Component

Mouse mitochondrial alanine aminotransferase / Gpt2

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. Hepatocyte-specific Gpt2 deletion reduced labeled alanine contribution to glucose production in mouse hepatocyte experiments.

    Mouse mitochondrial alanine aminotransferase / Gpt2 → Mouse hepatic glucose production from alanine source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Mouse liver Gpt2 genetic deletion; isotope tracing.
    limitations
    Does not mean GPT2 is the only route; lean knockout animals did not develop a general failure of glucose control. Correction record: Published correction adds the originally omitted disclosure that B.N.F. was a scientific advisory board member and stockholder of Cirius Therapeutics, which develops MPC inhibitors. Disclosure correction, not a data retraction. https://pmc.ncbi.nlm.nih.gov/articles/PMC9713851/
    nutrient_topic
    L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
    plain_language
    Mitochondrial transamination can feed alanine carbon into glucose.
    primary_references
    Silencing alanine transaminase 2 in diabetic liver attenuates hyperglycemia by reducing gluconeogenesis from amino acids. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35476997/ · DOI 10.1016/j.celrep.2022.110733
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 216–222

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse liver Gpt2 genetic deletion; isotope tracing. · source_derived_draft · unverified_draft

    ## alanine-liver-gpt2-flux Mitochondrial transamination can feed alanine carbon into glucose. Hepatocyte-specific Gpt2 deletion reduced labeled alanine contribution to glucose production in mouse hepatocyte experiments. Model: Mouse liver Gpt2 genetic deletion; isotope tracing. Limitations: Does not mean GPT2 is the only route; lean knockout animals did not develop a general failure of glucose control. Correction record: Published correction adds the originally omitted disclosure that B.N.F. was a scientific advisory board member and stockholder of Cirius Therapeutics, which develops MPC inhibitors. Disclosure correction, not a data retraction. https://pmc.ncbi.nlm.nih.gov/articles/PMC9713851/ Evidence access: Primary full text Silencing alanine transaminase 2 in diabetic liver attenuates hyperglycemia by reducing gluconeogenesis from amino acids. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35476997/ · DOI 10.1016/j.celrep.2022.110733
    Complete structured claim and evidence

  2. Neuron-specific Gpt2 deletion impaired alanine synthesis and metabolic replenishment and reproduced severe motor abnormalities and pre-weaning mortality.

    Mouse mitochondrial alanine aminotransferase / Gpt2 → Alanine synthesis and TCA replenishment in mouse neurons source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse neuron-specific deletion and metabolomic experiments.
    limitations
    The phenotype is not an ordinary dietary alanine deficiency.
    nutrient_topic
    L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
    plain_language
    Neurons require functioning synthesis machinery as well as available carbon and nitrogen.
    primary_references
    Mitochondrial enzyme GPT2 regulates metabolic mechanisms required for neuron growth and motor function in vivo. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34519342/ · DOI 10.1093/hmg/ddab269
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 304–310

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse neuron-specific deletion and metabolomic experiments. · source_derived_draft · unverified_draft

    ## alanine-neuron-gpt2 Neurons require functioning synthesis machinery as well as available carbon and nitrogen. Neuron-specific Gpt2 deletion impaired alanine synthesis and metabolic replenishment and reproduced severe motor abnormalities and pre-weaning mortality. Model: Mouse neuron-specific deletion and metabolomic experiments. Limitations: The phenotype is not an ordinary dietary alanine deficiency. Evidence access: Primary abstract Mitochondrial enzyme GPT2 regulates metabolic mechanisms required for neuron growth and motor function in vivo. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34519342/ · DOI 10.1093/hmg/ddab269
    Complete structured claim and evidence

What acts on it

  1. The study linked ATF4-dependent stress signaling to increased hepatic Gpt2 expression in the examined mouse ER-stress and obesity settings.

    Mouse activating transcription factor 4 / Atf4 → Mouse mitochondrial alanine aminotransferase / Gpt2 source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary full text
    experimental_model
    Mouse hepatocyte/liver interventions and expression assays.
    limitations
    Expression regulation is context-specific and does not establish a human supplementation response. Correction record: Published correction adds the originally omitted disclosure that B.N.F. was a scientific advisory board member and stockholder of Cirius Therapeutics, which develops MPC inhibitors. Disclosure correction, not a data retraction. https://pmc.ncbi.nlm.nih.gov/articles/PMC9713851/
    nutrient_topic
    L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
    plain_language
    Stress can change how much alanine-processing enzyme a liver expresses.
    primary_references
    Silencing alanine transaminase 2 in diabetic liver attenuates hyperglycemia by reducing gluconeogenesis from amino acids. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35476997/ · DOI 10.1016/j.celrep.2022.110733

    L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 224–230

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse hepatocyte/liver interventions and expression assays. · source_derived_draft · unverified_draft

    ## alanine-liver-atf4 Stress can change how much alanine-processing enzyme a liver expresses. The study linked ATF4-dependent stress signaling to increased hepatic Gpt2 expression in the examined mouse ER-stress and obesity settings. Model: Mouse hepatocyte/liver interventions and expression assays. Limitations: Expression regulation is context-specific and does not establish a human supplementation response. Correction record: Published correction adds the originally omitted disclosure that B.N.F. was a scientific advisory board member and stockholder of Cirius Therapeutics, which develops MPC inhibitors. Disclosure correction, not a data retraction. https://pmc.ncbi.nlm.nih.gov/articles/PMC9713851/ Evidence access: Primary full text Silencing alanine transaminase 2 in diabetic liver attenuates hyperglycemia by reducing gluconeogenesis from amino acids. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35476997/ · DOI 10.1016/j.celrep.2022.110733
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Hepatic Gpt2 suppression improved hyperglycemia in db/db mice, whereas liver-specific loss in lean mice did not similarly alter ordinary blood glucose.

    Hepatic Gpt2 suppression in mice → Hyperglycemia in db/db mice source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary full text
    experimental_model
    Diabetic and lean mouse genetic experiments.
    limitations
    Not a demonstrated human diabetes treatment; compensatory pathways remain. Correction record: Published correction adds the originally omitted disclosure that B.N.F. was a scientific advisory board member and stockholder of Cirius Therapeutics, which develops MPC inhibitors. Disclosure correction, not a data retraction. https://pmc.ncbi.nlm.nih.gov/articles/PMC9713851/
    nutrient_topic
    L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
    plain_language
    The consequence of blocking one pathway depended on metabolic state.
    primary_references
    Silencing alanine transaminase 2 in diabetic liver attenuates hyperglycemia by reducing gluconeogenesis from amino acids. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35476997/ · DOI 10.1016/j.celrep.2022.110733
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 232–238

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Diabetic and lean mouse genetic experiments. · source_derived_draft · unverified_draft

    ## alanine-liver-diabetes-context The consequence of blocking one pathway depended on metabolic state. Hepatic Gpt2 suppression improved hyperglycemia in db/db mice, whereas liver-specific loss in lean mice did not similarly alter ordinary blood glucose. Model: Diabetic and lean mouse genetic experiments. Limitations: Not a demonstrated human diabetes treatment; compensatory pathways remain. Correction record: Published correction adds the originally omitted disclosure that B.N.F. was a scientific advisory board member and stockholder of Cirius Therapeutics, which develops MPC inhibitors. Disclosure correction, not a data retraction. https://pmc.ncbi.nlm.nih.gov/articles/PMC9713851/ Evidence access: Primary full text Silencing alanine transaminase 2 in diabetic liver attenuates hyperglycemia by reducing gluconeogenesis from amino acids. · 2022 · https://pubmed.ncbi.nlm.nih.gov/35476997/ · DOI 10.1016/j.celrep.2022.110733
    Complete structured claim and evidence

  2. Exogenous alanine was necessary for survival of Gpt2-null neurons in culture, while Gpt2-null astrocytes did not show the same requirement.

    L-Alanine → Survival of Gpt2-null mouse neurons source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Mouse neuron and astrocyte cultures with Gpt2 loss.
    limitations
    Culture survival rescue is not proof of full neurological recovery.
    nutrient_topic
    L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
    plain_language
    Different brain cell types had different needs after the same enzyme loss.
    primary_references
    Mitochondrial enzyme GPT2 regulates metabolic mechanisms required for neuron growth and motor function in vivo. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34519342/ · DOI 10.1093/hmg/ddab269
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 312–318

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse neuron and astrocyte cultures with Gpt2 loss. · source_derived_draft · unverified_draft

    ## alanine-neuron-alanine-rescue Different brain cell types had different needs after the same enzyme loss. Exogenous alanine was necessary for survival of Gpt2-null neurons in culture, while Gpt2-null astrocytes did not show the same requirement. Model: Mouse neuron and astrocyte cultures with Gpt2 loss. Limitations: Culture survival rescue is not proof of full neurological recovery. Evidence access: Primary abstract Mitochondrial enzyme GPT2 regulates metabolic mechanisms required for neuron growth and motor function in vivo. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34519342/ · DOI 10.1093/hmg/ddab269
    Complete structured claim and evidence

  3. Dietary alanine supplementation improved survival and brain metabolic profiles in Gpt2-null mice but did not alone appear to correct motor function.

    L-Alanine → Survival and motor outcomes in Gpt2-null mice source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_access
    Primary abstract
    experimental_model
    Gpt2-null mouse dietary intervention.
    limitations
    No validated human treatment or dose follows; survival and motor outcomes are separate.
    nutrient_topic
    L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
    plain_language
    Restoring a metabolite helped some outcomes while leaving major problems unresolved.
    primary_references
    Mitochondrial enzyme GPT2 regulates metabolic mechanisms required for neuron growth and motor function in vivo. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34519342/ · DOI 10.1093/hmg/ddab269
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 320–326

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Gpt2-null mouse dietary intervention. · source_derived_draft · unverified_draft

    ## alanine-neuron-diet-limits Restoring a metabolite helped some outcomes while leaving major problems unresolved. Dietary alanine supplementation improved survival and brain metabolic profiles in Gpt2-null mice but did not alone appear to correct motor function. Model: Gpt2-null mouse dietary intervention. Limitations: No validated human treatment or dose follows; survival and motor outcomes are separate. Evidence access: Primary abstract Mitochondrial enzyme GPT2 regulates metabolic mechanisms required for neuron growth and motor function in vivo. · 2022 · https://pubmed.ncbi.nlm.nih.gov/34519342/ · DOI 10.1093/hmg/ddab269
    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