Component
Endogenous fecal iron loss
Fecal loss of iron previously within the body, distinguished from unabsorbed dietary iron.
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 acts on it
After intraperitoneal 59Fe, riboflavin-deficient rats lost about twice as much endogenous tracer in feces as weight-matched controls.
Experimental context and source evidence
- availability_state
- nutrient_deficiency Imported condition classification; unverified.
- cross_nutrient
- B2 status affected post-absorption iron retention in rats.
- evidence_location
- Abstract
- experimental_model
- Riboflavin-deficient weanling rats; weight-matched and ad-libitum controls; intestinal histology and intraperitoneal 59Fe tracing.
- exposure
- Dietary riboflavin deficiency plus intraperitoneal tracer
- limitations
- The proposed enterocyte-turnover mechanism is supported indirectly; this is not measurement of unabsorbed oral iron.
- nutrient_topic
- Riboflavin research collection; topical membership is not evidence of a direct dietary effect. · Riboflavin (vitamin B2)
- organism
- Rattus norvegicus
- plain_language
- Deficiency increased loss of iron already inside the body.
- primary_references
- [powers1993] A proposed intestinal mechanism for the effect of riboflavin deficiency on iron loss in the rat. (1993). https://pubmed.ncbi.nlm.nih.gov/8490008/ DOI: 10.1079/bjn19930055
- tissue_or_cell_type
- Gastrointestinal tract and feces
- trigger_kind
- nutrient_deficiency Imported condition classification; unverified.
Riboflavin: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1458–1470
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Riboflavin-deficient weanling rats; weight-matched and ad-libitum controls; intestinal histology and intraperitoneal 59Fe tracing. · source_derived_draft · unverified_draft
### b2-rat-endogenous-iron-loss After intraperitoneal 59Fe, riboflavin-deficient rats lost about twice as much endogenous tracer in feces as weight-matched controls. Condition category: nutrient_deficiency nutrient_topic: Riboflavin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Deficiency increased loss of iron already inside the body. organism: Rattus norvegicus tissue_or_cell_type: Gastrointestinal tract and feces experimental_model: Riboflavin-deficient weanling rats; weight-matched and ad-libitum controls; intestinal histology and intraperitoneal 59Fe tracing. limitations: The proposed enterocyte-turnover mechanism is supported indirectly; this is not measurement of unabsorbed oral iron. exposure: Dietary riboflavin deficiency plus intraperitoneal tracer cross_nutrient: B2 status affected post-absorption iron retention in rats. evidence_location: Abstract [powers1993] A proposed intestinal mechanism for the effect of riboflavin deficiency on iron loss in the rat. (1993). https://pubmed.ncbi.nlm.nih.gov/8490008/ DOI: 10.1079/bjn19930055
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.