Component
Rat AMP-activated protein kinase complex
Context-specific entity; species, compartment and exposure are stated on each claim.
4 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 acts on it
Acute alanine treatment increased AMPK and downstream ACC phosphorylation in rat H4IIE liver cells over the tested 0.25–10 mM range.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Rat H4IIE cells; acute millimolar alanine exposure.
- limitations
- Phosphorylation in culture is not proof of clinical benefit or a universal response to dietary alanine.
- nutrient_topic
- L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
- plain_language
- Alanine metabolism can generate an energy-stress signal in this experimental setting.
- primary_references
- l-Alanine activates hepatic AMP-activated protein kinase and modulates systemic glucose metabolism. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30190193/ · DOI 10.1016/j.molmet.2018.08.002
L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 248–254
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat H4IIE cells; acute millimolar alanine exposure. · source_derived_draft · unverified_draft
## alanine-ampk-acute Alanine metabolism can generate an energy-stress signal in this experimental setting. Acute alanine treatment increased AMPK and downstream ACC phosphorylation in rat H4IIE liver cells over the tested 0.25–10 mM range. Model: Rat H4IIE cells; acute millimolar alanine exposure. Limitations: Phosphorylation in culture is not proof of clinical benefit or a universal response to dietary alanine. Evidence access: Primary full text l-Alanine activates hepatic AMP-activated protein kinase and modulates systemic glucose metabolism. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30190193/ · DOI 10.1016/j.molmet.2018.08.002
Complete structured claim and evidenceALT1 siRNA reduced rat H4IIE ALT protein by about 77% and reduced alanine-stimulated AMPK activation by about 49%.
Experimental context and source evidence
- availability_state
- machinery_impairment Imported condition classification; unverified.
- evidence_access
- Primary full text
- experimental_model
- Rat H4IIE cells; siRNA knockdown with alanine challenge.
- limitations
- Partial knockdown and partial attenuation do not prove ALT1 is the only contributing pathway.
- nutrient_topic
- L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
- plain_language
- The response partly depended on processing alanine, rather than simply sensing it outside the cell.
- primary_references
- l-Alanine activates hepatic AMP-activated protein kinase and modulates systemic glucose metabolism. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30190193/ · DOI 10.1016/j.molmet.2018.08.002
- trigger_kind
- machinery_impairment Imported condition classification; unverified.
L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 256–262
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat H4IIE cells; siRNA knockdown with alanine challenge. · source_derived_draft · unverified_draft
## alanine-ampk-alt1-dependence The response partly depended on processing alanine, rather than simply sensing it outside the cell. ALT1 siRNA reduced rat H4IIE ALT protein by about 77% and reduced alanine-stimulated AMPK activation by about 49%. Model: Rat H4IIE cells; siRNA knockdown with alanine challenge. Limitations: Partial knockdown and partial attenuation do not prove ALT1 is the only contributing pathway. Evidence access: Primary full text l-Alanine activates hepatic AMP-activated protein kinase and modulates systemic glucose metabolism. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30190193/ · DOI 10.1016/j.molmet.2018.08.002
Complete structured claim and evidenceAmmonium chloride exposure reproduced increases in AMP/ATP and AMPK/ACC phosphorylation, and pyruvate attenuated these responses.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Rat H4IIE experiments; 2–5 mM ammonium chloride comparison.
- limitations
- Mimicry is not proof that ammonia is the sole mediator of alanine effects or that urea-cycle ATP use accounts for them.
- nutrient_topic
- L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
- plain_language
- A nitrogen-handling byproduct may contribute to the energy signal.
- primary_references
- l-Alanine activates hepatic AMP-activated protein kinase and modulates systemic glucose metabolism. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30190193/ · DOI 10.1016/j.molmet.2018.08.002
L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 280–286
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat H4IIE experiments; 2–5 mM ammonium chloride comparison. · source_derived_draft · unverified_draft
## alanine-ampk-ammonia A nitrogen-handling byproduct may contribute to the energy signal. Ammonium chloride exposure reproduced increases in AMP/ATP and AMPK/ACC phosphorylation, and pyruvate attenuated these responses. Model: Rat H4IIE experiments; 2–5 mM ammonium chloride comparison. Limitations: Mimicry is not proof that ammonia is the sole mediator of alanine effects or that urea-cycle ATP use accounts for them. Evidence access: Primary full text l-Alanine activates hepatic AMP-activated protein kinase and modulates systemic glucose metabolism. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30190193/ · DOI 10.1016/j.molmet.2018.08.002
Complete structured claim and evidencePyruvate or TCA-intermediate supplementation restored ATP and attenuated alanine-induced AMPK phosphorylation in the tested liver-cell experiments.
Experimental context and source evidence
- evidence_access
- Primary full text
- experimental_model
- Rat H4IIE nutrient-addition experiments.
- limitations
- A biochemical rescue does not establish a supplement combination for humans.
- nutrient_topic
- L-Alanine collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · L-Alanine
- plain_language
- Providing usable carbon changed the signaling response to alanine.
- primary_references
- l-Alanine activates hepatic AMP-activated protein kinase and modulates systemic glucose metabolism. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30190193/ · DOI 10.1016/j.molmet.2018.08.002
L-Alanine: carbon, nitrogen, protein synthesis and cross-nutrient mechanisms (2026-09-19) · lines 272–278
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Rat H4IIE nutrient-addition experiments. · source_derived_draft · unverified_draft
## alanine-ampk-carbon-rescue Providing usable carbon changed the signaling response to alanine. Pyruvate or TCA-intermediate supplementation restored ATP and attenuated alanine-induced AMPK phosphorylation in the tested liver-cell experiments. Model: Rat H4IIE nutrient-addition experiments. Limitations: A biochemical rescue does not establish a supplement combination for humans. Evidence access: Primary full text l-Alanine activates hepatic AMP-activated protein kinase and modulates systemic glucose metabolism. · 2018 · https://pubmed.ncbi.nlm.nih.gov/30190193/ · DOI 10.1016/j.molmet.2018.08.002
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.