Component

Nicotinic-acid-induced cutaneous flushing

Nicotinic-acid-induced cutaneous flushing. The model and exposure of each linked claim define its scope.

3 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

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.

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.

Recorded relationships

What acts on it

  1. Arrb1-null mice had less nicotinic-acid-induced flushing while retaining a serum free-fatty-acid response similar to wild-type mice.

    Mouse Arrb1 knockout genotype → Nicotinic-acid-induced cutaneous flushing source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Nicotinic acid (administered_agonist); Plasma free fatty acid concentration (preserved_separate_endpoint)
    evidence_span
    {"source_cache": "artifacts/niacin-clinical-sources/walters2009.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "2eb822534ed0c8ea9f71ec67288c302e4e375ed9e86cfe70b28f21ae65ffbd4b", "start_char": 0, "end_char": 1537, "text_sha256": "2eb822534ed0c8ea9f71ec67288c302e4e375ed9e86cfe70b28f21ae65ffbd4b"}
    experimental_model
    Human cell-line receptor signaling and separate Arrb1-null mouse physiology
    exposure
    Nicotinic-acid stimulation and beta-arrestin perturbation
    limitations
    Pharmacological receptor signaling, not an essential effect of every B3 precursor. Cell signaling and mouse physiology are distinct arms. Reduced fatty acids or flushing does not establish cardiovascular benefit.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Mus musculus
    plain_language
    The flushing and fatty-acid responses could be separated in mice; one is not a reliable measure of the other.
    primary_references
    [nia-clin-walters2009] beta-Arrestin1 mediates nicotinic acid-induced flushing, but not its antilipolytic effect, in mice. (2009). https://pubmed.ncbi.nlm.nih.gov/19349687/ DOI: 10.1172/jci36806
    tissue_or_cell_type
    Engineered cells; mouse skin and serum
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1319–1331

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cell-line receptor signaling and separate Arrb1-null mouse physiology · source_derived_draft · unverified_draft

    ### nia-clin-arrb1-mouse-flush Arrb1-null mice had less nicotinic-acid-induced flushing while retaining a serum free-fatty-acid response similar to wild-type mice. Condition category: machinery_impairment nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The flushing and fatty-acid responses could be separated in mice; one is not a reliable measure of the other. organism: Mus musculus tissue_or_cell_type: Engineered cells; mouse skin and serum experimental_model: Human cell-line receptor signaling and separate Arrb1-null mouse physiology limitations: Pharmacological receptor signaling, not an essential effect of every B3 precursor. Cell signaling and mouse physiology are distinct arms. Reduced fatty acids or flushing does not establish cardiovascular benefit. exposure: Nicotinic-acid stimulation and beta-arrestin perturbation cross_nutrient: Nicotinic acid (administered_agonist); Plasma free fatty acid concentration (preserved_separate_endpoint) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/walters2009.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "2eb822534ed0c8ea9f71ec67288c302e4e375ed9e86cfe70b28f21ae65ffbd4b", "start_char": 0, "end_char": 1537, "text_sha256": "2eb822534ed0c8ea9f71ec67288c302e4e375ed9e86cfe70b28f21ae65ffbd4b"} [nia-clin-walters2009] beta-Arrestin1 mediates nicotinic acid-induced flushing, but not its antilipolytic effect, in mice. (2009). https://pubmed.ncbi.nlm.nih.gov/19349687/ DOI: 10.1172/jci36806
    Complete structured claim and evidence

  2. PUMA-G-deficient mice did not flush after nicotinic acid; transplantation of wild-type bone marrow restored this response.

    Mouse Hcar2 knockout genotype → Nicotinic-acid-induced cutaneous flushing source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    cross_nutrient
    Nicotinic acid (agonist); Mouse Hcar2 / PUMA-G receptor (affected_receptor)
    evidence_span
    {"source_cache": "artifacts/niacin-clinical-sources/benyo2005.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "21dedb52cbd8fccaf810dabec7837e471525e0a5462827b21437d2f7b30c44a2", "start_char": 0, "end_char": 1388, "text_sha256": "21dedb52cbd8fccaf810dabec7837e471525e0a5462827b21437d2f7b30c44a2"}
    experimental_model
    PUMA-G/Hcar2 and prostaglandin-pathway mouse knockout experiments with bone-marrow transplantation
    exposure
    Nicotinic acid; receptor or cyclooxygenase deletion; wild-type bone-marrow rescue
    limitations
    Mouse pharmacological flushing experiment. HCAR2 historically GPR109A/HM74A in humans; mouse receptor PUMA-G. The location of the responsible immune cells was inferred, not every human flush directly measured.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Mus musculus
    plain_language
    The mouse flushing signal required the receptor in a population supplied by bone marrow.
    primary_references
    [nia-clin-benyo2005] GPR109A (PUMA-G/HM74A) mediates nicotinic acid-induced flushing. (2005). https://pubmed.ncbi.nlm.nih.gov/16322797/ DOI: 10.1172/jci23626
    tissue_or_cell_type
    Skin vasculature and hematopoietic cells
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1333–1345

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PUMA-G/Hcar2 and prostaglandin-pathway mouse knockout experiments with bone-marrow transplantation · source_derived_draft · unverified_draft

    ### nia-clin-hcar2-mouse-flush PUMA-G-deficient mice did not flush after nicotinic acid; transplantation of wild-type bone marrow restored this response. Condition category: machinery_impairment nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The mouse flushing signal required the receptor in a population supplied by bone marrow. organism: Mus musculus tissue_or_cell_type: Skin vasculature and hematopoietic cells experimental_model: PUMA-G/Hcar2 and prostaglandin-pathway mouse knockout experiments with bone-marrow transplantation limitations: Mouse pharmacological flushing experiment. HCAR2 historically GPR109A/HM74A in humans; mouse receptor PUMA-G. The location of the responsible immune cells was inferred, not every human flush directly measured. exposure: Nicotinic acid; receptor or cyclooxygenase deletion; wild-type bone-marrow rescue cross_nutrient: Nicotinic acid (agonist); Mouse Hcar2 / PUMA-G receptor (affected_receptor) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/benyo2005.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "21dedb52cbd8fccaf810dabec7837e471525e0a5462827b21437d2f7b30c44a2", "start_char": 0, "end_char": 1388, "text_sha256": "21dedb52cbd8fccaf810dabec7837e471525e0a5462827b21437d2f7b30c44a2"} [nia-clin-benyo2005] GPR109A (PUMA-G/HM74A) mediates nicotinic acid-induced flushing. (2005). https://pubmed.ncbi.nlm.nih.gov/16322797/ DOI: 10.1172/jci23626
    Complete structured claim and evidence

  3. Nicotinic-acid flushing was absent in cyclooxygenase-1-deficient mice and reduced in mice lacking the tested PGD2 or PGE2 receptors, supporting prostaglandin involvement.

    Prostaglandin D2 → Nicotinic-acid-induced cutaneous flushing source_derived_draftungraded
    Experimental context and source evidence
    cross_nutrient
    Prostaglandin E2 (additional_signal); Nicotinic acid (trigger)
    evidence_span
    {"source_cache": "artifacts/niacin-clinical-sources/benyo2005.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "21dedb52cbd8fccaf810dabec7837e471525e0a5462827b21437d2f7b30c44a2", "start_char": 0, "end_char": 1388, "text_sha256": "21dedb52cbd8fccaf810dabec7837e471525e0a5462827b21437d2f7b30c44a2"}
    experimental_model
    PUMA-G/Hcar2 and prostaglandin-pathway mouse knockout experiments with bone-marrow transplantation
    exposure
    Nicotinic acid; receptor or cyclooxygenase deletion; wild-type bone-marrow rescue
    limitations
    Mouse pharmacological flushing experiment. HCAR2 historically GPR109A/HM74A in humans; mouse receptor PUMA-G. The location of the responsible immune cells was inferred, not every human flush directly measured.
    nutrient_topic
    Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)
    organism
    Mus musculus
    plain_language
    Nicotinic acid triggers prostaglandin signals that widen skin vessels in this mouse model.
    primary_references
    [nia-clin-benyo2005] GPR109A (PUMA-G/HM74A) mediates nicotinic acid-induced flushing. (2005). https://pubmed.ncbi.nlm.nih.gov/16322797/ DOI: 10.1172/jci23626
    tissue_or_cell_type
    Skin vasculature and hematopoietic cells

    Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1347–1359

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · PUMA-G/Hcar2 and prostaglandin-pathway mouse knockout experiments with bone-marrow transplantation · source_derived_draft · unverified_draft

    ### nia-clin-prostaglandin-flush Nicotinic-acid flushing was absent in cyclooxygenase-1-deficient mice and reduced in mice lacking the tested PGD2 or PGE2 receptors, supporting prostaglandin involvement. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Nicotinic acid triggers prostaglandin signals that widen skin vessels in this mouse model. organism: Mus musculus tissue_or_cell_type: Skin vasculature and hematopoietic cells experimental_model: PUMA-G/Hcar2 and prostaglandin-pathway mouse knockout experiments with bone-marrow transplantation limitations: Mouse pharmacological flushing experiment. HCAR2 historically GPR109A/HM74A in humans; mouse receptor PUMA-G. The location of the responsible immune cells was inferred, not every human flush directly measured. exposure: Nicotinic acid; receptor or cyclooxygenase deletion; wild-type bone-marrow rescue cross_nutrient: Prostaglandin E2 (additional_signal); Nicotinic acid (trigger) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/benyo2005.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "21dedb52cbd8fccaf810dabec7837e471525e0a5462827b21437d2f7b30c44a2", "start_char": 0, "end_char": 1388, "text_sha256": "21dedb52cbd8fccaf810dabec7837e471525e0a5462827b21437d2f7b30c44a2"} [nia-clin-benyo2005] GPR109A (PUMA-G/HM74A) mediates nicotinic acid-induced flushing. (2005). https://pubmed.ncbi.nlm.nih.gov/16322797/ DOI: 10.1172/jci23626
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

    This is a research prototype built from draft material. It is not medical advice, and its statements still await verification against the original studies.

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