Component
Chenodeoxycholic acid
Chenodeoxycholic acid
1 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
Chenodeoxycholic acid increased ALAS1 mRNA and enzyme activity in primary human hepatocytes and liver slices through an FXR-linked regulatory mechanism.
Experimental context and source evidence
- cross_nutrient
- Hepatic heme synthesis; ALAS1 is distinct from erythroid ALAS2.
- experimental_model
- Primary human hepatocytes and human liver slices; reporter assays
- exposure
- Experimental bile-acid or FXR-agonist treatment
- limitations
- No B6 manipulation; this is regulation of the pathway, not proof of a B6 rescue effect.
- nutrient_topic
- Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6
- organism
- Homo sapiens
- plain_language
- The liver heme pathway has its own regulation in addition to its cofactor needs.
- primary_references
- [b6-alas1-2007] Regulation of human liver delta-aminolevulinic acid synthase by bile acids. (2007). https://pubmed.ncbi.nlm.nih.gov/17975826/ DOI: 10.1002/hep.21879
- tissue_or_cell_type
- Primary human hepatocytes and human liver slices
Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 835–846
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Primary human hepatocytes and human liver slices; reporter assays · source_derived_draft · unverified_draft
### b6-met-alas1-fxr Chenodeoxycholic acid increased ALAS1 mRNA and enzyme activity in primary human hepatocytes and liver slices through an FXR-linked regulatory mechanism. Condition category: normal nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: The liver heme pathway has its own regulation in addition to its cofactor needs. organism: Homo sapiens tissue_or_cell_type: Primary human hepatocytes and human liver slices experimental_model: Primary human hepatocytes and human liver slices; reporter assays limitations: No B6 manipulation; this is regulation of the pathway, not proof of a B6 rescue effect. cross_nutrient: Hepatic heme synthesis; ALAS1 is distinct from erythroid ALAS2. exposure: Experimental bile-acid or FXR-agonist treatment [b6-alas1-2007] Regulation of human liver delta-aminolevulinic acid synthase by bile acids. (2007). https://pubmed.ncbi.nlm.nih.gov/17975826/ DOI: 10.1002/hep.21879
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.