Component
Rat AMP-activated protein kinase complexes
Rat AMP-activated protein kinase complexes. Species, exposure and limitations are retained in each linked claim.
10 recorded relationships. Experimental role, claim status and evidence remain attached to each record.
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.
Other things that act on it
Enzymes, hormones, genes, and other components with a recorded effect. These are not nutrients, so they do not count toward the arrows above. Each finding names the chapter that recorded it.
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.
What it acts on
AMPK silencing abolished chromium picolinate’s protection against impaired GLUT4 regulation in hyperinsulinemic L6 myotubes.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"}
- experimental_model
- Hyperinsulinemia model with AMPK silencing
- exposure
- Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA
- limitations
- Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment.
- nutrient_topic
- Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
- organism
- Rat L6 skeletal muscle myotubes
- plain_language
- When AMPK was depleted, this transporter response to chromium picolinate was lost.
- primary_references
- [chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
- tissue_or_cell_type
- Cultured muscle plasma membrane and cortical actin
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 393–404
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hyperinsulinemia model with AMPK silencing · source_derived_draft · unverified_draft
### chromium-ampk-required-glut4 AMPK silencing abolished chromium picolinate’s protection against impaired GLUT4 regulation in hyperinsulinemic L6 myotubes. Condition category: machinery_impairment nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: When AMPK was depleted, this transporter response to chromium picolinate was lost. organism: Rat L6 skeletal muscle myotubes tissue_or_cell_type: Cultured muscle plasma membrane and cortical actin experimental_model: Hyperinsulinemia model with AMPK silencing limitations: Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment. exposure: Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA evidence_span: {"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"} [chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
Complete structured claim and evidenceAMPK silencing abolished chromium picolinate’s protection against impaired glucose transport in the same L6 model.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"}
- experimental_model
- Hyperinsulinemia model with AMPK silencing
- exposure
- Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA
- limitations
- Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment.
- nutrient_topic
- Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
- organism
- Rat L6 skeletal muscle myotubes
- plain_language
- The glucose-uptake benefit also depended on AMPK in this experiment.
- primary_references
- [chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
- tissue_or_cell_type
- Cultured muscle plasma membrane and cortical actin
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 406–417
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hyperinsulinemia model with AMPK silencing · source_derived_draft · unverified_draft
### chromium-ampk-required-uptake AMPK silencing abolished chromium picolinate’s protection against impaired glucose transport in the same L6 model. Condition category: machinery_impairment nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The glucose-uptake benefit also depended on AMPK in this experiment. organism: Rat L6 skeletal muscle myotubes tissue_or_cell_type: Cultured muscle plasma membrane and cortical actin experimental_model: Hyperinsulinemia model with AMPK silencing limitations: Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment. exposure: Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA evidence_span: {"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"} [chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
Complete structured claim and evidence
What acts on it
CGA increased AMPK phosphorylation and measured AMPK activity in L6 myotubes.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/chlorogenic_acid-research/22412912.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77c1ccf86d3fb56135a01d2d80b9f1eec3d657e825789f8be490fff93feb8fff", "start_char": 0, "end_char": 1896, "text_sha256": "77c1ccf86d3fb56135a01d2d80b9f1eec3d657e825789f8be490fff93feb8fff"}
- experimental_model
- L6 myotube signaling with siRNA and pharmacological tests; db/db mouse experiments
- exposure
- L6 experiments included 2 mmol/L CGA; mouse acute intervention 250 mg/kg intraperitoneally
- limitations
- Millimolar culture exposure and injected mouse doses are not dietary human exposures. Phosphorylation and abundance readouts do not by themselves prove every upstream causal step.
- nutrient_topic
- Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. · Chlorogenic acid / 5-O-caffeoylquinic acid
- organism
- Rattus norvegicus
- plain_language
- A cellular energy-sensing pathway responded in cultured rat muscle.
- primary_references
- [chlorogenic_acid-p22412912] Chlorogenic acid stimulates glucose transport in skeletal muscle via AMPK activation: a contributor to the beneficial effects of coffee on diabetes. (2012). https://pubmed.ncbi.nlm.nih.gov/22412912/ DOI: 10.1371/journal.pone.0032718
- tissue_or_cell_type
- L6 skeletal-muscle myotubes
Chlorogenic acid: metabolism, signaling and nutrient connections (2026-09-17) · lines 412–423
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · L6 myotube signaling with siRNA and pharmacological tests; db/db mouse experiments · source_derived_draft · unverified_draft
### chlorogenic_acid-ampk-activation CGA increased AMPK phosphorylation and measured AMPK activity in L6 myotubes. Condition category: normal nutrient_topic: Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: A cellular energy-sensing pathway responded in cultured rat muscle. organism: Rattus norvegicus tissue_or_cell_type: L6 skeletal-muscle myotubes experimental_model: L6 myotube signaling with siRNA and pharmacological tests; db/db mouse experiments limitations: Millimolar culture exposure and injected mouse doses are not dietary human exposures. Phosphorylation and abundance readouts do not by themselves prove every upstream causal step. exposure: L6 experiments included 2 mmol/L CGA; mouse acute intervention 250 mg/kg intraperitoneally evidence_span: {"source_cache": "artifacts/chlorogenic_acid-research/22412912.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77c1ccf86d3fb56135a01d2d80b9f1eec3d657e825789f8be490fff93feb8fff", "start_char": 0, "end_char": 1896, "text_sha256": "77c1ccf86d3fb56135a01d2d80b9f1eec3d657e825789f8be490fff93feb8fff"} [chlorogenic_acid-p22412912] Chlorogenic acid stimulates glucose transport in skeletal muscle via AMPK activation: a contributor to the beneficial effects of coffee on diabetes. (2012). https://pubmed.ncbi.nlm.nih.gov/22412912/ DOI: 10.1371/journal.pone.0032718
Complete structured claim and evidenceMangiferin increased AMPK phosphorylation in L6 myotubes.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"}
- experimental_model
- Normal and insulin-resistant L6 myotube comparison
- exposure
- Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin
- limitations
- Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering.
- nutrient_topic
- Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
- organism
- Rattus norvegicus
- plain_language
- The energy-sensing pathway responded in this cell model.
- primary_references
- [mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
- tissue_or_cell_type
- L6 myotubes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 379–390
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Normal and insulin-resistant L6 myotube comparison · source_derived_draft · unverified_draft
### mangiferin-mangiferin-ampk Mangiferin increased AMPK phosphorylation in L6 myotubes. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The energy-sensing pathway responded in this cell model. organism: Rattus norvegicus tissue_or_cell_type: L6 myotubes experimental_model: Normal and insulin-resistant L6 myotube comparison limitations: Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering. exposure: Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin evidence_span: {"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"} [mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
Complete structured claim and evidenceNorathyriol increased AMPK phosphorylation in L6 myotubes.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"}
- experimental_model
- Normal and insulin-resistant L6 myotube comparison
- exposure
- Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin
- limitations
- Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering.
- nutrient_topic
- Mangiferin research collection; topical membership is not evidence of a direct dietary effect. · Mangiferin
- organism
- Rattus norvegicus
- plain_language
- The energy-sensing pathway responded in this cell model.
- primary_references
- [mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
- tissue_or_cell_type
- L6 myotubes
Mangiferin: metabolism, signaling and nutrient connections (2026-09-17) · lines 392–403
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Normal and insulin-resistant L6 myotube comparison · source_derived_draft · unverified_draft
### mangiferin-norathyriol-ampk Norathyriol increased AMPK phosphorylation in L6 myotubes. Condition category: normal nutrient_topic: Mangiferin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The energy-sensing pathway responded in this cell model. organism: Rattus norvegicus tissue_or_cell_type: L6 myotubes experimental_model: Normal and insulin-resistant L6 myotube comparison limitations: Cell glucose consumption and phosphorylation assays; AMPK association alone does not prove direct binding or human glucose lowering. exposure: Micromolar mangiferin or norathyriol, with or without 0.05 nM insulin evidence_span: {"source_cache": "artifacts/mangiferin-research/24033319.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a", "start_char": 0, "end_char": 1791, "text_sha256": "9e8f13eba529ca6e56c33c3cee21d8fef473025e4bea72d81b375c96031ee84a"} [mangiferin-p24033319] Mangiferin and its aglycone, norathyriol, improve glucose metabolism by activation of AMP-activated protein kinase. (2014). https://pubmed.ncbi.nlm.nih.gov/24033319/ DOI: 10.3109/13880209.2013.814691
Complete structured claim and evidenceChromium picolinate increased AMPK signaling in L6 myotubes without enhancing the proximal insulin-signaling responses measured in that experiment.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"}
- experimental_model
- Hyperinsulinemia model with AMPK silencing
- exposure
- Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA
- limitations
- Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment.
- nutrient_topic
- Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium
- organism
- Rat L6 skeletal muscle myotubes
- plain_language
- The response involved the cell’s energy-sensing pathway rather than a measured increase in proximal insulin signaling.
- primary_references
- [chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
- tissue_or_cell_type
- Cultured muscle plasma membrane and cortical actin
Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 354–365
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Hyperinsulinemia model with AMPK silencing · source_derived_draft · unverified_draft
### chromium-ampk-response Chromium picolinate increased AMPK signaling in L6 myotubes without enhancing the proximal insulin-signaling responses measured in that experiment. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response involved the cell’s energy-sensing pathway rather than a measured increase in proximal insulin signaling. organism: Rat L6 skeletal muscle myotubes tissue_or_cell_type: Cultured muscle plasma membrane and cortical actin experimental_model: Hyperinsulinemia model with AMPK silencing limitations: Cell-culture mechanism. The indexed abstract identifies AMPK depletion without resolving the targeted catalytic isoform; family-level identity is retained. This is not a dietary repletion or human treatment experiment. exposure: Chromium picolinate during chronic low-dose insulin exposure, followed by acute insulin response; AMPK siRNA evidence_span: {"source_cache": "artifacts/chromium-research/24725432.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4", "start_char": 0, "end_char": 1788, "text_sha256": "f172a147ded27e509e27d5bcc53ad6dc3e8b22b424ab021515b205ae29bccbc4"} [chromium-p24725432] Chromium enhances insulin responsiveness via AMPK. (2014). https://pubmed.ncbi.nlm.nih.gov/24725432/ DOI: 10.1016/j.jnutbio.2014.01.007
Complete structured claim and evidenceBerberine increased AMPK phosphorylation in L6 myotubes.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/berberine-research/18285556.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cd721d78117d554be4fdb0403ac792f6723cf59cfd3679106607e8f17eafc257", "start_char": 0, "end_char": 1735, "text_sha256": "cd721d78117d554be4fdb0403ac792f6723cf59cfd3679106607e8f17eafc257"}
- experimental_model
- Cell respiration, isolated mitochondria and kinase perturbation
- exposure
- Berberine concentration-response; kinase deletion/inhibition
- limitations
- Functional respiratory inhibition does not by itself establish direct binding to complex I or improved mitochondrial health. Preclinical exposure, not human efficacy.
- nutrient_topic
- Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
- organism
- Rat L6 myotubes, muscle mitochondria and LKB1-deficient cells
- plain_language
- AMPK responds to the altered cellular energy state in this model.
- primary_references
- [berberine-p18285556] Berberine and its more biologically available derivative, dihydroberberine, inhibit mitochondrial respiratory complex I: a mechanism for the action of berberine to activate AMP-activated protein kinase and improve insulin action. (2008). https://pubmed.ncbi.nlm.nih.gov/18285556/ DOI: 10.2337/db07-1552
- tissue_or_cell_type
- Respiratory complex I and AMPK
Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 337–348
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cell respiration, isolated mitochondria and kinase perturbation · source_derived_draft · unverified_draft
### berberine-ampk Berberine increased AMPK phosphorylation in L6 myotubes. Condition category: normal nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: AMPK responds to the altered cellular energy state in this model. organism: Rat L6 myotubes, muscle mitochondria and LKB1-deficient cells tissue_or_cell_type: Respiratory complex I and AMPK experimental_model: Cell respiration, isolated mitochondria and kinase perturbation limitations: Functional respiratory inhibition does not by itself establish direct binding to complex I or improved mitochondrial health. Preclinical exposure, not human efficacy. exposure: Berberine concentration-response; kinase deletion/inhibition evidence_span: {"source_cache": "artifacts/berberine-research/18285556.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "cd721d78117d554be4fdb0403ac792f6723cf59cfd3679106607e8f17eafc257", "start_char": 0, "end_char": 1735, "text_sha256": "cd721d78117d554be4fdb0403ac792f6723cf59cfd3679106607e8f17eafc257"} [berberine-p18285556] Berberine and its more biologically available derivative, dihydroberberine, inhibit mitochondrial respiratory complex I: a mechanism for the action of berberine to activate AMP-activated protein kinase and improve insulin action. (2008). https://pubmed.ncbi.nlm.nih.gov/18285556/ DOI: 10.2337/db07-1552
Complete structured claim and evidenceAdding (S)-6-gingerol increased AMPK alpha Thr172 phosphorylation in rat L6 cells, with CaMKK-associated signaling.
Experimental context and source evidence
- dose
- (S)-6-Gingerol; dose-response, exact range not in accessed abstract
- duration
- Time-dependent response; exact times not in accessed abstract
- evidence_access
- Primary PubMed abstract.
- evidence_scope
- literature_reviewed; model-specific source-derived curation, not universally established human effects
- experimental_model
- Rat L6 skeletal muscle myotubes
- limitations
- Calcium/CaMKK-associated signaling does not demonstrate dietary calcium depletion or calcium-supplement synergy; no human glycemic outcome was tested. The accessed abstract does not identify a CaMKK isoform or establish genetic necessity.
- nutrient_topic
- Gingerols collection; each molecular form and experimental preparation remains explicit. · Gingerols
- organism
- Rat L6 skeletal muscle myotubes
- plain_language
- Adding (S)-6-gingerol increased AMPK alpha Thr172 phosphorylation in rat L6 cells, with CaMKK-associated signaling.
- primary_references
- (S)-[6]-Gingerol enhances glucose uptake in L6 myotubes by activation of AMPK in response to [Ca2+]i. (2013). https://pubmed.ncbi.nlm.nih.gov/23958199/ DOI: 10.18433/j34g7p
- route
- In vitro addition
- tissue
- Skeletal muscle cell model
Gingerols: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 162–171
Original AI-assisted curation of thirteen primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Rat L6 skeletal muscle myotubes · source_derived_draft · unverified_draft
## gingerols-6-l6-ampk Adding (S)-6-gingerol increased AMPK alpha Thr172 phosphorylation in rat L6 cells, with CaMKK-associated signaling. Model/species: Rat L6 skeletal muscle myotubes Tissue: Skeletal muscle cell model Exposure: (S)-6-Gingerol; dose-response, exact range not in accessed abstract Route: In vitro addition Duration: Time-dependent response; exact times not in accessed abstract Limits: Calcium/CaMKK-associated signaling does not demonstrate dietary calcium depletion or calcium-supplement synergy; no human glycemic outcome was tested. The accessed abstract does not identify a CaMKK isoform or establish genetic necessity. Primary reference: (S)-[6]-Gingerol enhances glucose uptake in L6 myotubes by activation of AMPK in response to [Ca2+]i. (2013). https://pubmed.ncbi.nlm.nih.gov/23958199/ DOI: 10.18433/j34g7p Access: Primary PubMed abstract.
Complete structured claim and evidence
Where it participates (unsigned role)
AMPK alpha1/alpha2 knockdown abrogated CGA-stimulated glucose transport.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_span
- {"source_cache": "artifacts/chlorogenic_acid-research/22412912.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77c1ccf86d3fb56135a01d2d80b9f1eec3d657e825789f8be490fff93feb8fff", "start_char": 0, "end_char": 1896, "text_sha256": "77c1ccf86d3fb56135a01d2d80b9f1eec3d657e825789f8be490fff93feb8fff"}
- experimental_model
- L6 myotube signaling with siRNA and pharmacological tests; db/db mouse experiments
- exposure
- L6 experiments included 2 mmol/L CGA; mouse acute intervention 250 mg/kg intraperitoneally
- limitations
- Millimolar culture exposure and injected mouse doses are not dietary human exposures. Phosphorylation and abundance readouts do not by themselves prove every upstream causal step.
- nutrient_topic
- Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. · Chlorogenic acid / 5-O-caffeoylquinic acid
- organism
- Rattus norvegicus
- plain_language
- The response depends on functioning machinery in this model.
- primary_references
- [chlorogenic_acid-p22412912] Chlorogenic acid stimulates glucose transport in skeletal muscle via AMPK activation: a contributor to the beneficial effects of coffee on diabetes. (2012). https://pubmed.ncbi.nlm.nih.gov/22412912/ DOI: 10.1371/journal.pone.0032718
- tissue_or_cell_type
- L6 myotubes
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
Chlorogenic acid: metabolism, signaling and nutrient connections (2026-09-17) · lines 490–501
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · L6 myotube signaling with siRNA and pharmacological tests; db/db mouse experiments · source_derived_draft · unverified_draft
### chlorogenic_acid-ampk-loss AMPK alpha1/alpha2 knockdown abrogated CGA-stimulated glucose transport. Condition category: machinery_impairment nutrient_topic: Chlorogenic acid research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response depends on functioning machinery in this model. organism: Rattus norvegicus tissue_or_cell_type: L6 myotubes experimental_model: L6 myotube signaling with siRNA and pharmacological tests; db/db mouse experiments limitations: Millimolar culture exposure and injected mouse doses are not dietary human exposures. Phosphorylation and abundance readouts do not by themselves prove every upstream causal step. exposure: L6 experiments included 2 mmol/L CGA; mouse acute intervention 250 mg/kg intraperitoneally evidence_span: {"source_cache": "artifacts/chlorogenic_acid-research/22412912.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "77c1ccf86d3fb56135a01d2d80b9f1eec3d657e825789f8be490fff93feb8fff", "start_char": 0, "end_char": 1896, "text_sha256": "77c1ccf86d3fb56135a01d2d80b9f1eec3d657e825789f8be490fff93feb8fff"} [chlorogenic_acid-p22412912] Chlorogenic acid stimulates glucose transport in skeletal muscle via AMPK activation: a contributor to the beneficial effects of coffee on diabetes. (2012). https://pubmed.ncbi.nlm.nih.gov/22412912/ DOI: 10.1371/journal.pone.0032718
Complete structured claim and evidenceAdding (S)-6-gingerol increased glucose uptake in rat L6 myotubes.
Experimental context and source evidence
- dose
- (S)-6-Gingerol; dose-response, exact range not in accessed abstract
- duration
- Time-dependent response; exact times not in accessed abstract
- evidence_access
- Primary PubMed abstract.
- evidence_scope
- literature_reviewed; model-specific source-derived curation, not universally established human effects
- experimental_model
- Rat L6 skeletal muscle myotubes
- limitations
- Calcium/CaMKK-associated signaling does not demonstrate dietary calcium depletion or calcium-supplement synergy; no human glycemic outcome was tested.
- nutrient_topic
- Gingerols collection; each molecular form and experimental preparation remains explicit. · Gingerols
- organism
- Rat L6 skeletal muscle myotubes
- plain_language
- Adding (S)-6-gingerol increased glucose uptake in rat L6 myotubes.
- primary_references
- (S)-[6]-Gingerol enhances glucose uptake in L6 myotubes by activation of AMPK in response to [Ca2+]i. (2013). https://pubmed.ncbi.nlm.nih.gov/23958199/ DOI: 10.18433/j34g7p
- route
- In vitro addition
- tissue
- Skeletal muscle cell model
Gingerols: mechanisms, molecular forms and cross-actor connections (2026-09-20) · lines 173–182
Original AI-assisted curation of thirteen primary research papers; study-specific PubMed/DOI links and limitations retained. Not publisher full text. · supports · Rat L6 skeletal muscle myotubes · source_derived_draft · unverified_draft
## gingerols-6-l6-glucose Adding (S)-6-gingerol increased glucose uptake in rat L6 myotubes. Model/species: Rat L6 skeletal muscle myotubes Tissue: Skeletal muscle cell model Exposure: (S)-6-Gingerol; dose-response, exact range not in accessed abstract Route: In vitro addition Duration: Time-dependent response; exact times not in accessed abstract Limits: Calcium/CaMKK-associated signaling does not demonstrate dietary calcium depletion or calcium-supplement synergy; no human glycemic outcome was tested. Primary reference: (S)-[6]-Gingerol enhances glucose uptake in L6 myotubes by activation of AMPK in response to [Ca2+]i. (2013). https://pubmed.ncbi.nlm.nih.gov/23958199/ DOI: 10.18433/j34g7p Access: Primary PubMed abstract.
Complete structured claim and evidence
The events it takes part in
A mechanism often involves more than two components. These are the full events, with every participant and its role.
Situations it appears in
Low-supply and faulty-machinery situations recorded in the chapters where this component plays a part.
In the sources
Preserved passages that mention this component, quoted exactly. Open one to read it in context.
Open hypotheses
Proposed ideas that involve this component. They are labeled as hypotheses and do not change any recorded statement.
This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.