Nicotinic acid

evidence_span

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experimental_model

Oral radiotracer retention and distribution experiments

exposure

Labeled oral chromium with dietary/metabolite coadministration

limitations

A negative retention result in this preparation does not exclude all chemical complexation or dose effects. Oral coadministration is not identical to a preformed chromium-nicotinate complex.

nutrient_topic

Chromium research collection; topical membership is not evidence of a direct dietary effect. · Chromium

organism

Rat

plain_language

Adding nicotinic acid did not make the rats retain more chromium in this experiment.

primary_references

[chromium-p8605085] Dietary and metabolite effects on trivalent chromium retention and distribution in rats. (1995). https://pubmed.ncbi.nlm.nih.gov/8605085/ DOI: 10.1007/bf02789412

tissue_or_cell_type

Whole-body and tissue chromium

Chromium: transport, insulin signaling, nutrient interactions and essentiality debate (2026-09-17) · lines 861–872

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Oral radiotracer retention and distribution experiments · source_derived_draft · unverified_draft

### chromium-niacin-retention-null Oral coadministration of nicotinic acid with labeled chromium did not significantly alter chromium retention in the rat study. Condition category: normal nutrient_topic: Chromium research collection; topical membership is not evidence of a direct dietary effect. plain_language: Adding nicotinic acid did not make the rats retain more chromium in this experiment. organism: Rat tissue_or_cell_type: Whole-body and tissue chromium experimental_model: Oral radiotracer retention and distribution experiments limitations: A negative retention result in this preparation does not exclude all chemical complexation or dose effects. Oral coadministration is not identical to a preformed chromium-nicotinate complex. exposure: Labeled oral chromium with dietary/metabolite coadministration evidence_span: {"source_cache": "artifacts/chromium-research/8605085.abstract.txt", "locator": "Exact primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "19976d36625bfcd29ba9739717e4b5ee7c2a641dc625a2bfed62947df7060889", "start_char": 0, "end_char": 1103, "text_sha256": "19976d36625bfcd29ba9739717e4b5ee7c2a641dc625a2bfed62947df7060889"} [chromium-p8605085] Dietary and metabolite effects on trivalent chromium retention and distribution in rats. (1995). https://pubmed.ncbi.nlm.nih.gov/8605085/ DOI: 10.1007/bf02789412

cross_nutrient

Niacin precursor form and the measured endpoint are separate graph entities.

evidence_span

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experimental_model

AIM-HIGH randomized trial; 3,414 patients with established cardiovascular disease on intensive statin therapy

exposure

Extended-release nicotinic acid 1,500–2,000 mg/day versus placebo; mean 3-year follow-up

limitations

Pharmacological dosing added to statin therapy. Lipid changes are not equivalent to clinical benefit. Trial stopped for lack of efficacy; no inference about treating dietary niacin deficiency.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Homo sapiens

plain_language

Improved lipid numbers did not translate into fewer trial cardiovascular events in these statin-treated patients.

primary_references

[nia-clin-aimhigh2011] Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. (2011). https://pubmed.ncbi.nlm.nih.gov/22085343/ DOI: 10.1056/nejmoa1107579

tissue_or_cell_type

Circulating lipids and cardiovascular outcomes

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1389–1401

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · AIM-HIGH randomized trial; 3,414 patients with established cardiovascular disease on intensive statin therapy · source_derived_draft · unverified_draft

### nia-clin-aimhigh-events The AIM-HIGH composite endpoint occurred in 16.4% versus 16.2% of niacin and placebo participants: hazard ratio 1.02, 95% CI 0.87–1.21. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Improved lipid numbers did not translate into fewer trial cardiovascular events in these statin-treated patients. organism: Homo sapiens tissue_or_cell_type: Circulating lipids and cardiovascular outcomes experimental_model: AIM-HIGH randomized trial; 3,414 patients with established cardiovascular disease on intensive statin therapy limitations: Pharmacological dosing added to statin therapy. Lipid changes are not equivalent to clinical benefit. Trial stopped for lack of efficacy; no inference about treating dietary niacin deficiency. exposure: Extended-release nicotinic acid 1,500–2,000 mg/day versus placebo; mean 3-year follow-up cross_nutrient: Niacin precursor form and the measured endpoint are separate graph entities. evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/aimhigh2011.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "eefcc0d7eed5694eb9d1861a06fc5a256986753607c2095996304fd0de25f3aa", "start_char": 0, "end_char": 2340, "text_sha256": "eefcc0d7eed5694eb9d1861a06fc5a256986753607c2095996304fd0de25f3aa"} [nia-clin-aimhigh2011] Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. (2011). https://pubmed.ncbi.nlm.nih.gov/22085343/ DOI: 10.1056/nejmoa1107579

cross_nutrient

Niacin precursor form and the measured endpoint are separate graph entities.

evidence_span

{"source_cache": "artifacts/niacin-clinical-sources/aimhigh2011.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "eefcc0d7eed5694eb9d1861a06fc5a256986753607c2095996304fd0de25f3aa", "start_char": 0, "end_char": 2340, "text_sha256": "eefcc0d7eed5694eb9d1861a06fc5a256986753607c2095996304fd0de25f3aa"}

experimental_model

AIM-HIGH randomized trial; 3,414 patients with established cardiovascular disease on intensive statin therapy

exposure

Extended-release nicotinic acid 1,500–2,000 mg/day versus placebo; mean 3-year follow-up

limitations

Pharmacological dosing added to statin therapy. Lipid changes are not equivalent to clinical benefit. Trial stopped for lack of efficacy; no inference about treating dietary niacin deficiency.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Homo sapiens

plain_language

The drug changed blood lipids in the intended direction.

primary_references

[nia-clin-aimhigh2011] Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. (2011). https://pubmed.ncbi.nlm.nih.gov/22085343/ DOI: 10.1056/nejmoa1107579

tissue_or_cell_type

Circulating lipids and cardiovascular outcomes

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1375–1387

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · AIM-HIGH randomized trial; 3,414 patients with established cardiovascular disease on intensive statin therapy · source_derived_draft · unverified_draft

### nia-clin-aimhigh-hdl In AIM-HIGH, median HDL cholesterol in the niacin arm rose from 35 to 42 mg/dL at two years, with concurrent triglyceride and LDL reductions. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The drug changed blood lipids in the intended direction. organism: Homo sapiens tissue_or_cell_type: Circulating lipids and cardiovascular outcomes experimental_model: AIM-HIGH randomized trial; 3,414 patients with established cardiovascular disease on intensive statin therapy limitations: Pharmacological dosing added to statin therapy. Lipid changes are not equivalent to clinical benefit. Trial stopped for lack of efficacy; no inference about treating dietary niacin deficiency. exposure: Extended-release nicotinic acid 1,500–2,000 mg/day versus placebo; mean 3-year follow-up cross_nutrient: Niacin precursor form and the measured endpoint are separate graph entities. evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/aimhigh2011.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "eefcc0d7eed5694eb9d1861a06fc5a256986753607c2095996304fd0de25f3aa", "start_char": 0, "end_char": 2340, "text_sha256": "eefcc0d7eed5694eb9d1861a06fc5a256986753607c2095996304fd0de25f3aa"} [nia-clin-aimhigh2011] Niacin in patients with low HDL cholesterol levels receiving intensive statin therapy. (2011). https://pubmed.ncbi.nlm.nih.gov/22085343/ DOI: 10.1056/nejmoa1107579

cross_nutrient

Laropiprant / MK-0524 (coadministered_drug)

evidence_span

{"source_cache": "artifacts/niacin-clinical-sources/hps2014.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05", "start_char": 0, "end_char": 2717, "text_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05"}

experimental_model

HPS2-THRIVE randomized trial; 25,673 adults with vascular disease on statin-based therapy

exposure

Extended-release nicotinic acid 2 g plus laropiprant 40 mg daily; median 3.9 years

limitations

Combination regimen; observed harm cannot all be assigned to nicotinic acid alone. Run-in selected participants able to tolerate initial therapy. Outcomes do not address deficiency replacement.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Homo sapiens

plain_language

This large trial also found no clear event benefit when the combination was added to statin treatment.

primary_references

[nia-clin-hps2014] Effects of extended-release niacin with laropiprant in high-risk patients. (2014). https://pubmed.ncbi.nlm.nih.gov/25014686/ DOI: 10.1056/nejmoa1300955

tissue_or_cell_type

Major vascular events and adverse events

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1403–1415

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HPS2-THRIVE randomized trial; 25,673 adults with vascular disease on statin-based therapy · source_derived_draft · unverified_draft

### nia-clin-hps-events Niacin–laropiprant produced major vascular-event rates of 13.2% versus 13.7% with placebo: rate ratio 0.96, 95% CI 0.90–1.03, without a significant benefit. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: This large trial also found no clear event benefit when the combination was added to statin treatment. organism: Homo sapiens tissue_or_cell_type: Major vascular events and adverse events experimental_model: HPS2-THRIVE randomized trial; 25,673 adults with vascular disease on statin-based therapy limitations: Combination regimen; observed harm cannot all be assigned to nicotinic acid alone. Run-in selected participants able to tolerate initial therapy. Outcomes do not address deficiency replacement. exposure: Extended-release nicotinic acid 2 g plus laropiprant 40 mg daily; median 3.9 years cross_nutrient: Laropiprant / MK-0524 (coadministered_drug) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/hps2014.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05", "start_char": 0, "end_char": 2717, "text_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05"} [nia-clin-hps2014] Effects of extended-release niacin with laropiprant in high-risk patients. (2014). https://pubmed.ncbi.nlm.nih.gov/25014686/ DOI: 10.1056/nejmoa1300955

cross_nutrient

Laropiprant / MK-0524 (coadministered_drug)

evidence_span

{"source_cache": "artifacts/niacin-clinical-sources/hps2014.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05", "start_char": 0, "end_char": 2717, "text_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05"}

experimental_model

HPS2-THRIVE randomized trial; 25,673 adults with vascular disease on statin-based therapy

exposure

Extended-release nicotinic acid 2 g plus laropiprant 40 mg daily; median 3.9 years

limitations

Combination regimen; observed harm cannot all be assigned to nicotinic acid alone. Run-in selected participants able to tolerate initial therapy. Outcomes do not address deficiency replacement.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Homo sapiens

plain_language

The combination had measurable harms as well as lipid effects.

primary_references

[nia-clin-hps2014] Effects of extended-release niacin with laropiprant in high-risk patients. (2014). https://pubmed.ncbi.nlm.nih.gov/25014686/ DOI: 10.1056/nejmoa1300955

tissue_or_cell_type

Major vascular events and adverse events

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1417–1429

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · HPS2-THRIVE randomized trial; 25,673 adults with vascular disease on statin-based therapy · source_derived_draft · unverified_draft

### nia-clin-hps-glycemic-harm Niacin–laropiprant increased serious diabetes-control disturbances by 3.7 percentage points and new diabetes diagnoses by 1.3 points; gastrointestinal, musculoskeletal, skin, infection and bleeding serious adverse events also increased. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: The combination had measurable harms as well as lipid effects. organism: Homo sapiens tissue_or_cell_type: Major vascular events and adverse events experimental_model: HPS2-THRIVE randomized trial; 25,673 adults with vascular disease on statin-based therapy limitations: Combination regimen; observed harm cannot all be assigned to nicotinic acid alone. Run-in selected participants able to tolerate initial therapy. Outcomes do not address deficiency replacement. exposure: Extended-release nicotinic acid 2 g plus laropiprant 40 mg daily; median 3.9 years cross_nutrient: Laropiprant / MK-0524 (coadministered_drug) evidence_span: {"source_cache": "artifacts/niacin-clinical-sources/hps2014.abstract.txt", "locator": "Indexed primary abstract", "file_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05", "start_char": 0, "end_char": 2717, "text_sha256": "9f12db5e258418187e65c3b921cffd01bf3cc0f400d3caa19cb4005c5e6f4f05"} [nia-clin-hps2014] Effects of extended-release niacin with laropiprant in high-risk patients. (2014). https://pubmed.ncbi.nlm.nih.gov/25014686/ DOI: 10.1056/nejmoa1300955

evidence_access

Primary full text

experimental_model

E. coli PncA genetic experiments, mammalian cancer cells and xenografts.

limitations

PncA is bacterial; do not create a human nicotinamidase from this result.

nutrient_topic

NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+

plain_language

Microbes can redirect one vitamin form into another route around a blocked enzyme.

primary_references

Bacteria Boost Mammalian Host NAD Metabolism by Engaging the Deamidated Biosynthesis Pathway. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32130883/ · DOI 10.1016/j.cmet.2020.02.001

NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 164–170

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · E. coli PncA genetic experiments, mammalian cancer cells and xenografts. · source_derived_draft · unverified_draft

## nad-plus-microbial-deamidation Microbes can redirect one vitamin form into another route around a blocked enzyme. Bacterial PncA converted nicotinamide to nicotinic acid, enabling an alternative deamidated NAD synthesis route in mammalian cells. Model: E. coli PncA genetic experiments, mammalian cancer cells and xenografts. Limitations: PncA is bacterial; do not create a human nicotinamidase from this result. Evidence access: Primary full text Bacteria Boost Mammalian Host NAD Metabolism by Engaging the Deamidated Biosynthesis Pathway. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32130883/ · DOI 10.1016/j.cmet.2020.02.001

evidence_access

Primary abstract

experimental_model

Human receptor/cell assays with separate mouse tissue observations.

limitations

Low affinity makes exposure compartment important; sharing a receptor does not make butyrate and niacin nutritionally interchangeable.

nutrient_topic

Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate

plain_language

A receptor also used by nicotinic acid senses sufficiently high local butyrate.

primary_references

GPR109A is a G-protein-coupled receptor for the bacterial fermentation product butyrate and functions as a tumor suppressor in colon. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19276343/ · DOI 10.1158/0008-5472.CAN-08-4466

Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 350–356

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human receptor/cell assays with separate mouse tissue observations. · source_derived_draft · unverified_draft

## butyrate-hcar2-agonism A receptor also used by nicotinic acid senses sufficiently high local butyrate. Butyrate activated GPR109A/HCAR2 at millimolar concentrations in the study of receptor signaling in human colonic cells. Model: Human receptor/cell assays with separate mouse tissue observations. Limitations: Low affinity makes exposure compartment important; sharing a receptor does not make butyrate and niacin nutritionally interchangeable. Evidence access: Primary abstract GPR109A is a G-protein-coupled receptor for the bacterial fermentation product butyrate and functions as a tumor suppressor in colon. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19276343/ · DOI 10.1158/0008-5472.CAN-08-4466

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_access

Primary abstract

experimental_model

Human colon cancer-cell receptor reexpression.

limitations

An engineered culture rescue does not show that oral supplements restore silenced receptors in patients.

nutrient_topic

Butyrate collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Butyrate

plain_language

Restoring the receptor enabled a response distinct from the HDAC pathway.

primary_references

GPR109A is a G-protein-coupled receptor for the bacterial fermentation product butyrate and functions as a tumor suppressor in colon. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19276343/ · DOI 10.1158/0008-5472.CAN-08-4466

trigger_kind

machinery_impairment Imported condition classification; unverified.

Butyrate: microbial production, fuel use, signaling and nutrient interactions (2026-09-19) · lines 358–364

AI-assisted research curation; primary-abstract references and experimental limitations individually identified. Not publisher full text. · supports · Human colon cancer-cell receptor reexpression. · source_derived_draft · unverified_draft

## butyrate-hcar2-restoration Restoring the receptor enabled a response distinct from the HDAC pathway. Restoring GPR109A expression in human colon cancer cells enabled apoptosis in the presence of butyrate or nicotinate; the receptor-mediated response did not require histone deacetylation inhibition. Model: Human colon cancer-cell receptor reexpression. Limitations: An engineered culture rescue does not show that oral supplements restore silenced receptors in patients. Evidence access: Primary abstract GPR109A is a G-protein-coupled receptor for the bacterial fermentation product butyrate and functions as a tumor suppressor in colon. · 2009 · https://pubmed.ncbi.nlm.nih.gov/19276343/ · DOI 10.1158/0008-5472.CAN-08-4466

availability_state

nutrient_deficiency Imported condition classification; unverified.

cross_nutrient

Dietary B6 status affected apparent tryptophan-to-niacin conversion.

experimental_model

Young male Wistar rats; four controlled diets for 19 days

exposure

Young male Wistar rats; 19-day diets; conversion contrast within niacin-free groups

limitations

Apparent urinary conversion, not net synthesis or a human requirement.

nutrient_topic

Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. · Vitamin B6

organism

Rattus norvegicus

plain_language

B6 shortage reduced this dietary study's estimate of niacin production from tryptophan.

primary_references

[b6-niacin-1995] Effects of Vitamin B6 Deficiency on the Conversion Ratio of Tryptophan to Niacin (1995). https://doi.org/10.1271/bbb.59.2060 DOI: 10.1271/bbb.59.2060

tissue_or_cell_type

Whole-animal dietary intake and urine

trigger_kind

nutrient_deficiency Imported condition classification; unverified.

Vitamin B6: mechanisms, deficiency and nutrient interactions (2026-09-17) · lines 898–909

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Young male Wistar rats; four controlled diets for 19 days · source_derived_draft · unverified_draft

### b6-met-rat-niacin-conversion Under niacin-free feeding, B6-free rats had lower apparent tryptophan-to-niacin conversion than rats receiving B6. Condition category: nutrient_deficiency nutrient_topic: Vitamin B6 research collection; topical membership is not evidence of a direct dietary effect. plain_language: B6 shortage reduced this dietary study's estimate of niacin production from tryptophan. organism: Rattus norvegicus tissue_or_cell_type: Whole-animal dietary intake and urine experimental_model: Young male Wistar rats; four controlled diets for 19 days limitations: Apparent urinary conversion, not net synthesis or a human requirement. cross_nutrient: Dietary B6 status affected apparent tryptophan-to-niacin conversion. exposure: Young male Wistar rats; 19-day diets; conversion contrast within niacin-free groups [b6-niacin-1995] Effects of Vitamin B6 Deficiency on the Conversion Ratio of Tryptophan to Niacin (1995). https://doi.org/10.1271/bbb.59.2060 DOI: 10.1271/bbb.59.2060

evidence_access

Primary full text

experimental_model

Mouse isotope tracing and microbiota-depletion experiments.

limitations

Not a measured human conversion fraction or proof that all formulations use the same route.

nutrient_topic

NAD+ collection; molecular form, preparation, species, exposure and manipulation remain explicit. · NAD+

plain_language

An oral precursor may reach tissues through a microbially altered route.

primary_references

Bacteria Boost Mammalian Host NAD Metabolism by Engaging the Deamidated Biosynthesis Pathway. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32130883/ · DOI 10.1016/j.cmet.2020.02.001

NAD+: compartmental supply, consumption and cross-nutrient mechanisms (2026-09-19) · lines 180–186

AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Mouse isotope tracing and microbiota-depletion experiments. · source_derived_draft · unverified_draft

## nad-plus-microbiota-oral-precursors An oral precursor may reach tissues through a microbially altered route. Stable-isotope tracing and microbiota depletion showed bacterial deamidation contributed substantially to tissue NAD increases after oral nicotinamide or NR in mice. Model: Mouse isotope tracing and microbiota-depletion experiments. Limitations: Not a measured human conversion fraction or proof that all formulations use the same route. Evidence access: Primary full text Bacteria Boost Mammalian Host NAD Metabolism by Engaging the Deamidated Biosynthesis Pathway. · 2020 · https://pubmed.ncbi.nlm.nih.gov/32130883/ · DOI 10.1016/j.cmet.2020.02.001

availability_state

machinery_impairment Imported condition classification; unverified.

evidence_span

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experimental_model

Cultured human cells with endogenous NAPRT and experimental NAPRT knockdown; separate mouse expression measurements

exposure

NAPRT knockdown plus nicotinic acid; concentration and duration not independently available in indexed abstract

limitations

The abstract does not specify the cell line or dosing details; no inference to oral intake or patient response.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Homo sapiens

plain_language

Nicotinic acid could not produce the same NAD rise after its entry enzyme was suppressed.

primary_references

[b3-pre-hara2007] Elevation of cellular NAD levels by nicotinic acid and involvement of nicotinic acid phosphoribosyltransferase in human cells. (2007). https://pubmed.ncbi.nlm.nih.gov/17604275/ DOI: 10.1074/jbc.m610357200

tissue_or_cell_type

Cultured human cells expressing endogenous NAPRT

trigger_kind

machinery_impairment Imported condition classification; unverified.

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 289–300

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Cultured human cells with endogenous NAPRT and experimental NAPRT knockdown; separate mouse expression measurements · source_derived_draft · unverified_draft

### b3-pre-naprt-knockdown-na NAPRT knockdown reversed the rise in cellular NAD caused by nicotinic acid in the cultured human cells studied. Condition category: machinery_impairment nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Nicotinic acid could not produce the same NAD rise after its entry enzyme was suppressed. organism: Homo sapiens tissue_or_cell_type: Cultured human cells expressing endogenous NAPRT experimental_model: Cultured human cells with endogenous NAPRT and experimental NAPRT knockdown; separate mouse expression measurements limitations: The abstract does not specify the cell line or dosing details; no inference to oral intake or patient response. exposure: NAPRT knockdown plus nicotinic acid; concentration and duration not independently available in indexed abstract evidence_span: {"source_cache": "artifacts/niacin-precursors-sources/hara2007.abstract.txt", "locator": "Indexed primary abstract", "start_char": 0, "end_char": 1634, "file_sha256": "4a605e0551bc9453dec63e8aa1e0fcd78985ae7dfca8d4b785039de0e0382547", "text_sha256": "4a605e0551bc9453dec63e8aa1e0fcd78985ae7dfca8d4b785039de0e0382547"} [b3-pre-hara2007] Elevation of cellular NAD levels by nicotinic acid and involvement of nicotinic acid phosphoribosyltransferase in human cells. (2007). https://pubmed.ncbi.nlm.nih.gov/17604275/ DOI: 10.1074/jbc.m610357200

evidence_span

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experimental_model

Recombinant human NAPRT crystallography and docking; purified protein, no intact tissue

exposure

Biochemical or structural assay; no dietary intervention

limitations

Purified-enzyme evidence does not establish dietary intake requirements or clinical outcomes.

nutrient_topic

Niacin research collection; topical membership is not evidence of a direct dietary effect. · Niacin (vitamin B3)

organism

Homo sapiens

plain_language

Nicotinic acid enters its NAD-building route through NAPRT.

primary_references

[b3-pre-naprt2015] Crystal structure of human nicotinic acid phosphoribosyltransferase. (2015). https://pubmed.ncbi.nlm.nih.gov/26042198/ DOI: 10.1016/j.fob.2015.05.002

tissue_or_cell_type

Purified recombinant protein; no intact tissue

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 249–260

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Recombinant human NAPRT crystallography and docking; purified protein, no intact tissue · source_derived_draft · unverified_draft

### b3-pre-naprt-reaction Human NAPRT catalyzes phosphoribosyl transfer from PRPP to nicotinic acid, producing nicotinic acid mononucleotide and pyrophosphate. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Nicotinic acid enters its NAD-building route through NAPRT. organism: Homo sapiens tissue_or_cell_type: Purified recombinant protein; no intact tissue experimental_model: Recombinant human NAPRT crystallography and docking; purified protein, no intact tissue limitations: Purified-enzyme evidence does not establish dietary intake requirements or clinical outcomes. exposure: Biochemical or structural assay; no dietary intervention evidence_span: {"source_cache": "artifacts/niacin-precursors-sources/naprt2015.abstract.txt", "locator": "Indexed primary abstract", "start_char": 0, "end_char": 1606, "file_sha256": "df6e36cf3464d4cda171d06ee24065532dee0d8b5fd5c3ccafcb1cc8df951bbe", "text_sha256": "df6e36cf3464d4cda171d06ee24065532dee0d8b5fd5c3ccafcb1cc8df951bbe"} [b3-pre-naprt2015] Crystal structure of human nicotinic acid phosphoribosyltransferase. (2015). https://pubmed.ncbi.nlm.nih.gov/26042198/ DOI: 10.1016/j.fob.2015.05.002

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

cross_nutrient

Human hydroxycarboxylic acid receptor 2 / HCAR2 (upstream_receptor); Nicotinic acid (agonist); arachidonic acid (released_substrate)

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 nicotinic-acid receptor signaling assay

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

Homo sapiens

plain_language

A separate receptor branch recruits beta-arrestin and releases the fatty-acid material used to make flushing signals.

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

Cultured human cells

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1305–1317

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cell-line nicotinic-acid receptor signaling assay · source_derived_draft · unverified_draft

### nia-clin-arrb1-pla2 Nicotinic acid promoted beta-arrestin1 association with activated cytosolic phospholipase A2 and beta-arrestin1-dependent phospholipase activation with arachidonate release in the cell assay. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: A separate receptor branch recruits beta-arrestin and releases the fatty-acid material used to make flushing signals. organism: Homo sapiens tissue_or_cell_type: Cultured human cells experimental_model: Human cell-line nicotinic-acid receptor signaling assay 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: Human hydroxycarboxylic acid receptor 2 / HCAR2 (upstream_receptor); Nicotinic acid (agonist); arachidonic acid (released_substrate) 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

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

cross_nutrient

Nicotinic acid (agonist); Cyclic adenosine monophosphate (measured_signal)

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 nicotinic-acid receptor signaling assay

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

Homo sapiens

plain_language

Nicotinic acid can act as a receptor signal as well as a vitamin precursor, switching down a cellular signaling molecule.

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

Cultured human cells

Niacin: NAD metabolism, deficiency and nutrient interactions (2026-09-17) · lines 1291–1303

AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Human cell-line nicotinic-acid receptor signaling assay · source_derived_draft · unverified_draft

### nia-clin-hcar2-camp Nicotinic-acid activation of GPR109A/HCAR2 in the human cell-line assay lowered cAMP through a pertussis-toxin-sensitive pathway. Condition category: normal nutrient_topic: Niacin research collection; topical membership is not evidence of a direct dietary effect. plain_language: Nicotinic acid can act as a receptor signal as well as a vitamin precursor, switching down a cellular signaling molecule. organism: Homo sapiens tissue_or_cell_type: Cultured human cells experimental_model: Human cell-line nicotinic-acid receptor signaling assay 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 (agonist); Cyclic adenosine monophosphate (measured_signal) 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

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

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