more readily than a human.
    primary_references
    Exogenous aralar/slc25a12 can replace citrin/slc25a13 as malate aspartate shuttle component in liver. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36967723/ · DOI 10.1016/j.ymgmr.2023.100967

    L-Aspartate: redox transfer, nitrogen partitioning and cross-nutrient mechanisms (2026-09-19) · lines 138–144

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse and human liver quantitative proteomics. · source_derived_draft · unverified_draft

    ## l-aspartate-carrier-species-expression A mouse may compensate for a missing carrier more readily than a human. Absolute proteomics found citrin/aralar molar ratios of about 7.8 in mouse liver and 397 in human liver, indicating much less endogenous aralar relative to citrin in humans. Model: Mouse and human liver quantitative proteomics. Limitations: Sampled expression ratios are not universal constants or proof of a clinical rescue strategy. Evidence access: Primary full text Exogenous aralar/slc25a12 can replace citrin/slc25a13 as malate aspartate shuttle component in liver. · 2023 · https://pubmed.ncbi.nlm.nih.gov/36967723/ · DOI 10.1016/j.ymgmr.2023.100967
    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.

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