Open Access Articles- Top Results for Niacin


This article is about the nutrient. For the neo-fusion band, see Niacin (band). For niacins, see Nicotinic acids.
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IUPAC name
pyridine-3-carboxylic acid[1]
Systematic IUPAC name
Pyridine-3-carboxylic acid[2]
Other names
Nicotinic Acid
Vitamin B3
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3DMet B00073 ATC code C04AC01
C10AD02 109591 59-67-6 7pxY ChEBI CHEBI:15940 7pxY ChEMBL ChEMBL573 7pxY ChemSpider 913 7pxY DrugBank DB00627 7pxY EC number 200-441-0 3340 IUPHAR ligand 1588 Jmol-3D images Image
Image KEGG D00049 7pxY MeSH Niacin PubChem Template:Chembox PubChem/format RTECS number QT0525000 Template:Chembox UNII colspan=2 style="background:#f8eaba; border-top:2px solid transparent; border-bottom:2px solid transparent; text-align:center;" #REDIRECTmw:Help:Magic words#Other
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Template:Chem/atomTemplate:Chem/atomTemplate:Chem/atomTemplate:Chem/atomTemplate:Chem/atomTemplate:Chem/atom Molar mass 123.1094 g mol−1 Appearance White, translucent crystals Density 1.473 g cm−3 Melting point Script error: No such module "convert". 18 g L−1 log P 0.219 Acidity (pKa) 4.85 Basicity (pKb) 9.15 Isoelectric point 4.75 1.4936 Dipole moment 0.1271305813 D colspan=2 style="background:#f8eaba; border-top:2px solid transparent; border-bottom:2px solid transparent; text-align:center;" #REDIRECTmw:Help:Magic words#Other
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−344.9 kJ mol−1 −2.73083 MJ mol−1 colspan=2 style="background:#f8eaba; border-top:2px solid transparent; border-bottom:2px solid transparent; text-align:center;" #REDIRECTmw:Help:Magic words#Other
This page is a soft redirect. Pharmacology

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Intramuscular, Oral 20–45 min colspan=2 style="background:#f8eaba; border-top:2px solid transparent; border-bottom:2px solid transparent; text-align:center;" #REDIRECTmw:Help:Magic words#Other
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EU classification Irritant Xi R-phrases R36/37/38 S-phrases S26, S36 NFPA 704

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Except where otherwise noted, data are given for materials in their standard state (at 25 °C [77 °F], 100 kPa).
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Niacin (also known as vitamin B3 or nicotinic acid) is an organic compound with the formula Template:Chem/atomTemplate:Chem/atomTemplate:Chem/atomTemplate:Chem/atomTemplate:Chem/atomTemplate:Chem/atom and, depending on the definition used, one of the 20 to 80 essential human nutrients.

This colorless, water-soluble solid is a derivative of pyridine, with a carboxyl group (COOH) at the 3-position. Other forms of vitamin B3 include the corresponding amide and nicotinamide ("niacinamide"), where the carboxyl group has been replaced by a carboxamide group (Template:Chem/atomTemplate:Chem/atom), as well as more complex amides and a variety of esters. Nicotinic acid and niacinamide are convertible to each other with steady world demand rising from 8,500 tonnes per year in the 1980s to 40,000 in recent years.[3]

Niacin cannot be directly converted to nicotinamide, but both compounds are precursors of the coenzymes nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) in vivo.[4] NAD converts to NADP by phosphorylation in the presence of the enzyme NAD+ kinase. NADP and NAD are coenzymes for many dehydrogenases, participating in many hydrogen transfer processes.[5] 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.[5] High energy requirements (brain) or high turnover rate (gut, skin) organs are usually the most susceptible to their deficiency.[6] Although the two are identical in their vitamin activity, nicotinamide does not have the same pharmacological effects (lipid modifying effects) as niacin. Nicotinamide does not reduce cholesterol or cause flushing.[7] Niacin is involved in both DNA repair and the production of steroid hormones in the adrenal gland.

Insufficient niacin in the diet can cause nausea, skin and mouth lesions, anemia, headaches, and tiredness. Chronic niacin deficiency leads to a disease called pellagra. The lack of niacin may also be observed in pandemic deficiency disease, which is caused by a lack of five crucial vitamins (niacin, vitamin C, thiamin, vitamin D, and vitamin A) and is usually found in areas of widespread poverty and malnutrition. Niacin has not been found to be useful in decreasing the risk of cardiovascular disease in those already on a statin[8] but appears to be effective in those not taking a statin.[9]

Dietary needs

One recommended daily allowance of niacin is 2–12 mg/day for children, 14 mg/day for women, 16 mg/day for men, and 18 mg/day for pregnant or breast-feeding women.[10] Tolerable upper intake levels (UL) for adult men and women is considered to be 35 mg/day by the Dietary Reference Intake system to avoid flushing. In general, niacin status is tested through urinary biomarkers,[11] which are believed to be more reliable than plasma levels.[12]


Main article: Pellagra

Between 1906 and 1940 more than 3 million Americans were affected by pellagra with more than 100,000 deaths. Dr. Joseph Goldberger was assigned to study pellagra by the Surgeon General of the United States and produced good results. In the late 1930s, studies by Dr. Tom Spies, Marion Blankenhorn, and Clark Cooper established that niacin cured pellagra in humans. The disease was greatly reduced as a result.

File:Pellagra NIH.jpg
A man with pellagra, which is caused by a chronic lack of vitamin B3 in the diet

At present, niacin deficiency is sometimes seen in developed countries, and it is usually apparent in conditions of poverty, malnutrition, and chronic alcoholism.[13] It also tends to occur in areas where people eat maize (corn) as a staple food, since it is the only grain low in digestible niacin. A special cooking technique called nixtamalization is needed to increase the bioavailability of niacin during maize meal/flour production.

Mild niacin deficiency has been shown to slow metabolism, causing decreased tolerance to cold.

Severe deficiency of niacin in the diet causes the disease pellagra, which is characterized by diarrhea, dermatitis, and dementia, as well as “Casal's necklace” lesions on the lower neck, hyperpigmentation, thickening of the skin, inflammation of the mouth and tongue, digestive disturbances, amnesia, delirium, and eventually death, if left untreated.[14] Common psychiatric symptoms of niacin deficiency include irritability, poor concentration, anxiety, fatigue, restlessness, apathy, and depression.[14] Studies have indicated that, in patients with alcoholic pellagra, niacin deficiency may be an important factor influencing both the onset and severity of this condition. Patients with alcoholism typically experience increased intestinal permeability, leading to negative health outcomes.

Hartnup’s disease is a hereditary nutritional disorder resulting in niacin deficiency.[14] This condition was first identified in the 1950s by the Hartnup family in London. It is due to a deficit in the intestines and kidneys, making it difficult for the body to break down and absorb dietary tryptophan. The resulting condition is similar to pellagra, including symptoms of red, scaly rash, and sensitivity to sunlight. Oral niacin is given as a treatment for this condition in doses ranging from 40–200 mg, with a good prognosis if identified and treated early.[14] Niacin synthesis is also deficient in carcinoid syndrome, because of metabolic diversion of its precursor tryptophan to form serotonin.

Medical uses

A 2014 review of niacin did not find that it affected either cardiovascular disease or risk of death in those already taking a statin.[8] Niacin alone appears to reduce the risk of cardiovascular disease.[15][16]

The National Cholesterol Education Program (NCEP) in 2002 recommended niacin alone for cardiovascular and atherogenic dyslipidemia in mild or normal LDL levels or in combination for higher HDL levels.[17] By lowering VLDL levels, niacin also increases the level of high-density lipoprotein (HDL) or "good" cholesterol in blood, and therefore it is sometimes prescribed for people with low HDL, who are also at high risk of a heart attack.[18]

Nicotinic acid has been also approved by the FDA for pellagra. Moreover nicotinic acid has been used as a topical vasodilator or skin cream. Several cosmetic products contain vitamin B3 as a key ingredient due to its antioxidant, antiwrinkle, and whitening effects. Niacin exerts antioxidant properties through redox reaction of nicotinic acid metabolites; thus, it can scavenge ROS which is the key etiology of skin aging such as wrinkles, sag, poor texture, hyperpigmentation, and skin yellowness. Moreover, niacin is applied for lip plumper due to its vasodilation effect. Niacin acts as the vasodilator which can dilate the capillaries of lip. The vasodilated lips are slightly swelled and redder making them appear as full blooming lips which is a typically desired appearance.[19]


Pharmacological doses of niacin (1.5 – 6 g per day) lead to side effects that can include dermatological conditions such as skin flushing and itching, dry skin, and skin rashes including eczema exacerbation and acanthosis nigricans. Some of these symptoms are generally related to niacin's role as the rate limiting cofactor in the histidine decarboxylase enzyme which converts l-histidine into histamine.[citation needed] H1 and H2 receptor mediated histamine is metabolized via a sequence of mono (or di-) amine oxidase and COMT into methylhistamine which is then conjugated through the liver's CYP450 pathways. Persistent flushing and other symptoms may indicate deficiencies in one or more of the cofactors responsible for this enzymatic cascade. Gastrointestinal complaints, such as dyspepsia (indigestion), nausea and liver toxicity fulminant hepatic failure, have also been reported. Side effects of hyperglycemia, cardiac arrhythmias and "birth defects in experimental animals" have also been reported.[20][page needed]

Flushing usually lasts for about 15 to 30 minutes, though it can sometimes last up to two hours. It is sometimes accompanied by a prickly or itching sensation, in particular, in areas covered by clothing. Flushing is mediated by prostaglandin E2 and D2 due to GPR109A activation of epidermal Langerhans cells and keratinocytes.[21][22] Langerhans cells use cyclooxygenase type 1 (COX-1) for PGE2 production and are more responsible for acute flushing while keratinocytes are COX-2 dependent and are in active continued vaso-dilation.[23][24] To reduce flushing many studies focused on altering or blocking the prostaglandin mediated pathway.[25] This effect is mediated by GPR109A-mediated prostaglandin release from the Langerhans cells of the skin and can be blocked by taking 300 mg of aspirin half an hour before taking niacin, by taking one tablet of ibuprofen per day or by co-administering the prostaglandin receptor antagonist laropiprant. Taking niacin with meals also helps reduce this side effect. After several weeks of a consistent dose, most patients no longer flush.[26] Slow- or "sustained"-release forms of niacin have been developed to lessen these side effects.[27][28] One study showed the incidence of flushing was significantly lower with a sustained release formulation[29] though doses above 2 g per day have been associated with liver damage, in particular, with slow-release formulations.[20] Flushing is often thought to involve histamine, but histamine has been shown not to be involved in the reaction.[30] Prostaglandin (PGD2) is the primary cause of the flushing reaction, with serotonin appearing to have a secondary role in this reaction.[30]

Hepatotoxicity is another side effect of niacin. This is possibly related to metabolism via amidation resulting in NAD production.[31] The time-release form has a lower therapeutic index for lowering serum lipids relative to this form of toxicity.[32]

Although high doses of niacin may elevate blood sugar, thereby worsening diabetes mellitus,[20] recent studies show the actual effect on blood sugar to be only 5–10%. Patients with diabetes who continued to take anti-diabetes drugs containing niacin did not experience major blood glucose changes. Thus overall, niacin continues to be recommended as a drug for preventing cardiovascular disease in patients with diabetes.

Hyperuricemia is another side effect of taking high-dose niacin, and may exacerbate gout.[33]

Niacin in doses used to lower cholesterol levels has been associated with birth defects in laboratory animals, with possible consequences for infant development in pregnant women.[20]

Niacin, particularly the time-release variety, at extremely high doses can cause acute toxic reactions.[34] Extremely high doses of niacin can also cause niacin maculopathy, a thickening of the macula and retina, which leads to blurred vision and blindness. This maculopathy is reversible after niacin intake ceases.[35]

Mechanism of action

Niacin therapeutic effect is mostly through its binding to G protein coupled receptors, niacin receptor 1 (NIACR1) and niacin receptor 2 (NIACR2), that are highly expressed in adipose tissue, spleen, immune cells and keratinocytes but not in other expected organs such as liver, kidney, heart or intestine.[36][37] A carboxyl group of nicotinic acid is a crucial moiety for the binding in which both oxygen atoms of the carboxyl group can bind to positively charged residue of arginine 111 of transmembrane helices (TMH) 3 via electrostatic interaction. Moreover, nitrogen atom of pyridine ring of nicotinic acid interacts with serine 178 of extracellular loop (ECL) 2 by embedding between TMH2/ECL1 junction and TMH7. [19] NIACR1 and NIACR2 inhibit cyclic adenosine monophosphate (cAMP) production and thus fat breakdown in adipose tissue and free fatty acids available for liver to produce triglycerides and very-low-density lipoproteins (VLDL) and consequently low-density lipoprotein (LDL) or "bad" cholesterol.[31][38] Decrease in free fatty acids also suppress hepatic expression of apolipoprotein C3 (APOC3) and PPARg coactivator-1b (PGC-1b) thus increase VLDL turn over and reduce its production.[39] It also inhibits diacylglycerol acyltransferase-2 (important hepatic TG synthesis).

The mechanism behind increasing HDL is not totally understood but it seems to be done in various ways. Niacin increases apolipoprotein A1 levels due to anti catabolic effects resulting in higher reverse cholesterol transport. It also inhibits HDL hepatic uptake, down-regulating production of the cholesterol ester transfer protein (CETP) gene.[40] Finally, it stimulates the ABCA1 transporter in monocytes and macrophages and up-regulates peroxisome proliferator-activated receptor γ results in reverse cholesterol transport.[41]

It reduces secondary outcomes associated with atherosclerosis, such as low density lipoprotein cholesterol (LDL), very low-density lipoprotein cholesterol (VLDL-C), and triglycerides (TG), but increases high density lipoprotein cholesterol (HDL).[40] Despite the importance of other cardiovascular risk factors, high HDL was associated with fewer cardiovascular events independent of LDL reduction.[42][43] Other effects include anti-thrombotic and vascular inflammation, improving endothelial function, and plaque stability.[44] Adipokines are the adipocytes’ produced mediators. Some adipokines such as tumor necrosis factor (TNF)-a, interleukins and chemokines, have pro-inflammatory effect and some others such as adiponectin have anti-inflammatory effect that regulates inflammatory process, decrease vascular progression and atherosclerosis.[45]

Niacin also appears to upregulate brain-derived neurotrophic factor (BDNF) and tropomyosin receptor kinase B (TrkB) expression.[46]

Research has been able to show the function of niacin in the pathway lipid metabolism. It is seen that this vitamin can decrease the synthesis of apoB-containing lipoproteins such as VLDL, LDL, IDL and Lipoprotein (a) via several mechanisms: (1) Directly inhibiting the action of DGAT2, a key enzyme for triglyceride synthesis; (2) It has the ability to bind to the receptor HCAR2 thereby decreasing lipolysis and FFA flux to the liver for triglyceride synthesis;[11] and (3) increased apoB catabolism. On the other hand HDL cholesterol levels are increased by niacin through direct and indirect pathways. (4) Niacin decreases CETP mass and activity, and this synergistic effect with the decrease in triglyceride levels, can indirectly raise HDL cholesterol levels. The study has also been able to show direct effects on the beta chain of ATP synthase (5) and on production (6) and hepatic uptake (7) of apoA-I also increase HDL cholesterol levels. Thus by affecting the pathway reducing lipid levels help in reducing CVD.[47]


Nicotinamide may be obtained from the diet where it is present primarily as NAD+ and NADP+. These are hydrolysed in the intestine and the resulting nicotinamide is absorbed either as such, or following its hydrolysis to nicotinic acid. Nicotinamide is present in nature in only small amounts. In unprepared foods, niacin is present mainly in the form of the cellular pyridine nucleotides NAD and NADP. Enzymatic hydrolysis of the co-enzymes can occur during the course of food preparation. Boiling releases most of the total niacin present in sweet corn as nicotinamide (up to 55 mg/kg).[48]

Nicotinamide may be toxic to the liver at doses exceeding 3 g/day for adults.[49]

Inositol hexanicotinate

One form of dietary supplement is inositol hexanicotinate (IHN), which is inositol that has been esterified with niacin on all six of inositol's alcohol groups. IHN is usually sold as "flush-free" or "no-flush" niacin in units of 250, 500, or 1000 mg/tablets or capsules. It is sold as an over-the-counter formulation, and often is marketed and labeled as niacin, thus misleading consumers into thinking they are getting the active form of the medication. While this form of niacin does not cause the flushing associated with the immediate-release products, the evidence that it has lipid-modifying functions is contradictory, at best. As the clinical trials date from the early 1960s (Dorner, Welsh) or the late 1970s (Ziliotto, Kruse, Agusti), it is difficult to assess them by today's standards.[50] One of the last of those studies affirmed the superiority of inositol and xantinol esters of nicotinic acid for reducing serum free fatty acid,[51] but other studies conducted during the same period found no benefit.[52] Studies explain that this is primarily because "flush-free" preparations do not contain any free nicotinic acid. A more recent placebo-controlled trial was small (n=11/group), but results after three months at 1500 mg/day showed no trend for improvements in total cholesterol, LDL-C, HDL-C or triglycerides.[53] Thus, so far there is not enough evidence to recommend IHN to treat dyslipidemia. Furthermore, the American Heart Association and the National Cholesterol Education Program both take the position that only prescription niacin should be used to treat dyslipidemias, and only under the management of a physician. The reason given is that niacin at effective intakes of 1500–3000 mg/day can also potentially have severe adverse effects. Thus liver function tests to monitor liver enzymes are necessary when taking therapeutic doses of niacin, including alkaline phosphatase (ALP), aspartate transaminase (AST), and alanine transaminase (ALT).

Biosynthesis and chemical synthesis

The liver can synthesize niacin from the essential amino acid tryptophan, requiring 60 mg of tryptophan to make one mg of niacin.[54] The 5-membered aromatic heterocycle of tryptophan is cleaved and rearranged with the alpha amino group of tryptophan into the 6-membered aromatic heterocycle of niacin. Riboflavin, vitamin B6 and iron are required in some of the reactions involved in the conversion of tryptophan to NAD.

Several thousand tons of niacin are manufactured each year, starting from 3-methylpyridine.

Food sources

Niacin is found in variety of foods, including liver, chicken, beef, fish, cereal, peanuts, and legumes, and is also synthesized from tryptophan, an essential amino acid found in most forms of protein.

Animal products:

Fruits and vegetables:






Many preparations of niacin are available over-the-counter as dietary supplements. Immediate release niacin is effective at lowering cholesterol levels, and has minimal hepatotoxic side effects due to its rapid elimination from the body. However, it has the main drawback of causing strong vasodilation side effects with sensations of flushing and skin tingling that can be unpleasant to many patients. Non-prescription extended release niacin, such as Endur-acin, which uses a wax matrix to delay release is available as well.[59][60] A prescription extended release niacin, Niaspan, has a film coating that delays release of the niacin, resulting in an absorption over a period of 8–12 hours. The extended release formulations generally reduce vasodilation and flushing side effects, but increase the risk of hepatotoxicity compared to the immediate release forms.[61][62][63]

A formulation of laropiprant (Merck & Co., Inc.) and niacin had previously been approved for use in Europe and marketed as Tredaptive. Laropiprant is a prostaglandin D2 binding drug shown to reduce vasodilatation and flushing up to 73%.[40][64][65][66] The HPS2-THRIVE study,[67] a study sponsored by Merck, showed no additional efficacy of Tredaptive in lowering cholesterol when used together with other statin drugs, but did show an increase in other side effects. The study resulted in the complete withdrawal of Tredaptive from the international market.[68][69]

Over-the counter niacin dietary supplements generally lack the safety and efficacy data required for FDA regulatory approval. Some “no flush” types, such as inositol hexanicotinate contain convertible niacin compounds, but have little clinical efficacy in reducing cholesterol levels.[70][71] “Slow release” varieties have higher hepatotoxic activity, hence non-prescription niacin is not recommended due to potential harm.[40]


Niacin was first described by chemist Hugo Weidel in 1873 in his studies of nicotine.[72] The original preparation remains useful: The oxidation of nicotine using nitric acid.[73] For the first time, niacin was extracted by Casimir Funk, but he thought that it was thiamine and due to the discovered amine group he coined the term "vitamine". Niacin was extracted from livers by biochemist Conrad Elvehjem in 1937, who later identified the active ingredient, then referred to as the "pellagra-preventing factor" and the "anti-blacktongue factor."[74] Soon after, in studies conducted in Alabama and Cincinnati, Dr. Tom Spies found that nicotinic acid cured the sufferers of pellagra.[75]

Niacin is referred to as vitamin B3 because it was the third of the B vitamins to be discovered. It has historically been referred to as "vitamin PP", "vitamin P-P" and "PP-factor", that are derived from the term "pellagra-preventive factor".[76] When the biological significance of nicotinic acid was realized, it was thought appropriate to choose a name to dissociate it from nicotine, to avoid the perception that vitamins or niacin-rich food contains nicotine, or that cigarettes contain vitamins. The resulting name 'niacin' was derived from nicotinic acid + vitamin.[76]

Carpenter found in 1951 that niacin in corn is biologically unavailable, and can be released only in very alkaline lime water of pH 11.[77]

In 1955, Altschul and colleagues described niacin as having a lipid lowering property.[78] Niacin is the oldest lipid lowering drug.

On April 22, 2014, Pennsylvania State University researchers working with NASA at the Goddard Astrobiology Analytical Laboratory reported[79] of finding niacin within eight CM-2 type carbonaceous chondrite meteorites. The meteorite’s vitamin B3 levels ranged from 30–600 parts per billion, the study reports. Related molecules discovered in the meteorites include pyridine carboxylic acids and pyridine dicarboxylic acids.


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