Component
FXR transcriptional activity
FXR transcriptional activity. Species, exposure and limitations are retained in each linked claim.
2 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
Metformin inhibited FXR agonist induction of FXR target genes in mouse liver and intestine.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/metformin-research/24531544.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e34abf954452e017d254058f7e611697560bba87a53cf726c88f0b77d6673ad", "start_char": 0, "end_char": 1358, "text_sha256": "9e34abf954452e017d254058f7e611697560bba87a53cf726c88f0b77d6673ad"}
- experimental_model
- Mass-spectrometry interaction screen in human hepatoma cells with mouse liver, intestine and a cholestasis model
- exposure
- Metformin and other AMPK activators with FXR agonists
- limitations
- An adverse-direction finding: in a cholestasis model metformin worsened liver injury. Recorded because a mechanism record should not be filtered for favourable outcomes.
- nutrient_topic
- Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
- organism
- Human cells and mouse
- plain_language
- The drug reaches that receptor’s gene programme in both organs.
- primary_references
- [metformin-p24531544] Metformin interferes with bile acid homeostasis through AMPK-FXR crosstalk. (2014). https://pubmed.ncbi.nlm.nih.gov/24531544/ DOI: 10.1172/jci68815
- tissue_or_cell_type
- Liver and intestine
Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 1009–1020
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mass-spectrometry interaction screen in human hepatoma cells with mouse liver, intestine and a cholestasis model · source_derived_draft · unverified_draft
### metformin-metformin-fxr-target-genes Metformin inhibited FXR agonist induction of FXR target genes in mouse liver and intestine. 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 drug reaches that receptor’s gene programme in both organs. organism: Human cells and mouse tissue_or_cell_type: Liver and intestine experimental_model: Mass-spectrometry interaction screen in human hepatoma cells with mouse liver, intestine and a cholestasis model limitations: An adverse-direction finding: in a cholestasis model metformin worsened liver injury. Recorded because a mechanism record should not be filtered for favourable outcomes. exposure: Metformin and other AMPK activators with FXR agonists evidence_span: {"source_cache": "artifacts/metformin-research/24531544.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e34abf954452e017d254058f7e611697560bba87a53cf726c88f0b77d6673ad", "start_char": 0, "end_char": 1358, "text_sha256": "9e34abf954452e017d254058f7e611697560bba87a53cf726c88f0b77d6673ad"} [metformin-p24531544] Metformin interferes with bile acid homeostasis through AMPK-FXR crosstalk. (2014). https://pubmed.ncbi.nlm.nih.gov/24531544/ DOI: 10.1172/jci68815
Complete structured claim and evidence
Where it participates (unsigned role)
AMPK interacted with FXR in the cytoplasm and phosphorylated it in its hinge domain, inhibiting FXR transcriptional activity and preventing coactivator recruitment.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/metformin-research/24531544.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e34abf954452e017d254058f7e611697560bba87a53cf726c88f0b77d6673ad", "start_char": 0, "end_char": 1358, "text_sha256": "9e34abf954452e017d254058f7e611697560bba87a53cf726c88f0b77d6673ad"}
- experimental_model
- Mass-spectrometry interaction screen in human hepatoma cells with mouse liver, intestine and a cholestasis model
- exposure
- Metformin and other AMPK activators with FXR agonists
- limitations
- An adverse-direction finding: in a cholestasis model metformin worsened liver injury. Recorded because a mechanism record should not be filtered for favourable outcomes.
- nutrient_topic
- Metformin research collection; topical membership is not evidence of a direct clinical effect, and pharmacological exposure is not dietary intake. · Metformin
- organism
- Human cells and mouse
- plain_language
- The energy sensor directly switches down the bile-acid receptor.
- primary_references
- [metformin-p24531544] Metformin interferes with bile acid homeostasis through AMPK-FXR crosstalk. (2014). https://pubmed.ncbi.nlm.nih.gov/24531544/ DOI: 10.1172/jci68815
- tissue_or_cell_type
- Liver and intestine
Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 996–1007
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mass-spectrometry interaction screen in human hepatoma cells with mouse liver, intestine and a cholestasis model · source_derived_draft · unverified_draft
### metformin-ampk-fxr AMPK interacted with FXR in the cytoplasm and phosphorylated it in its hinge domain, inhibiting FXR transcriptional activity and preventing coactivator recruitment. 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 energy sensor directly switches down the bile-acid receptor. organism: Human cells and mouse tissue_or_cell_type: Liver and intestine experimental_model: Mass-spectrometry interaction screen in human hepatoma cells with mouse liver, intestine and a cholestasis model limitations: An adverse-direction finding: in a cholestasis model metformin worsened liver injury. Recorded because a mechanism record should not be filtered for favourable outcomes. exposure: Metformin and other AMPK activators with FXR agonists evidence_span: {"source_cache": "artifacts/metformin-research/24531544.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "9e34abf954452e017d254058f7e611697560bba87a53cf726c88f0b77d6673ad", "start_char": 0, "end_char": 1358, "text_sha256": "9e34abf954452e017d254058f7e611697560bba87a53cf726c88f0b77d6673ad"} [metformin-p24531544] Metformin interferes with bile acid homeostasis through AMPK-FXR crosstalk. (2014). https://pubmed.ncbi.nlm.nih.gov/24531544/ DOI: 10.1172/jci68815
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.