Niacin appearance

Reducing LDL cholesterol while substantially raising HDL cholesterol (statin + niacin) appears to reduce the risk of atherosclerotic disease progression to a greater degree than statin monotherapy. 

Niacin positively impacts lipoprotein metabolism through multiple mechanisms. Niacin appears to block HDL particle uptake and catabo-... 

Several different niacin formulations are available niacin immediate-release (IR), niacin sustained-release (SR), and niacin extended-release (ER).28,29 These formulations differ in terms of dissolution and absorption rates, metabolism, efficacy, and side effects. Limitations of niacin IR and SR are flushing and hepatotoxicity, respectively. These differences appear related to the dissolution and absorption rates of niacin formulations and its subsequent metabolism. Niacin IR is available by prescription (Niacor ) as well as a dietary supplement which is not regulated by the FDA.28 Currently, there are no FDA-approved niacin SR products, thus, all SR products are available only as dietary supplements. 

Niacin can raise uric acid levels, and in diabetics can raise blood glucose levels. However, several clinical trials have shown that niacin can be used safely and effectively in patients with diabetes.33 Due to the high cardiovascular risk of patients with diabetes, the benefits of improving the lipid profile appear to outweigh any adjustment in diabetic medication(s) that is needed.33... 

With well-established animal models to evaluate vasodilation and FFA reduction, several compounds were profiled in vivo and they indeed displayed improved TIs relative to niacin. Furthermore, these models appeared to correlate to humans as two candidates including both... 

Niacin, riboflavin, pantothenic acid and vitamin B6 contents are greatly increased in tempeh during fermentation, whereas thiamin exhibits no significant change. H. oligosporus appears to have a great synthetic capacity for niacin, riboflavin, pantothenic acid, and vitamin B, but not for thiamin. 

The same authors (G8, G7) also found very substantial decreases in riboflavin (approx. 80%), and niacin (P9) fared little better. When mixtures were irradiated unusual events occurred. Riboflavin and ascorbic acid were each protected by niacin. Addition of cystine or cysteine apparently sensitized the niacin (P10). Since initial rates were not given, and the doses were considerably above the oxygen breakpoint (Sec. IIIA2), no mechanistic interpretation is possible. There also appears to be some doubt about the reliability of the colormetric assay used by these workers. 

Milk contains about 0.1 mg niacin per 100 g and thus is not a rich source of the preformed vitamin. Tryptophan contributes roughly 0.7 mg NE per 100 g milk. In milk, niacin exists primarily as nicotinamide and its concentration does not appear to be affected greatly by breed of cow, feed, season or stage of lactation. Pasteurized goats (0.3 mg niacin and 0.7 mg NE from tryptophan per 100 g) and raw sheep s (0.4 mg niacin and 1.3 mg NE from tryptophan per 100 g) milk are somewhat richer than cows milk. Niacin levels in human milk are 0.2 mg niacin and 0.5 mg NE from tryptophan per 100 g. The concentration of niacin in most dairy products is low (Appendix 6A) but is compensated somewhat by tryptophan released on hydrolysis of the proteins. 

The physiologically active forms of niacin are nicotinic acid, nicotinamide, and their coenzymes (93,96). Niacytin and the niacynogens appear to have limited bioavailability, although more work is needed in this area. The absorption and metabolism of niacin has been reviewed (20,93). 

The excretion of methyl pyridone carboxamide is more severely reduced in marginal niacin deficiency than is that of -methyl nicotinamide. The excretion of methyl pyridone carboxamide decreases rapidly in subjects fed on a niacin-deficient diet, and virtually ceases several weeks before the appearance of clinical signs of deficiency by contrast, a number of studies have shown continuing excretion of -methyl nicotinamide even in pellagrins. A better estimate of niacin nutritional status can be obtained by determining the ratio of urinary methyl pyridone carboxamide Ai -methyl nicotinamide, which is relatively constant, despite the administration of loading doses of tryptophan or niacin to adequately nourished subjects (between 1.3 to 4.0), and a ratio of less than 1.0 indicates depletion of niacin reserves (de Eange and Joubert, 1964 Dillon et al., 1992). 

Allergic skin reactions (17) and other adverse effects, including dermatological problems and neurological symptoms, have been described in individuals using such formulations. Heavy chronic consumption of kava-kava can lead to a pellagroid dermopathy that appears to be unrelated to niacin deficiency (18). 

Niacin (nicotinic acid) may be administered as aluminum nicotinate (Nicalex). This is acomplex of aluminum hydroxy nicotinate and niacin. The aluminum salt is hydrolyzed to aluminum hydroxide and niacin in the stomach. The aluminum salt seems to have no advantage nver the free acid. Hepatic reaction appears more prevalent than with niacin. 

Certain vitamins can be synthesized by humans in limited quantities. Niacin can be formed from tryptophan (Chapter 17). This pathway is not active enough to satisfy all the body s needs however, in calculating the RDA for niacin, 60 mg of dietary tryptophan is considered equivalent to 1 mg of dietary niacin. In Hartnup s disease (see Table 38-1 and Chapter 17), a rare hereditary disorder in the transport of monoaminomonocarboxylic acids (e.g., tryptophan), a pellagra-like rash may appear, suggesting that over a long period of time dietary intake of niacin is insufficient for metabolic needs. This pattern also occurs in carcinoid syndrome in which much tryptophan is shunted into the synthesis of 5-hydroxytryptamine. 

The answer is d. (Murray, pp 627-661. Scriver, pp 3897-3964. Sack, pp 121-138. Wilson, pp 287-320.) The vitamin whose structure appears in the question is nicotinic acid (niacin), which gives rise to the nicotinamide adenine dinucleotide coenzymes NAD and NADP. NAD is a cofactor required by all dehydrogenases. NADPII is a cofactor produced by the pentose phosphate shunt. It is utilized in reductive synthesis of compounds such as fatty acids. 

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