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| Names | |||
|---|---|---|---|
| Pronunciation | /ˈnaɪəsɪn/ | ||
| Preferred IUPAC name
Pyridine-3-carboxylic acid[1] | |||
Other names
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| Identifiers | |||
3D model (JSmol)
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|||
| 3DMet | |||
| 109591 | |||
| ChEBI | |||
| ChEMBL | |||
| ChemSpider | |||
| DrugBank | |||
| ECHA InfoCard | 100.000.401 | ||
| EC Number |
| ||
| 3340 | |||
| KEGG | |||
| MeSH | Niacin | ||
PubChem CID
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| RTECS number |
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| UNII | |||
CompTox Dashboard (EPA)
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| Properties | |||
| C6H5NO2 | |||
| Molar mass | 123.111 g·mol−1 | ||
| Appearance | White, translucent crystals | ||
| Density | 1.473 g cm−3 | ||
| Melting point | 237 °C; 458 °F; 510 K | ||
| 18 g L−1 | |||
| log P | 0.219 | ||
| Acidity (pKa) | 2.0, 4.85 | ||
| Isoelectric point | 4.75 | ||
Refractive index (nD)
|
1.4936 | ||
| 0.1271305813 D[citation needed] | |||
| Thermochemistry | |||
Std enthalpy of
formation (ΔfH⦵298) |
−344.9 kJ mol−1 | ||
Std enthalpy of
combustion (ΔcH⦵298) |
−2.73083 MJ mol−1 | ||
| Pharmacology | |||
| C04AC01 (WHO) C10BA01 (WHO) C10AD02 (WHO) C10AD52 (WHO) | |||
| License data |
| ||
| Intramuscular, by mouth | |||
| Pharmacokinetics: | |||
| 20–45 min | |||
| Hazards | |||
| GHS labelling: | |||
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| Warning | |||
| H319 | |||
| P264, P280, P305+P351+P338, P337+P313, P501 | |||
| NFPA 704 (fire diamond) | |||
| Flash point | 193 °C (379 °F; 466 K) | ||
| 365 °C (689 °F; 638 K) | |||
Except where otherwise noted, data are given for materials in their standard state (at 25 °C , 100 kPa).
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| Clinical data | |
|---|---|
| Trade names | Niacor, Niaspan, others |
| AHFS/Drugs.com | Monograph |
| MedlinePlus | a682518 |
| License data |
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| Pregnancy category |
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| Routes of administration | Intramuscular, by mouth |
| Legal status | |
| Legal status |
|
| Identifiers | |
| PDB ligand | |
| CompTox Dashboard (EPA) | |
| ECHA InfoCard | 100.000.401 |
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Niacin, also known as nicotinic acid, is an organic compound and a vitamer of vitamin B3, an essential human nutrient.[3] It is produced by plants and animals from the amino acid tryptophan.[4] Niacin is obtained in the diet from a variety of whole and processed foods, with highest contents in fortified packaged foods, meat, poultry, red fish such as tuna and salmon, lesser amounts in nuts, legumes and seeds.[3][5] Niacin as a dietary supplement is used to treat pellagra, a disease caused by niacin deficiency. Signs and symptoms of pellagra include skin and mouth lesions, anemia, headaches, and tiredness.[6] Many countries mandate its addition to wheat flour or other food grains, thereby reducing the risk of pellagra.[3][7]
The amide derivative nicotinamide (niacinamide) is a component of the coenzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP+). Although niacin and nicotinamide are identical in their vitamin activity, nicotinamide does not have the same pharmacological, lipid-modifying effects or side effects as niacin, i.e., when niacin takes on the -amide group, it does not reduce cholesterol nor cause flushing.[8][9] Nicotinamide is recommended as a treatment for niacin deficiency because it can be administered in remedial amounts without causing the flushing, considered an adverse effect.[10]
Niacin is also a prescription medication.[11] Amounts far in excess of the recommended dietary intake for vitamin functions will lower blood triglycerides and low density lipoprotein cholesterol (LDL-C), and raise blood high density lipoprotein cholesterol (HDL-C, often referred to as "good" cholesterol). There are two forms: immediate-release and sustained-release niacin. Initial prescription amounts are 500 mg/day, increased over time until a therapeutic effect is achieved. Immediate-release doses can be as high as 3,000 mg/day; sustained-release as high as 2,000 mg/day.[11] Despite the proven lipid changes, niacin has not been found useful for decreasing the risk of cardiovascular disease in those already on a statin.[12] A 2010 review had concluded that niacin was effective as a mono-therapy,[13] but a 2017 review incorporating twice as many trials concluded that prescription niacin, while affecting lipid levels, did not reduce all-cause mortality, cardiovascular mortality, myocardial infarctions, nor fatal or non-fatal strokes.[14] Prescription niacin was shown to cause hepatotoxicity[15] and increase risk of type 2 diabetes.[16][17] Niacin prescriptions in the U.S. had peaked in 2009, at 9.4 million,[citation needed] declining to 800 thousand by 2020.[18]
Niacin has the formula C
6H
5NO
2 and belongs to the group of the pyridinecarboxylic acids.[3] As the precursor for nicotinamide adenine dinucleotide and nicotinamide adenine dinucleotide phosphate, niacin is involved in DNA repair.[19]
Definition
Niacin is both a vitamin, i.e., an essential nutrient, marketed as a dietary supplement, and in the US, a prescription medicine. As a vitamin, it is precursor of the coenzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP). These compounds are coenzymes for many dehydrogenases, participating in many hydrogen transfer processes. NAD is important in catabolism of fat, carbohydrate, protein, and alcohol, as well as cell signaling and DNA repair, and NADP mostly in anabolism reactions such as fatty acid and cholesterol synthesis.[20] Vitamin intake recommendations made by several countries are that intakes of 14–18 mg/day are sufficient to meet the needs of healthy adults.[4][21][22] Niacin but also nicotinamide (niacinamide) are used for prevention and treatment of pellagra, a disease caused by lack of the vitamin.[6][20] When niacin is used as a medicine to treat elevated cholesterol and triglycerides, daily doses range from 500 to 3,000 mg/day.[23][24] High-dose nicotinamide does not have this medicinal effect.[20]
Vitamin deficiency
Severe deficiency of niacin in the diet causes the disease pellagra, characterized by diarrhea, sun-sensitive dermatitis involving hyperpigmentation and thickening of the skin (see image), inflammation of the mouth and tongue, delirium, dementia, and if left untreated, death.[6] Common psychiatric symptoms include irritability, poor concentration, anxiety, fatigue, loss of memory, restlessness, apathy, and depression.[20] The biochemical mechanism(s) for the observed deficiency-caused neurodegeneration are not well understood, but may rest on: A) the requirement for nicotinamide adenine dinucleotide (NAD+) to suppress the creation of neurotoxic tryptophan metabolites, B) inhibition of mitochondrial ATP generation, resulting in cell damage; C), activation of the poly (ADP-ribose) polymerase (PARP) pathway, as PARP is a nuclear enzyme involved in DNA repair, but in the absence of NAD+ can lead to cell death; D) reduced synthesis of neuro-protective brain-derived neurotrophic factor or its receptor tropomyosin receptor kinase B; or E) changes to genome expression directly due to the niacin deficiency.[25]
Niacin deficiency is rarely seen in developed countries, and it is more typically associated with poverty, malnutrition or malnutrition secondary to chronic alcoholism.[26] It also tends to occur in less developed areas where people eat maize (corn) as a staple food, as maize is the only grain low in digestible niacin. A cooking technique called nixtamalization i.e., pretreating with alkali ingredients, increases the bioavailability of niacin during maize meal/flour production.[27] For this reason, people who consume maize as tortillas or hominy are at less risk of niacin deficiency.
For treating deficiency, the World Health Organization (WHO) recommends administering niacinamide i.e., nicotinamide, instead of niacin, to avoid the flushing side effect commonly caused by the latter. Guidelines suggest using 300 mg/day for three to four weeks.[10] Dementia and dermatitis show improvement within a week. Because deficiencies of other B-vitamins may be present, the WHO recommends a multi-vitamin in addition to the niacinamide.[10]
Hartnup disease is a hereditary nutritional disorder resulting in niacin deficiency.[28] It is named after an English family with a genetic disorder that resulted in a failure to absorb the essential amino acid tryptophan, tryptophan being a precursor for niacin synthesis. The symptoms are similar to pellagra, including red, scaly rash and sensitivity to sunlight. Oral niacin or niacinamide is given as a treatment for this condition in doses ranging from 50 to 100 mg twice a day, with a good prognosis if identified and treated early.[28] Niacin synthesis is also deficient in carcinoid syndrome, because of metabolic diversion of its precursor tryptophan to form serotonin.[3]
Measuring vitamin status
Plasma concentrations of niacin and niacin metabolites are not useful markers of niacin status.[4] Urinary excretion of the methylated metabolite N1-methyl-nicotinamide is considered reliable and sensitive. The measurement requires a 24-hour urine collection. For adults, a value of less than 5.8 μmol/day represent deficient niacin status and 5.8 to 17.5 μmol/day represents low.[4] According to the World Health Organization, an alternative mean of expressing urinary N1-methyl-nicotinamide is as mg/g creatinine in a 24-hour urine collection, with deficient defined as <0.5, low 0.5-1.59, acceptable 1.6-4.29, and high >4.3[10] Niacin deficiency occurs before the signs and symptoms of pellagra appear.[4] Erythrocyte nicotinamide adenine dinucleotide (NAD) concentrations potentially provide another sensitive indicator of niacin depletion, although definitions of deficient, low and adequate have not been established. Lastly, plasma tryptophan decreases on a low niacin diet because tryptophan converts to niacin. However, low tryptophan could also be caused by a diet low in this essential amino acid, so it is not specific to confirming vitamin status.[4]
Dietary recommendations
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