Component

Human liver kinase B1 / STK11

Human liver kinase B1 / STK11. Species, exposure and limitations are retained in each linked 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. Deletion of LKB1 in adult mouse liver resulted in a nearly complete loss of AMPK activity, with hyperglycaemia and increased gluconeogenic and lipogenic gene expression.

    Human liver kinase B1 / STK11 → AMP-activated protein kinase complexes source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/metformin-research/16308421.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e4762199db357f0f8002a9da8ff2ecad8e9bfcb48c963eb4b2cde7ffa363eec4", "start_char": 0, "end_char": 1103, "text_sha256": "e4762199db357f0f8002a9da8ff2ecad8e9bfcb48c963eb4b2cde7ffa363eec4"}
    experimental_model
    Liver-specific LKB1 deletion in adult mice with adenoviral TORC2 knockdown
    exposure
    Metformin in LKB1-deficient livers
    limitations
    A genetic requirement in this model. The same year’s consensus was later challenged by AMPK-independent findings recorded in this collection.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Mouse
    plain_language
    The upstream kinase is what turns the energy sensor on in the liver.
    primary_references
    [metformin-p16308421] The kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin. (2005). https://pubmed.ncbi.nlm.nih.gov/16308421/ DOI: 10.1126/science.1120781
    tissue_or_cell_type
    Liver

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 567–578

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Liver-specific LKB1 deletion in adult mice with adenoviral TORC2 knockdown · source_derived_draft · unverified_draft

    ### metformin-lkb1-ampk-axis Deletion of LKB1 in adult mouse liver resulted in a nearly complete loss of AMPK activity, with hyperglycaemia and increased gluconeogenic and lipogenic gene expression. Condition category: normal nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: The upstream kinase is what turns the energy sensor on in the liver. organism: Mouse tissue_or_cell_type: Liver experimental_model: Liver-specific LKB1 deletion in adult mice with adenoviral TORC2 knockdown limitations: A genetic requirement in this model. The same year’s consensus was later challenged by AMPK-independent findings recorded in this collection. exposure: Metformin in LKB1-deficient livers evidence_span: {"source_cache": "artifacts/metformin-research/16308421.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e4762199db357f0f8002a9da8ff2ecad8e9bfcb48c963eb4b2cde7ffa363eec4", "start_char": 0, "end_char": 1103, "text_sha256": "e4762199db357f0f8002a9da8ff2ecad8e9bfcb48c963eb4b2cde7ffa363eec4"} [metformin-p16308421] The kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin. (2005). https://pubmed.ncbi.nlm.nih.gov/16308421/ DOI: 10.1126/science.1120781
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. LKB1 knockdown prevented the norathyriol-associated increase in ACC phosphorylation.

    Experimental human STK11 / LKB1 siRNA knockdown → Human acetyl-CoA carboxylase activity, isoform unresolved in assay source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"}
    experimental_model
    KK-Ay mouse liver experiments and mechanistic HepG2 studies
    exposure
    Norathyriol in sodium-oleate lipid-loading model; micromolar range
    limitations
    Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim.
    nutrient_topic
    Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
    organism
    Homo sapiens for HepG2 experiments; mouse findings separately scoped
    plain_language
    Removing an upstream component interrupted the response.
    primary_references
    [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
    tissue_or_cell_type
    HepG2 cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 510–521

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KK-Ay mouse liver experiments and mechanistic HepG2 studies · source_derived_draft · unverified_draft

    ### mangiferin-lkb1-acc LKB1 knockdown prevented the norathyriol-associated increase in ACC phosphorylation. Condition category: machinery_impairment nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing an upstream component interrupted the response. organism: Homo sapiens for HepG2 experiments; mouse findings separately scoped tissue_or_cell_type: HepG2 cells experimental_model: KK-Ay mouse liver experiments and mechanistic HepG2 studies limitations: Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim. exposure: Norathyriol in sodium-oleate lipid-loading model; micromolar range evidence_span: {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"} [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
    Complete structured claim and evidence

  2. Norathyriol lowered measured LKB1 acetylation in HepG2 cells.

    Norathyriol → Human LKB1 acetylation in HepG2 cells source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 35295, "end_char": 36269, "text_sha256": "4b69cb6e7f09043eda3312b226bc03bbf8e0cbf25a4f6b51505c0aebed3b7d04"}
    experimental_model
    KK-Ay mouse liver experiments and mechanistic HepG2 studies
    exposure
    Norathyriol in sodium-oleate lipid-loading model; micromolar range
    limitations
    Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim.
    nutrient_topic
    Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
    organism
    Homo sapiens for HepG2 experiments; mouse findings separately scoped
    plain_language
    A chemical modification of an upstream kinase changed.
    primary_references
    [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
    tissue_or_cell_type
    HepG2 cells

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 458–469

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KK-Ay mouse liver experiments and mechanistic HepG2 studies · source_derived_draft · unverified_draft

    ### mangiferin-lkb1-acetylation Norathyriol lowered measured LKB1 acetylation in HepG2 cells. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A chemical modification of an upstream kinase changed. organism: Homo sapiens for HepG2 experiments; mouse findings separately scoped tissue_or_cell_type: HepG2 cells experimental_model: KK-Ay mouse liver experiments and mechanistic HepG2 studies limitations: Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim. exposure: Norathyriol in sodium-oleate lipid-loading model; micromolar range evidence_span: {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 35295, "end_char": 36269, "text_sha256": "4b69cb6e7f09043eda3312b226bc03bbf8e0cbf25a4f6b51505c0aebed3b7d04"} [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
    Complete structured claim and evidence

  3. LKB1 knockdown prevented the norathyriol-associated increase in AMPK phosphorylation.

    Experimental human STK11 / LKB1 siRNA knockdown → Human AMP-activated protein kinase complexes source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"}
    experimental_model
    KK-Ay mouse liver experiments and mechanistic HepG2 studies
    exposure
    Norathyriol in sodium-oleate lipid-loading model; micromolar range
    limitations
    Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim.
    nutrient_topic
    Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
    organism
    Homo sapiens for HepG2 experiments; mouse findings separately scoped
    plain_language
    Removing an upstream component interrupted the response.
    primary_references
    [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
    tissue_or_cell_type
    HepG2 cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 497–508

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KK-Ay mouse liver experiments and mechanistic HepG2 studies · source_derived_draft · unverified_draft

    ### mangiferin-lkb1-ampk LKB1 knockdown prevented the norathyriol-associated increase in AMPK phosphorylation. Condition category: machinery_impairment nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing an upstream component interrupted the response. organism: Homo sapiens for HepG2 experiments; mouse findings separately scoped tissue_or_cell_type: HepG2 cells experimental_model: KK-Ay mouse liver experiments and mechanistic HepG2 studies limitations: Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim. exposure: Norathyriol in sodium-oleate lipid-loading model; micromolar range evidence_span: {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"} [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
    Complete structured claim and evidence

  4. LKB1 knockdown blocked the triglyceride-lowering response to norathyriol.

    Experimental human STK11 / LKB1 siRNA knockdown → Triglyceride accumulation in human HepG2 cells source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"}
    experimental_model
    KK-Ay mouse liver experiments and mechanistic HepG2 studies
    exposure
    Norathyriol in sodium-oleate lipid-loading model; micromolar range
    limitations
    Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim.
    nutrient_topic
    Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
    organism
    Homo sapiens for HepG2 experiments; mouse findings separately scoped
    plain_language
    Removing an upstream component interrupted the response.
    primary_references
    [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
    tissue_or_cell_type
    HepG2 cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 484–495

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · KK-Ay mouse liver experiments and mechanistic HepG2 studies · source_derived_draft · unverified_draft

    ### mangiferin-lkb1-tg LKB1 knockdown blocked the triglyceride-lowering response to norathyriol. Condition category: machinery_impairment nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Removing an upstream component interrupted the response. organism: Homo sapiens for HepG2 experiments; mouse findings separately scoped tissue_or_cell_type: HepG2 cells experimental_model: KK-Ay mouse liver experiments and mechanistic HepG2 studies limitations: Phosphorylation and expression are scoped to experiments; no established human fatty-liver therapy or direct SIRT1 ligand claim. exposure: Norathyriol in sodium-oleate lipid-loading model; micromolar range evidence_span: {"source_cache": "artifacts/mangiferin-research/29563875.fulltext.txt", "locator": "Primary full-text span; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a48a1f92d67cd91638969bb1ec3cb9f18cb3cb4e29c7e5f2bacf627dda76415", "start_char": 33073, "end_char": 35334, "text_sha256": "166efaa83fd229a3e036a60bf4e23173a7b50a3044686fe1a324d6dc604354a9"} [mangiferin-p29563875] Mangiferin Improves Hepatic Lipid Metabolism Mainly Through Its Metabolite-Norathyriol by Modulating SIRT-1/AMPK/SREBP-1c Signaling. (2018). https://pubmed.ncbi.nlm.nih.gov/29563875/ DOI: 10.3389/fphar.2018.00201
    Complete structured claim and evidence

  5. Metformin required LKB1 in the liver to lower blood glucose levels in these mice.

    Liver-specific LKB1-deficient mouse hepatocytes in the 2010 and 2005 studies → Serum glucose concentration source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/metformin-research/16308421.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e4762199db357f0f8002a9da8ff2ecad8e9bfcb48c963eb4b2cde7ffa363eec4", "start_char": 0, "end_char": 1103, "text_sha256": "e4762199db357f0f8002a9da8ff2ecad8e9bfcb48c963eb4b2cde7ffa363eec4"}
    experimental_model
    Liver-specific LKB1 deletion in adult mice with adenoviral TORC2 knockdown
    exposure
    Metformin in LKB1-deficient livers
    limitations
    A genetic requirement in this model. The same year’s consensus was later challenged by AMPK-independent findings recorded in this collection.
    nutrient_topic
    Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
    organism
    Mouse
    plain_language
    Without the upstream kinase, the drug did not lower glucose in this model.
    primary_references
    [metformin-p16308421] The kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin. (2005). https://pubmed.ncbi.nlm.nih.gov/16308421/ DOI: 10.1126/science.1120781
    tissue_or_cell_type
    Liver
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 580–591

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Liver-specific LKB1 deletion in adult mice with adenoviral TORC2 knockdown · source_derived_draft · unverified_draft

    ### metformin-lkb1-required-metformin Metformin required LKB1 in the liver to lower blood glucose levels in these mice. Condition category: machinery_impairment nutrient_topic: Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. plain_language: Without the upstream kinase, the drug did not lower glucose in this model. organism: Mouse tissue_or_cell_type: Liver experimental_model: Liver-specific LKB1 deletion in adult mice with adenoviral TORC2 knockdown limitations: A genetic requirement in this model. The same year’s consensus was later challenged by AMPK-independent findings recorded in this collection. exposure: Metformin in LKB1-deficient livers evidence_span: {"source_cache": "artifacts/metformin-research/16308421.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "e4762199db357f0f8002a9da8ff2ecad8e9bfcb48c963eb4b2cde7ffa363eec4", "start_char": 0, "end_char": 1103, "text_sha256": "e4762199db357f0f8002a9da8ff2ecad8e9bfcb48c963eb4b2cde7ffa363eec4"} [metformin-p16308421] The kinase LKB1 mediates glucose homeostasis in liver and therapeutic effects of metformin. (2005). https://pubmed.ncbi.nlm.nih.gov/16308421/ DOI: 10.1126/science.1120781
    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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