Component
Liver fibrosis
Independent biological entity. Read linked claims for experimental scope and context.
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
Chronic vitamin A hepatotoxicity cases included cirrhosis and portal hypertension with characteristic hepatic storage-cell changes.
Experimental context and source evidence
- experimental_model
- 41 selected clinical cases with liver histology.
- exposure
- Chronic preformed-vitamin-A exposure; excess, not deficiency.
- limitations
- Case series cannot estimate population incidence or define a safe-dose threshold.
- nutrient_topic
- Vitamin A research collection; topical membership is not evidence of a direct dietary effect. · Vitamin A
- organism
- Homo sapiens
- plain_language
- Prolonged excess can damage the organ that stores vitamin A.
- primary_references
- [va-geubel1991] Liver damage caused by therapeutic vitamin A administration: estimate of dose-related toxicity in 41 cases (1991). https://pubmed.ncbi.nlm.nih.gov/2019375/ DOI: 10.1016/0016-5085(91)90672-8
- tissue_or_cell_type
- Liver
Vitamin A: forms, mechanisms, deficiency and excess (2026-09-17) · lines 1834–1844
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · 41 selected clinical cases with liver histology. · source_derived_draft · unverified_draft
### va-chronic-excess-liver-injury Chronic vitamin A hepatotoxicity cases included cirrhosis and portal hypertension with characteristic hepatic storage-cell changes. Condition category: normal nutrient_topic: Vitamin A research collection; topical membership is not evidence of a direct dietary effect. plain_language: Prolonged excess can damage the organ that stores vitamin A. organism: Homo sapiens tissue_or_cell_type: Liver experimental_model: 41 selected clinical cases with liver histology. limitations: Case series cannot estimate population incidence or define a safe-dose threshold. exposure: Chronic preformed-vitamin-A exposure; excess, not deficiency. [va-geubel1991] Liver damage caused by therapeutic vitamin A administration: estimate of dose-related toxicity in 41 cases (1991). https://pubmed.ncbi.nlm.nih.gov/2019375/ DOI: 10.1016/0016-5085(91)90672-8
Complete structured claim and evidence
Where it participates (unsigned role)
Fructose promoted leaky gut, endotoxaemia and liver fibrosis through ethanol-inducible cytochrome P450-2E1-mediated oxidative and nitrative stress.
Experimental context and source evidence
- evidence_span
- {"source_cache": "artifacts/alcohol-research/30959577.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a80ad0b106d815118c6c4174ff22f9a86c4e41f549edb39e5d663c6efd7af3d", "start_char": 0, "end_char": 1961, "text_sha256": "1a80ad0b106d815118c6c4174ff22f9a86c4e41f549edb39e5d663c6efd7af3d"}
- experimental_model
- Fructose feeding in mice with CYP2E1 deletion and gut barrier measurement
- exposure
- Fructose feeding with and without CYP2E1
- limitations
- Recorded because it isolates the enzyme: the leak and fibrosis required CYP2E1, which ethanol induces. The driver here is fructose, not ethanol.
- nutrient_topic
- Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. · Ethanol
- organism
- Mouse
- plain_language
- The enzyme alcohol stabilises is itself enough to open the gut barrier.
- primary_references
- [alcohol-p30959577] Fructose Promotes Leaky Gut, Endotoxemia, and Liver Fibrosis Through Ethanol-Inducible Cytochrome P450-2E1-Mediated Oxidative and Nitrative Stress. (2021). https://pubmed.ncbi.nlm.nih.gov/30959577/ DOI: 10.1002/hep.30652
- tissue_or_cell_type
- Intestine and liver
Alcohol: ethanol clearance, acetaldehyde, the channels it binds, organ injury and nutrient collisions (2026-09-21) · lines 501–512
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Fructose feeding in mice with CYP2E1 deletion and gut barrier measurement · source_derived_draft · unverified_draft
### alcohol-cyp2e1-leaky-gut Fructose promoted leaky gut, endotoxaemia and liver fibrosis through ethanol-inducible cytochrome P450-2E1-mediated oxidative and nitrative stress. Condition category: normal nutrient_topic: Alcohol research collection; topical membership is not evidence of a direct clinical effect, and ethanol is recorded separately from the acetaldehyde it becomes. plain_language: The enzyme alcohol stabilises is itself enough to open the gut barrier. organism: Mouse tissue_or_cell_type: Intestine and liver experimental_model: Fructose feeding in mice with CYP2E1 deletion and gut barrier measurement limitations: Recorded because it isolates the enzyme: the leak and fibrosis required CYP2E1, which ethanol induces. The driver here is fructose, not ethanol. exposure: Fructose feeding with and without CYP2E1 evidence_span: {"source_cache": "artifacts/alcohol-research/30959577.abstract.txt", "locator": "Indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "1a80ad0b106d815118c6c4174ff22f9a86c4e41f549edb39e5d663c6efd7af3d", "start_char": 0, "end_char": 1961, "text_sha256": "1a80ad0b106d815118c6c4174ff22f9a86c4e41f549edb39e5d663c6efd7af3d"} [alcohol-p30959577] Fructose Promotes Leaky Gut, Endotoxemia, and Liver Fibrosis Through Ethanol-Inducible Cytochrome P450-2E1-Mediated Oxidative and Nitrative Stress. (2021). https://pubmed.ncbi.nlm.nih.gov/30959577/ DOI: 10.1002/hep.30652
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.