WordNet
- street name for lysergic acid diethylamide (同)back breaker, battery-acid, dose, dot, Elvis, loony toons, Lucy in the sky with diamonds, pane, superman, window pane, Zen
- any of various water-soluble compounds having a sour taste and capable of turning litmus red and reacting with a base to form a salt
- having the characteristics of an acid; "an acid reaction"
PrepTutorEJDIC
- 酸性の / 酸味のある,すっぱい(sour) / (言葉・態度などが)厳しい,しんらつな / 酸 / すっぱいもの / 《俗》=LSD
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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2014/08/25 11:57:22」(JST)
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This article is about the nutrient. For the neo-fusion band, see Niacin (band). For niacins, see Nicotinic acids.
| Niacin | |||
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IUPAC name
pyridine-3-carboxylic acid[1] |
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Systematic name
Pyridine-3-carboxylic acid[2] |
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Other names
Nicotinic Acid |
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| Identifiers | |||
| CAS number | 59-67-6 Y | ||
| PubChem | 938 | ||
| ChemSpider | 913 Y | ||
| UNII | 2679MF687A Y | ||
| EC number | 200-441-0 | ||
| DrugBank | DB00627 | ||
| KEGG | D00049 Y | ||
| MeSH | Niacin | ||
| ChEBI | CHEBI:15940 Y | ||
| ChEMBL | CHEMBL573 Y | ||
| IUPHAR ligand | 1588 | ||
| RTECS number | QT0525000 | ||
| ATC code | C04AC01,C10AD02 | ||
| Beilstein Reference | 109591 | ||
| Gmelin Reference | 3340 | ||
| 3DMet | B00073 | ||
| Jmol-3D images | Image 1 Image 2 |
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SMILES
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InChI
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| Properties | |||
| Molecular formula | C 6NH |
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| Molar mass | 123.1094 g mol−1 | ||
| Appearance | White, translucent crystals | ||
| Density | 1.473 g cm−3 | ||
| Melting point | 237 °C; 458 °F; 510 K | ||
| Solubility in water | 18 g L−1 | ||
| log P | 0.219 | ||
| Acidity (pKa) | 4.85 | ||
| Basicity (pKb) | 9.15 | ||
| Isoelectric point | 4.75 | ||
| Refractive index (nD) | 1.4936 | ||
| Dipole moment | 0.1271305813 D | ||
| Thermochemistry | |||
| Std enthalpy of formation ΔfH |
−344.9 kJ mol−1 | ||
| Std enthalpy of combustion ΔcH |
−2.73083 MJ mol−1 | ||
| Pharmacology | |||
| Routes of administration |
Intramuscular, Oral | ||
| Elimination half-life |
20-45 min | ||
| Hazards | |||
| EU classification | Xi | ||
| R-phrases | R36/37/38 | ||
| S-phrases | S26, S36 | ||
| NFPA 704 |
1
1
0
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| Flash point | 193 °C (379 °F; 466 K) | ||
| Except where noted otherwise, data are given for materials in their standard state (at 25 °C (77 °F), 100 kPa) | |||
| Y (verify) (what is: Y/N?) | |||
| Infobox references | |||
Niacin (also known as vitamin B3 and nicotinic acid) is an organic compound with the formula C
6H
5NO
2 and, depending on the definition used, one of the 20 to 80 essential human nutrients.
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 been used for over 50 years to increase levels of HDL in the blood and has been found to decrease the risk of cardiovascular events modestly in a number of controlled human trials.[3]
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, nicotinamide ("niacinamide"), where the carboxyl group has been replaced by a carboxamide group (CONH
2), 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 1980s to 40,000 in recent years.[4]
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.[5] 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.[6] 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.[6] High energy requirements (brain) or high turnover rate (gut, skin) organs are usually the most susceptible to their deficiency.[7]
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.[8] Niacin is involved in both DNA repair, and the production of steroid hormones in the adrenal gland.
Contents
- 1 Dietary needs
- 2 Deficiency
- 3 Therapeutic effects
- 4 Niacin prescriptions
- 5 Toxicity
- 6 Nicotinamide
- 7 Inositol hexanicotinate
- 8 Biosynthesis and chemical synthesis
- 9 Food sources
- 10 History
- 11 References
- 12 External links
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.[9] 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,[10] which are believed to be more reliable than plasma levels.[11]
Deficiency
Main article: Pellagra
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.[12] It also tends to occur in areas where people eat maize (corn, the only grain low in digestible niacin) as a staple food. 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.[13] Common psychiatric symptoms of niacin deficiency include irritability, poor concentration, anxiety, fatigue, restlessness, apathy, and depression.[13] 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.[13] 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.[13] Niacin synthesis is also deficient in carcinoid syndrome, because of metabolic diversion of its precursor tryptophan to form serotonin.
Therapeutic effects
In 1955, Altschul and colleagues described niacin as having a lipid lowering property.[14] Niacin is the oldest lipid lowering drug. 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).[15] Despite the importance of other cardiovascular risk factors, high HDL was associated with fewer cardiovascular events independent of LDL reduction.[16][17] Other effects include anti-thrombotic and vascular inflammation, improving endothelial function, and plaque stability.[18] Niacin alone[19] or in combination with other lipid lowering agents such as statin[20] or ezetimibe[21] significantly reduces risk of cardiovascular disease and arthrosclerosis progression.[22]
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.[23][24] NIACR1 inhibits 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.[25][26][27] 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.[28] 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.[15] Finally, it stimulates ABCA1 transporter in monocytes and macrophages and up-regulates peroxisome proliferator-activated receptor γ results in reverse cholesterol transport.[29]
Improving vascular endothelial function has been reported in few experiments using niacin. In an experiment on type 2 diabetes, nicotinic acid improved endothelial function comparing with control. Daily dose of 1 g niacin shows significant lipid modifying properties and reach the plateau using 2 grams. NIACR1 in immune cells such as monocytes, macrophages, and dendritic cells is responsible for atherosclerosis effects of niacin by reducing the immune cells’ infiltration of vessel wall[30][31] It also down regulates endothelial adhesion molecules such as vascular cell adhesion molecule 1 (VCAM-1) or of chemokines such as monocyte chemotactic protein 1 (MCP-1) and inflammatory proteins which results in atherosclerotic stabilization and antithrombotic effects.[18] The changes in adhesion molecules and chemokines might be through activation of receptor NIACR1 on immune cells.[30]
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.[32][33] Nicotinic acid increase adiponectin plasma levels in humans and mice[34][35] but inhibits pro-inflammatory chemokines such as MCP-1 and fractalkin.[36] Other recently explored therapeutic effect of nicotinic acid are neuroprotective and anti-inflammatory effects, beneficial in animal models of arthritis, chronic renal failure, or sepsis; however, more work is needed in this area. Niacin may also be used as an insect repellent.[citation needed]
Following Coronary Drug Project (CDP), one of the first experiments done to study long term clinical lipid-lowering effect of niacin in the 1960s to early 1970’s,[37] many other experiments have been done. Their results, summarized in two meta-analyses, concluded that therapeutic doses of niacin alone or in combination with other lipid-modifying agents such as statin reduce cardiovascular events and atherosclerosis progression significantly.[19][38] This agrees with the current National Cholesterol Education Program (NCEP) on high cholesterol treatment. NCEP recommends niacin alone for cardiovascular and atherogenic dyslipidemia in mild or normal LDL levels or in combination for higher LDL levels (NCEP, 2002).[39] 1500 mg Immediate release niacin daily results in 13% LDL, 20% LP, 10% TG reduction and 19% HDL increase comparing to placebo.[40] Extended release niacin alone or with anti-flushing agent (laropiprant) shows similar effects.[41][42]
The ARBITER 6-HALTS study, reported at the 2009 annual meeting of the American Heart Association and in the New England Journal of Medicine[43] concluded that, when added to statins, 2000 mg/day of extended-release niacin was more effective than ezetimibe (Zetia) in reducing carotid intima-media thickness, a marker of atherosclerosis.[44] Additionally, a recent meta-analysis covering 11 randomized controlled clinical trials found positive effects of niacin alone or in combination on all cardiovascular events and on atherosclerosis evolution.[19]
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.[45][46]
However, a 2011 study (AIM-HIGH) was halted early because patients showed no decrease in cardiovascular events, but did experience an increase in the risk of stroke. These patients already had LDL levels well controlled by a statin drug, and the aim of the study was to evaluate extended-release niacin (2000 mg per day) to see if raising HDL levels had an additional positive effect on risk. In this study, it did not have such an effect, and appeared to increase stroke risk.[47] The role of niacin in patients whose LDL is not well-controlled (as in the majority of previous studies with niacin) is still under study and debate. However, it does not seem to offer benefits via raising HDL, in patients already lowering LDL by taking a statin. [48]
Niacin prescriptions
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.[49][50] 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.[51][52][53]
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%.[15][54][55][56] The HPS2-THRIVE study,[57] 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.[58][59]
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.[60][61] “Slow release” varieties have higher hepatotoxic activity, hence non-prescription niacin is not recommended due to potential harm.[15]
Toxicity
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.[62]
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.[63][64] 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.[65][66] To reduce flushing many studies focused on altering or blocking the prostaglandin mediated pathway.[67] 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 the niacin with meals also helps reduce this side effect. After several weeks of a consistent dose, most patients no longer flush.[68] Slow- or "sustained"-release forms of niacin have been developed to lessen these side effects.[69][70] One study showed the incidence of flushing was significantly lower with a sustained release formulation[71] though doses above 2 g per day have been associated with liver damage, in particular, with slow-release formulations.[62] Flushing is often thought to involve histamine, but histamine has been shown not to be involved in the reaction.[72] Prostaglandin (PGD2) is the primary cause of the flushing reaction, with serotonin appearing to have a secondary role in this reaction.[72]
Hepatotoxicity is another side effect of niacin. This is possibly related to metabolism via amidation resulting in NAD production.[25] The time-release form has a lower therapeutic index for lowering serum lipids relative to this form of toxicity.[73]
Although high doses of niacin may elevate blood sugar, thereby worsening diabetes mellitus,[62] 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.[74]
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.[62]
Niacin, particularly the time-release variety, at extremely high doses can cause acute toxic reactions.[75] 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.[76]
Nicotinamide
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).[77]
Nicotinamide may be toxic to the liver at doses exceeding 3 g/day for adults.[78]
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.[79] One of the last of those studies affirmed the superiority of inositol and xantinol esters of nicotinic acid for reducing serum free fatty acid,[80] but other studies conducted during the same period found no benefit.[81] 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.[82] 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
Biosynthesis
The liver can synthesize niacin from the essential amino acid tryptophan, requiring 60 mg of tryptophan to make one mg of niacin.[83] 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:
- liver, heart and kidney (9 – 15 mg niacin per 100 grams)
- chicken, chicken breast (6.5 mg)
- beef (5 – 6 mg)
- fish: tuna, salmon, halibut (2.5 – 13 mg)
- eggs (0.1 mg)
- venison (8.43 mg)
Fruits and vegetables:
- avocados (1 mg niacin per 100 grams)
- dates (2 mg)
- tomatoes (0.7 mg)
- leaf vegetables (0.3 - 0.4 mg)
- broccoli (0.6 mg)
- carrots (0.3 - 0.6 mg)
- sweet potatoes (0.5 - 0.6 mg)
- asparagus (0.4 mg)
Seeds:
- nuts (2 mg niacin per 100 grams)
- whole grain products (4 - 29.5 mg)
- legumes (0.4 – 16 mg)
- saltbush seeds
Fungi:
- mushrooms, shiitake mushrooms (3.5 – 4 mg niacin per 100 grams)
- brewer's yeast (36 mg)
Other:
- beer (6 mg per pint,[84] less if filtered)
- Ovaltine (18 mg)
- Peanut butter (15 mg)
- Tofu
- Soy sauce (0.4 mg)
- Vegemite (from spent brewer's yeast) (50 mg niacin per 100 grams)[85]
- Marmite (from spent brewer's yeast) (110 mg niacin per 100 grams)
[86]
History
Niacin was first described by chemist Hugo Weidel in 1873 in his studies of nicotine.[87] The original preparation remains useful: The oxidation of nicotine using nitric acid.[88] 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."[89] Soon after, in studies conducted in Alabama and Cincinnati, Dr. Tom Spies found that nicotinic acid cured the sufferers of pellagra.[90]
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.[citation needed]
Carpenter found in 1951 that niacin in corn is biologically unavailable, and can be released only in very alkaline lime water of pH 11.[91] This process, known as nixtamalization, was discovered by the prehistoric civilizations of Mesoamerica.[92]
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".[citation needed]
On April 22, 2014, Pennsylvania State University researchers working with NASA at the Goddard Astrobiology Analytical Laboratory reported[93] of finding niacin within eight CM-2 type carbonaceous chondrite meteorites. The meteorite’s vitamin B3 levels ranged from 30 to 600 parts per billion, the study reports. Related molecules discovered in the meteorites include pyridine carboxylic acids and pyridine dicarboxylic acids.
References
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- ^ a b c Bruckert E, Labreuche J, Amarenco P (2010). "Meta-analysis of the effect of nicotinic acid alone or in combination on cardiovascular events and atherosclerosis". Atherosclerosis 210 (2): 353–61. doi:10.1016/j.atherosclerosis.2009.12.023. PMID 20079494.
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External links
- Vitamin B3 MS Spectrum
- Niacin bound to proteins in the PDB
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UpToDate Contents
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- 1. スタチン系およびフィブラート系以外の薬剤による脂質低下 lipid lowering with drugs other than statins and fibrates
- 2. 成人の顔面紅潮に対するアプローチ approach to flushing in adults
- 3. 高トリグリセリド血症患者に対するアプローチ approach to the patient with hypertriglyceridemia
- 4. 小児の脂質異常症ののマネージメント management of pediatric dyslipidemia
- 5. HDL代謝およびHDLコレステロール値異常の患者に対するアプローチ hdl metabolism and approach to the patient with abnormal hdl cholesterol levels
English Journal
- Water-soluble vitamin homeostasis in fasting northern elephant seals (Mirounga angustirostris) measured by metabolomics analysis and standard methods.
- Boaz SM, Champagne CD, Fowler MA, Houser DH, Crocker DE.SourceSonoma State University, Department of Biology, 1801 E. Cotati Ave., Rohnert Park, CA 94928, USA.
- Comparative biochemistry and physiology. Part A, Molecular & integrative physiology.Comp Biochem Physiol A Mol Integr Physiol.2012 Feb;161(2):114-21. Epub 2011 Oct 1.
- Despite the importance of water-soluble vitamins to metabolism, there is limited knowledge of their serum availability in fasting wildlife. We evaluated changes in water-soluble vitamins in northern elephant seals, a species with an exceptional ability to withstand nutrient deprivation. We used a me
- PMID 21983145
- A Review of the Rationale for Additional Therapeutic Interventions to Attain Lower LDL-C When Statin Therapy Is Not Enough.
- Shanes JG.SourceClinical Medicine, Rosalind Franklin University of Medicine and Science, Melrose Park, IL, USA, jeffsh@ccmconsultants.com.
- Current atherosclerosis reports.Curr Atheroscler Rep.2012 Feb;14(1):33-40.
- Statins alone are not always adequate therapy to achieve low-density lipoprotein (LDL) goals in many patients. Many options are available either alone or in combination with statins that makes it possible to reach recommended goals in a safe and tolerable fashion for most patients. Ezetimibe and bil
- PMID 22109348
- Residual Cardiovascular Risk Despite Optimal LDL Cholesterol Reduction with Statins: The Evidence, Etiology, and Therapeutic Challenges.
- Sampson UK, Fazio S, Linton MF.SourceDepartment of Medicine, Vanderbilt University Medical Center, Atherosclerosis Research Unit, 383 PRB - 2220 Pierce Avenue, Nashville, TN, 37232-6300, USA, u.sampson@vanderbilt.edu.
- Current atherosclerosis reports.Curr Atheroscler Rep.2012 Feb;14(1):1-10.
- This review captures the existence, cause, and treatment challenges of residual cardiovascular risk (CVR) after aggressive low-density lipoprotein cholesterol (LDL-C) reduction. Scientific evidence implicates low high-density lipoprotein cholesterol (HDL-C) and high triglycerides (TG) in the CVR obs
- PMID 22102062
Japanese Journal
- An amino acid outside the classical acetylcholine binding loops strongly influence the actions of neonicotinoids on recombinant nicotinic acetylcholine receptors expressed in Xenopus laevis oocytes(Molecular Target & Mode of Action,Poster,1) Pest Management, Crop Protection and Vector Control)
- Matsui M.
- Journal of pesticide science 36(1), 153, 2011-02-20
- NAID 110008463091
- Fluorescent Derivatization of Xanthurenic Acid and Nicotinic Acid with Horseradish Peroxidase in the Presence of Excess Hydrogen Peroxide
- ODO Junichi,SOGAWA Yuto,INOGUCHI Masahiko,HIRAI Akihito
- Analytical sciences : the international journal of the Japan Society for Analytical Chemistry 27(1), 105-109, 2011-01-10
- NAID 10027739906
- Convenient synthesis of aminopyridinecarboxylic acids
- Okamoto Iwao,Terashima Masayuki,Yoshioka Rempei [他]
- Heterocycles 83(10), 2343-2352, 2011-10-01
- NAID 40019008606
Related Links
- Niacin (also known as vitamin B3, nicotinic acid and vitamin PP) is an organic compound with the formula C6H5NO2 and, depending ... Niacin and Vitamin B3 are the generic terms for both nicotinic acid and nicotinamide, which are often used ...
Related Pictures
★リンクテーブル★
| リンク元 | 「ナイアシン」「ニコチン酸」「ニコチン酸系薬」 |
| 拡張検索 | 「nicotinic acid adenine dinucleotide phosphate」「isonicotinic acid hydrazide」 |
| 関連記事 | 「nicotinic」 |
「ナイアシン」
- 英
- niacin
- 同
- ビタミンB3？
- 関
- nicotinamide, ニコチン酸 nicotinic acid nicotinic acid、ビタミン
- Nicobid？
- ⇔FB.196では ナイアシン = ニコチン酸、ナイアシンアミド = ニコチン酸アミドとしている。
- 厳密に言えば、生体内でトロプトファンから合成できる(その際にビタミンB6とriboflavinが必要)ので、ビタミンではない。トリプトファン60mgでナイアシン1mgに換算できる。ナイアシンはNADとなって、生体内で、酸化還元酵素の補酵素として機能するが、その他に、蛋白のADPリボシル化におけるADPリボースの供給源として、またDNA修復機構に関与するnucleoproteinのポリADPリボシル化にも関与している。(HBC.498)
臨床関連
- ペラグラ：ナイアシン欠乏症
- 過剰摂取：(1-6g/dayのナイアシン服用は高脂血症治療のために用いられる)血管拡張・紅潮、皮膚の刺激感。(500mg/day以上の摂取)肝障害。(HBC.498)
「ニコチン酸」
- 英
- nicotinic acid nicotinate NiA
- 同
- ナイアシン niacin、ビタミンB3、3-ピリジンカルボン酸 3-pyridinecarboxylic acid
- 商
- ナイクリン
- 関
- NAD、ペラグラ、ビタミン
概念
- ビタミンの一つ。
- ビタミンB複合体の一つで、ビタミンB3。別名、ナイアシン(和文ではニコチン酸、英文ではナイアシンという記載をよく見かける、気がする)
臨床関連
- ペラグラを来す
参考
- 構造
- wiki ja
- wiki en
「ニコチン酸系薬」
- あまり使われないらしい
ニコチン酸系薬
特徴
構造
作用機序
- 遊離脂肪酸の動員↓。肝でのVLDL合成↓。→LPL↑→VLDL-TG分解↑→TG↓ Cho排泄↑ LP(a)↓
- コレステロール排泄促進作用
薬理作用
- 血清TG：低下
- Cho排泄：促進
- 血清LP(a)：低下
動態
適応
注意
禁忌
副作用
- 皮膚障害(発赤(顔面紅潮←アスピリンで軽減)、かゆみ)
相互作用
「nicotinic acid adenine dinucleotide phosphate」
- 関
- NAADP
「isonicotinic acid hydrazide」
- 同
- INAPI
「nicotinic」
- ニコチン性の、ニコチンの