Component
Cutaneous perfusion
Cutaneous perfusion. The model and exposure of each linked claim define its scope.
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
In healthy men and women, the DP1 antagonist MK-0524 reduced nicotinic-acid-induced flushing symptoms and the rise in skin perfusion.
Experimental context and source evidence
- cross_nutrient
- Human prostaglandin D2 receptor 1 / PTGDR (antagonized_receptor); Prostaglandin D2 (receptor_ligand); Nicotinic acid (trigger)
- evidence_span
- {"source_cache": "artifacts/niacin-clinical-sources/cheng2006.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24", "start_char": 0, "end_char": 1708, "text_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24"}
- experimental_model
- Mouse receptor pharmacology with separate healthy-human flushing study
- exposure
- Nicotinic acid with or without the DP1 antagonist MK-0524
- limitations
- Human reduction in flushing is separate from lipid outcomes. Dose details not present in indexed abstract. Antagonism did not prove all flushing depends on one prostaglandin receptor; male knockout mice retained an aspirin-sensitive component.
- nutrient_topic
- Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
- organism
- Homo sapiens
- plain_language
- Blocking a prostaglandin receptor reduced the flush in people; that result alone says nothing about long-term cardiovascular outcomes.
- primary_references
- [nia-clin-cheng2006] Antagonism of the prostaglandin D2 receptor 1 suppresses nicotinic acid-induced vasodilation in mice and humans. (2006). https://pubmed.ncbi.nlm.nih.gov/16617107/ DOI: 10.1073/pnas.0601574103
- tissue_or_cell_type
- Skin perfusion
Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1361–1373
AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Mouse receptor pharmacology with separate healthy-human flushing study · source_derived_draft · unverified_draft
### nia-clin-dp1-human-flush In healthy men and women, the DP1 antagonist MK-0524 reduced nicotinic-acid-induced flushing symptoms and the rise in skin perfusion. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Blocking a prostaglandin receptor reduced the flush in people; that result alone says nothing about long-term cardiovascular outcomes. organism: Homo sapiens tissue_or_cell_type: Skin perfusion experimental_model: Mouse receptor pharmacology with separate healthy-human flushing study limitations: Human reduction in flushing is separate from lipid outcomes. Dose details not present in indexed abstract. Antagonism did not prove all flushing depends on one prostaglandin receptor; male knockout mice retained an aspirin-sensitive component. exposure: Nicotinic acid with or without the DP1 antagonist MK-0524 cross_nutrient: Human prostaglandin D2 receptor 1 / PTGDR (antagonized_receptor); Prostaglandin D2 (receptor_ligand); Nicotinic acid (trigger) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/cheng2006.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24", "start_char": 0, "end_char": 1708, "text_sha256": "3484f8e99487e3991c36a62fd4cdf3972f81de279a50f040f82356da18d74a24"} [nia-clin-cheng2006] Antagonism of the prostaglandin D2 receptor 1 suppresses nicotinic acid-induced vasodilation in mice and humans. (2006). https://pubmed.ncbi.nlm.nih.gov/16617107/ DOI: 10.1073/pnas.0601574103
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.