Component
Glycoursodeoxycholic acid / GUDCA
Glycoursodeoxycholic acid / GUDCA. 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 it acts on
GUDCA was identified as an intestinal FXR antagonist, and these changes were accompanied by inhibition of intestinal FXR signalling.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/metformin-research/30397356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf", "start_char": 0, "end_char": 1433, "text_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf"}
- experimental_model
- Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments
- exposure
- Three days of metformin in treatment-naive people; B. fragilis colonisation in high-fat-diet mice
- limitations
- A three-day human exposure with a mouse causal test. GUDCA is identified as an intestinal FXR antagonist; whole-body FXR biology is not claimed.
- 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 and mouse
- plain_language
- That bile acid switches off a gut receptor that controls metabolism.
- primary_references
- [metformin-p30397356] Gut microbiota and intestinal FXR mediate the clinical benefits of metformin. (2018). https://pubmed.ncbi.nlm.nih.gov/30397356/ DOI: 10.1038/s41591-018-0222-4
- tissue_or_cell_type
- Gut lumen and intestinal epithelium
Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 879–890
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments · source_derived_draft · unverified_draft
### metformin-gudca-fxr GUDCA was identified as an intestinal FXR antagonist, and these changes were accompanied by inhibition of intestinal FXR signalling. 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: That bile acid switches off a gut receptor that controls metabolism. organism: Human and mouse tissue_or_cell_type: Gut lumen and intestinal epithelium experimental_model: Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments limitations: A three-day human exposure with a mouse causal test. GUDCA is identified as an intestinal FXR antagonist; whole-body FXR biology is not claimed. exposure: Three days of metformin in treatment-naive people; B. fragilis colonisation in high-fat-diet mice evidence_span: {"source_cache": "artifacts/metformin-research/30397356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf", "start_char": 0, "end_char": 1433, "text_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf"} [metformin-p30397356] Gut microbiota and intestinal FXR mediate the clinical benefits of metformin. (2018). https://pubmed.ncbi.nlm.nih.gov/30397356/ DOI: 10.1038/s41591-018-0222-4
Complete structured claim and evidence
Where it participates (unsigned role)
Three days of metformin in newly diagnosed type 2 diabetes decreased Bacteroides fragilis and increased the bile acid glycoursodeoxycholic acid in the gut.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/metformin-research/30397356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf", "start_char": 0, "end_char": 1433, "text_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf"}
- experimental_model
- Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments
- exposure
- Three days of metformin in treatment-naive people; B. fragilis colonisation in high-fat-diet mice
- limitations
- A three-day human exposure with a mouse causal test. GUDCA is identified as an intestinal FXR antagonist; whole-body FXR biology is not claimed.
- 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 and mouse
- plain_language
- The drug changed which bacteria were present and which bile acid built up.
- primary_references
- [metformin-p30397356] Gut microbiota and intestinal FXR mediate the clinical benefits of metformin. (2018). https://pubmed.ncbi.nlm.nih.gov/30397356/ DOI: 10.1038/s41591-018-0222-4
- tissue_or_cell_type
- Gut lumen and intestinal epithelium
Metformin: transport, molecular targets, gut mechanisms and nutrient interactions (2026-09-19) · lines 866–877
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments · source_derived_draft · unverified_draft
### metformin-bfragilis-decrease Three days of metformin in newly diagnosed type 2 diabetes decreased Bacteroides fragilis and increased the bile acid glycoursodeoxycholic acid in the gut. 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 changed which bacteria were present and which bile acid built up. organism: Human and mouse tissue_or_cell_type: Gut lumen and intestinal epithelium experimental_model: Metagenomic and metabolomic analysis in newly diagnosed type 2 diabetes with mouse colonisation experiments limitations: A three-day human exposure with a mouse causal test. GUDCA is identified as an intestinal FXR antagonist; whole-body FXR biology is not claimed. exposure: Three days of metformin in treatment-naive people; B. fragilis colonisation in high-fat-diet mice evidence_span: {"source_cache": "artifacts/metformin-research/30397356.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf", "start_char": 0, "end_char": 1433, "text_sha256": "0dbf1f5a262207595ede745deeb9fc79ba7732dc4d6af6b5c9d654712d79c1cf"} [metformin-p30397356] Gut microbiota and intestinal FXR mediate the clinical benefits of metformin. (2018). https://pubmed.ncbi.nlm.nih.gov/30397356/ DOI: 10.1038/s41591-018-0222-4
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.