Component

Cellular glucose consumption

Cellular glucose consumption. Species, exposure and limitations are retained in each linked claim.

2 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. Berberine still increased glucose utilization after AMPK inhibition, AMPK-alpha silencing or dominant-negative AMPK expression.

    Berberine → Cellular glucose consumption source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/berberine-research/25072399.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aa8c67580ab0a69c335873a80e94bbe418ac93b88bcad42c72e1eeb564ff828a", "start_char": 0, "end_char": 1385, "text_sha256": "aa8c67580ab0a69c335873a80e94bbe418ac93b88bcad42c72e1eeb564ff828a"}
    experimental_model
    Pharmacological inhibition, siRNA and dominant-negative AMPK experiments
    exposure
    Berberine concentration-response; 20 micromolar in phosphorylation experiments
    limitations
    AMPK is not necessary for every glucose response. This does not show that all other berberine actions are AMPK-independent; cell concentrations may exceed circulating parent drug.
    nutrient_topic
    Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
    organism
    Human HepG2 hepatocytes and mouse C2C12 myotubes
    plain_language
    Cells can use more glucose even when this proposed signaling route is blocked.
    primary_references
    [berberine-p25072399] Berberine promotes glucose consumption independently of AMP-activated protein kinase activation. (2014). https://pubmed.ncbi.nlm.nih.gov/25072399/ DOI: 10.1371/journal.pone.0103702
    tissue_or_cell_type
    Glucose consumption, lactate release and mitochondrial respiration

    Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 350–361

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Pharmacological inhibition, siRNA and dominant-negative AMPK experiments · source_derived_draft · unverified_draft

    ### berberine-ampk-independent-glucose Berberine still increased glucose utilization after AMPK inhibition, AMPK-alpha silencing or dominant-negative AMPK expression. Condition category: normal nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Cells can use more glucose even when this proposed signaling route is blocked. organism: Human HepG2 hepatocytes and mouse C2C12 myotubes tissue_or_cell_type: Glucose consumption, lactate release and mitochondrial respiration experimental_model: Pharmacological inhibition, siRNA and dominant-negative AMPK experiments limitations: AMPK is not necessary for every glucose response. This does not show that all other berberine actions are AMPK-independent; cell concentrations may exceed circulating parent drug. exposure: Berberine concentration-response; 20 micromolar in phosphorylation experiments evidence_span: {"source_cache": "artifacts/berberine-research/25072399.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "aa8c67580ab0a69c335873a80e94bbe418ac93b88bcad42c72e1eeb564ff828a", "start_char": 0, "end_char": 1385, "text_sha256": "aa8c67580ab0a69c335873a80e94bbe418ac93b88bcad42c72e1eeb564ff828a"} [berberine-p25072399] Berberine promotes glucose consumption independently of AMP-activated protein kinase activation. (2014). https://pubmed.ncbi.nlm.nih.gov/25072399/ DOI: 10.1371/journal.pone.0103702
    Complete structured claim and evidence

  2. INSR silencing diminished the insulin-dependent increase in glucose consumption associated with berberine-enhanced receptor expression.

    Insulin receptor / INSR → Cellular glucose consumption source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/berberine-research/19059538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23", "start_char": 0, "end_char": 1461, "text_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23"}
    experimental_model
    Promoter assays, gene silencing and insulin-dependence experiments
    exposure
    Berberine with or without insulin, INSR siRNA or PKC inhibition
    limitations
    This insulin-dependent route does not replace insulin in insulin-deficient disease. Other models show insulin-independent routes; those observations are not discarded.
    nutrient_topic
    Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
    organism
    Human liver cells and separate rodent experiments
    plain_language
    A sensitizing signal cannot substitute for missing receptor machinery.
    primary_references
    [berberine-p19059538] Berberine reduces insulin resistance through protein kinase C-dependent up-regulation of insulin receptor expression. (2009). https://pubmed.ncbi.nlm.nih.gov/19059538/ DOI: 10.1016/j.metabol.2008.08.013
    tissue_or_cell_type
    Insulin receptor expression and glucose consumption
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 506–517

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Promoter assays, gene silencing and insulin-dependence experiments · source_derived_draft · unverified_draft

    ### berberine-insr-loss INSR silencing diminished the insulin-dependent increase in glucose consumption associated with berberine-enhanced receptor expression. Condition category: machinery_impairment nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sensitizing signal cannot substitute for missing receptor machinery. organism: Human liver cells and separate rodent experiments tissue_or_cell_type: Insulin receptor expression and glucose consumption experimental_model: Promoter assays, gene silencing and insulin-dependence experiments limitations: This insulin-dependent route does not replace insulin in insulin-deficient disease. Other models show insulin-independent routes; those observations are not discarded. exposure: Berberine with or without insulin, INSR siRNA or PKC inhibition evidence_span: {"source_cache": "artifacts/berberine-research/19059538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23", "start_char": 0, "end_char": 1461, "text_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23"} [berberine-p19059538] Berberine reduces insulin resistance through protein kinase C-dependent up-regulation of insulin receptor expression. (2009). https://pubmed.ncbi.nlm.nih.gov/19059538/ DOI: 10.1016/j.metabol.2008.08.013
    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