Component
Advanced glycation end-product formation
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
A high-nattokinase diet inhibited the rise in circulating advanced glycation end products in streptozotocin-diabetic rats.
Experimental context and source evidence
- duration
- 14 days
- evidence_access
- Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
- experimental_model
- Rat (streptozotocin-induced diabetes)
- exposure
- Diet containing 0.6 mg nattokinase per gram
- limitations
- The low-dose diet at 0.2 mg/g did nothing, so this is dose-dependent. The authors state explicitly that it is unclear whether the effect is caused by intact nattokinase or by peptides derived from it during digestion, which is the same open question this whole chapter turns on.
- organism
- Rat (streptozotocin-induced diabetes)
- plain_language
- A high-nattokinase diet inhibited the rise in circulating advanced glycation end products in streptozotocin-diabetic rats.
- primary_references
- Effect of nattokinase on the pathological conditions in streptozotocin induced diabetic rats. (2024) https://pubmed.ncbi.nlm.nih.gov/38586318/ DOI: 10.1016/j.heliyon.2024.e28835
- route
- In vivo, oral
- tissue
- Circulating AGEs and renal histopathology
Nattokinase: what the purified enzyme cleaves, what survives being eaten, and the gap between the two (2026-09-23) · lines 1313–1313
Original AI-assisted curation built from a supplied entity-first document of 105 entities and 129 claims. Every reference in that document was resolved against live PubMed with its abstract read and its DOI cross-checked on 2026-09-23, and the EFSA novel-food opinion was retrieved and read in full. That check corrected two PMIDs that pointed at unrelated papers, two DOIs, and two papers recorded as carrying no erratum that do carry one; it also reversed three findings the supplied document had stated backwards. Two papers carry a published correction, recorded as such and not as a retraction. Three sources are not indexed in PubMed and are cited by what they have. Laboratory lineages are recorded, so the four papers from one group, the three from another and the two readings of a single applicant dossier cannot be counted as separate lines of support. Study-specific doses, units, populations and limitations retained; activity units are never converted between systems. Not publisher full text. · supports · Rat (streptozotocin-induced diabetes) · source_derived_draft · unverified_draft
A high-nattokinase diet inhibited the rise in circulating advanced glycation end products in streptozotocin-diabetic rats.
Complete structured claim and evidenceBenfotiamine inhibited AGE-pathway activation in the experimental hyperglycemia models.
Experimental context and source evidence
- experimental_model
- High-glucose bovine endothelial cells and diabetic rat retinal experiments.
- exposure
- Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine.
- limitations
- Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase.
- nutrient_topic
- Thiamine research collection; topical membership is not evidence of a direct dietary effect. · Thiamine (vitamin B1)
- organism
- Bos taurus; Rattus norvegicus
- plain_language
- Less activation of a glycation pathway accompanied the intervention.
- primary_references
- [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
- tissue_or_cell_type
- Endothelial cultures and retina
Thiamine: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 1903–1913
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · High-glucose bovine endothelial cells and diabetic rat retinal experiments. · source_derived_draft · unverified_draft
### b1-benfotiamine-age Benfotiamine inhibited AGE-pathway activation in the experimental hyperglycemia models. Condition category: normal nutrient_topic: Thiamine research collection; topical membership is not evidence of a direct dietary effect. plain_language: Less activation of a glycation pathway accompanied the intervention. organism: Bos taurus; Rattus norvegicus tissue_or_cell_type: Endothelial cultures and retina experimental_model: High-glucose bovine endothelial cells and diabetic rat retinal experiments. limitations: Pharmacological derivative in bovine endothelial cells/diabetic rats; not proof of human dietary-thiamine benefit or direct NADPH production by transketolase. exposure: Pharmacological benfotiamine in high-glucose bovine endothelial cells and diabetic rat retina; not ordinary dietary thiamine. [b1-hammes2003] Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy (2003). https://pubmed.ncbi.nlm.nih.gov/12592403/ DOI: 10.1038/nm834
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.