Component

Alanine-stimulated insulin secretion in BRIN-BD11 cells

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

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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. Prolonged alanine culture reduced subsequent acute alanine-stimulated insulin secretion by 74%, without reducing responses to glucose, KCl or ketoisocaproate; 18 hours without alanine partly restored responsiveness.

    L-Alanine → Alanine-stimulated insulin secretion in BRIN-BD11 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Rat BRIN-BD11 culture, washout and rechallenge experiments.
    limitations
    Exposure concentration/duration before washout are not resolved in the accessed abstract; no human chronic-use threshold is inferred.
    nutrient_topic
    L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
    plain_language
    A strong acute response need not persist after prolonged exposure.
    primary_references
    Prolonged L-alanine exposure induces changes in metabolism, Ca(2+) handling and desensitization of insulin secretion in clonal pancreatic beta-cells. · 2009 · https://pubmed.ncbi.nlm.nih.gov/18702613/ · DOI 10.1042/CS20080138

    L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 400–406

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat BRIN-BD11 culture, washout and rechallenge experiments. · source_derived_draft · unverified_draft

    ## alanine-beta-chronic-desensitization A strong acute response need not persist after prolonged exposure. Prolonged alanine culture reduced subsequent acute alanine-stimulated insulin secretion by 74%, without reducing responses to glucose, KCl or ketoisocaproate; 18 hours without alanine partly restored responsiveness. Model: Rat BRIN-BD11 culture, washout and rechallenge experiments. Limitations: Exposure concentration/duration before washout are not resolved in the accessed abstract; no human chronic-use threshold is inferred. Evidence access: Primary abstract Prolonged L-alanine exposure induces changes in metabolism, Ca(2+) handling and desensitization of insulin secretion in clonal pancreatic beta-cells. · 2009 · https://pubmed.ncbi.nlm.nih.gov/18702613/ · DOI 10.1042/CS20080138
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Prior prolonged alanine culture attenuated subsequent alanine-evoked depolarization and intracellular calcium rise in BRIN-BD11 cells.

    L-Alanine → Depolarization and calcium rise after alanine rechallenge source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Rat clonal beta-cell chronic exposure and acute rechallenge.
    limitations
    Linked measurements do not prove which upstream molecular change caused desensitization.
    nutrient_topic
    L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
    plain_language
    The weakened insulin response was accompanied by weaker electrical and calcium signals.
    primary_references
    Prolonged L-alanine exposure induces changes in metabolism, Ca(2+) handling and desensitization of insulin secretion in clonal pancreatic beta-cells. · 2009 · https://pubmed.ncbi.nlm.nih.gov/18702613/ · DOI 10.1042/CS20080138

    L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 408–414

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat clonal beta-cell chronic exposure and acute rechallenge. · source_derived_draft · unverified_draft

    ## alanine-beta-chronic-calcium The weakened insulin response was accompanied by weaker electrical and calcium signals. Prior prolonged alanine culture attenuated subsequent alanine-evoked depolarization and intracellular calcium rise in BRIN-BD11 cells. Model: Rat clonal beta-cell chronic exposure and acute rechallenge. Limitations: Linked measurements do not prove which upstream molecular change caused desensitization. Evidence access: Primary abstract Prolonged L-alanine exposure induces changes in metabolism, Ca(2+) handling and desensitization of insulin secretion in clonal pancreatic beta-cells. · 2009 · https://pubmed.ncbi.nlm.nih.gov/18702613/ · DOI 10.1042/CS20080138
    Complete structured claim and evidence

  2. Carbon-13 NMR detected alanine-derived glutamate and aspartate in BRIN-BD11 cells; oligomycin attenuated alanine-stimulated insulin secretion.

    L-Alanine → Alanine oxidative metabolism in rat BRIN-BD11 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Rat clonal BRIN-BD11 beta-cell experiments.
    limitations
    Oligomycin broadly blocks oxidative phosphorylation; this is not a selective proof of one alanine enzyme.
    nutrient_topic
    L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
    plain_language
    Oxidative metabolism contributed to the secretory response in this cell line.
    primary_references
    A nuclear magnetic resonance-based demonstration of substantial oxidative L-alanine metabolism and L-alanine-enhanced glucose metabolism in a clonal pancreatic beta-cell line: metabolism of L-alanine is important to the regulation of insulin secretion. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12031957/ · DOI 10.2337/diabetes.51.6.1714

    L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 360–366

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat clonal BRIN-BD11 beta-cell experiments. · source_derived_draft · unverified_draft

    ## alanine-beta-oxidation Oxidative metabolism contributed to the secretory response in this cell line. Carbon-13 NMR detected alanine-derived glutamate and aspartate in BRIN-BD11 cells; oligomycin attenuated alanine-stimulated insulin secretion. Model: Rat clonal BRIN-BD11 beta-cell experiments. Limitations: Oligomycin broadly blocks oxidative phosphorylation; this is not a selective proof of one alanine enzyme. Evidence access: Primary abstract A nuclear magnetic resonance-based demonstration of substantial oxidative L-alanine metabolism and L-alanine-enhanced glucose metabolism in a clonal pancreatic beta-cell line: metabolism of L-alanine is important to the regulation of insulin secretion. · 2002 · https://pubmed.ncbi.nlm.nih.gov/12031957/ · DOI 10.2337/diabetes.51.6.1714
    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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