Component
Quercetin
Context-specific entity; species, compartment and exposure are stated on each claim.
3 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
Quercetin inhibited OAT3-mediated steviol-glucuronide uptake, with IC50 1.8 micromolar.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- In vitro transport inhibition assay.
- limitations
- Free tissue exposure and a human pharmacokinetic interaction were not established.
- nutrient_topic
- Stevia collection; species, compartment, exposure, co-substrates and manipulation remain explicit. · Stevia
- plain_language
- A food-derived flavonoid intersects the metabolite clearance route.
- primary_references
- Transmembrane transport of steviol glucuronide and its potential interaction with selected drugs and natural compounds. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26525112/ · DOI 10.1016/j.fct.2015.10.011
Stevia: glycoside metabolism, taste, ion channels and cross-nutrient mechanisms (2026-09-19) · lines 130–136
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · In vitro transport inhibition assay. · source_derived_draft · unverified_draft
## stevia-quercetin-oat3 A food-derived flavonoid intersects the metabolite clearance route. Quercetin inhibited OAT3-mediated steviol-glucuronide uptake, with IC50 1.8 micromolar. Model: In vitro transport inhibition assay. Limitations: Free tissue exposure and a human pharmacokinetic interaction were not established. Evidence access: Primary abstract Transmembrane transport of steviol glucuronide and its potential interaction with selected drugs and natural compounds. · 2015 · https://pubmed.ncbi.nlm.nih.gov/26525112/ · DOI 10.1016/j.fct.2015.10.011
Complete structured claim and evidence
What acts on it
Human-donor intestinal bacterial cultures yielded Quercetin through the reported subsequent deglycosylation route.
Experimental context and source evidence
- evidence_access
- Primary abstract
- experimental_model
- Four active isolates selected from about 100 colonies from one healthy female donor; most identified as Escherichia.
- limitations
- Mass-spectrometric pathway assignment; no specific enzyme or population-wide conversion rate established.
- nutrient_topic
- Myricetin collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Myricetin
- plain_language
- Gut processing produces a chemically different molecule.
- primary_references
- Identification of the metabolites of myricitrin produced by human intestinal bacteria in vitro using ultra-performance liquid chromatography/quadrupole time-of-flight mass spectrometry. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24882500/ · DOI 10.1517/17425255.2014.918954
Myricetin: metabolism, immune signaling, redox chemistry and cross-nutrient mechanisms (2026-09-19) · lines 36–42
AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Four active isolates selected from about 100 colonies from one healthy female donor; most identified as Escherichia. · source_derived_draft · unverified_draft
## myricetin-microbial-quercetin Gut processing produces a chemically different molecule. Human-donor intestinal bacterial cultures yielded Quercetin through the reported subsequent deglycosylation route. Model: Four active isolates selected from about 100 colonies from one healthy female donor; most identified as Escherichia. Limitations: Mass-spectrometric pathway assignment; no specific enzyme or population-wide conversion rate established. Evidence access: Primary abstract Identification of the metabolites of myricitrin produced by human intestinal bacteria in vitro using ultra-performance liquid chromatography/quadrupole time-of-flight mass spectrometry. · 2014 · https://pubmed.ncbi.nlm.nih.gov/24882500/ · DOI 10.1517/17425255.2014.918954
Complete structured claim and evidence
Where it participates (unsigned role)
Glucosylation improved net quercetin absorption as isoquercitrin but reduced phloretin absorption as phlorizin, demonstrating substrate-specific effects of glycosylation.
Experimental context and source evidence
- dose
- Quercetin/isoquercitrin and phloretin/phlorizin pairs
- duration
- 30 minutes
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- evidence_scope
- literature_reviewed; model-specific source-derived curation
- experimental_model
- In-situ rat intestinal perfusion
- limitations
- This is a mechanistic nutrient-to-nutrient comparison in rats, not evidence that the flavonoids compete in humans.
- nutrient_topic
- Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
- organism
- In-situ rat intestinal perfusion
- plain_language
- Glucosylation improved net quercetin absorption as isoquercitrin but reduced phloretin absorption as phlorizin, demonstrating substrate-specific effects of glycosylation.
- primary_references
- Comparison of the intestinal absorption of quercetin, phloretin and their glucosides in rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11481403/ DOI: 10.1093/jn/131.8.2109
- route
- Intestinal perfusion
- tissue
- Comparative flavonoid absorption
Phlorizin: mechanism of action and interactions (2026-09-20) · lines 66–75
Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · In-situ rat intestinal perfusion · source_derived_draft · unverified_draft
## phlorizin-quercetin-comparison Glucosylation improved net quercetin absorption as isoquercitrin but reduced phloretin absorption as phlorizin, demonstrating substrate-specific effects of glycosylation. Model/species: In-situ rat intestinal perfusion Tissue/system: Comparative flavonoid absorption Exposure: Quercetin/isoquercitrin and phloretin/phlorizin pairs Route: Intestinal perfusion Duration: 30 minutes Limits: This is a mechanistic nutrient-to-nutrient comparison in rats, not evidence that the flavonoids compete in humans. Primary reference: Comparison of the intestinal absorption of quercetin, phloretin and their glucosides in rats. (2001). https://pubmed.ncbi.nlm.nih.gov/11481403/ DOI: 10.1093/jn/131.8.2109 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
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.