Page 133 - Small Animal Clinical Nutrition 5th Edition

134 Small Animal Clinical Nutrition

METABOLISM occurs in animal tissues as NAD and NADP and in plants
Niacin in foods is found mainly as NADH and NADPH,
VetBooks.ir which may be free or bound to other macromolecules. After mostly as protein-bound forms. Niacin is generally added to
most pet foods as nicotinic acid or nicotinamide.
ingestion, NADH and NADPH undergo hydrolysis by the
intestinal mucosa to release free nicotinamide, which is read- Pyridoxine
ily absorbed (Brody, 1994a). Dietary niacin (nicotinic acid and Pyridoxine is also generally called vitamin B . However, vita-
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nicotinamide) is absorbed readily through the gastric and min B is a generic descriptor for all 3-hydroxy-2-methylpyri-
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small intestinal mucosa. Both free nicotinic acid and nicoti- dine derivatives exhibiting the biologic activity of pyridoxine.
namide are found in blood.Tissues readily take up these com- The three naturally occurring forms of vitamin B are pyridox-
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pounds to synthesize required cofactors, which also trap the al, pyridoxine and pyridoxamine.
compound in cells. Excess niacin is methylated and excreted
in urine. FUNCTION
Niacin may also be synthesized from tryptophan via the The biologically active forms of vitamin B are the coen-
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kynurenin pathway, which results in formation of nicotinic acid zymes pyridoxal phosphate (PLP) and pyridoxamine phos-
ribonucleotide. Some enzymes in this pathway require vitamin phate (PMP). PLP is involved in most reactions of amino acid
B and iron as cofactors. In most mammals, foods high in tryp- metabolism, including transamination, decarboxylation,
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tophan can alleviate signs of niacin deficiency. However, cats desulfhydration and nonoxidative deamination. PLP is also
cannot efficiently use tryptophan to synthesize niacin because involved in the catabolism of glycogen and metabolism of
they have a very high enzymatic activity of picolinic carboxylase lipids. As a coenzyme for decarboxylase enzymes, PLP func-
that decisively leads the metabolism of tryptophan to acetyl- tions in the synthesis of serotonin, epinephrine, norepinephrine
CoA and CO instead of NAD (Sudadolnik et al, 1957; Baker and γ-aminobutyric acid (GABA). Pyridoxine is involved in
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and Czarnecki-Maulden, 1991).Thus, cats have a strict dietary vasodilatation through the production of histamine and is
requirement for preformed niacin. required in the pathway where niacin is produced from trypto-
phan. Pyridoxine helps catalyze the synthesis of taurine from
REQUIREMENTS cysteine and participates with ascorbic acid and NAD in the
The AAFCO (2007) recommended allowance for niacin is synthesis of carnitine from the amino acid lysine. Pyridoxine is
11.4 mg/kg DM for dogs and 60 mg/kg DM for cats for all also involved with the synthesis of the heme precursor por-
lifestages.The NRC (2006) recommended allowance for niacin phyrin (as a coenzyme for δ-aminolevulinate synthase).
is 17 mg/kg DM for dogs and 40 mg/kg DM for cats for all
lifestages. Table 6-5 lists AAFCO and NRC allowances for METABOLISM
dogs and cats. The various forms of vitamin B (pyridoxine, pyridoxal, pyri-
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doxamine, PLP, PMP) are freely absorbed via passive diffusion
DEFICIENCY AND TOXICITY in the small intestine. The glucuronide form is not absorbed.
Deficiency of niacin results in pellagra with its classic 4D The predominant form of vitamin B in blood is PLP, which
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signs: dermatitis, diarrhea, dementia and death. Clinical is tightly bound to proteins. Pyridoxal crosses cell membranes
deficiency is uncommon in dogs because most commercial more readily than PLP does. After uptake by cells, the vitamin
pet foods are supplemented with niacin. Cats, however, are is again phosphorylated by pyridoxal kinase to yield the pre-
more likely to develop signs of deficiency because of their dominant tissue form, PLP, which is considered to be the most
strict requirement for niacin. Niacin is a fairly stable vita- active vitamin B form.
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min. Processing conditions may release some bound niacin, The vitamin B forms are readily interconverted metaboli-
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which increases availability. Niacin deficiency may occur cally by reactions involving phosphorylation/dephosphoryla-
when foods with low quantities of niacin and tryptophan are tion, oxidation/reduction and amination/deamination. Phos-
ingested. phorylation appears to be an important means of retaining the
Measurement of methylated nicotinamide levels in urine best vitamin intracellularly. Only small quantities of vitamin B are
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substantiates niacin deficiency. Niacin metabolites in whole stored in the body.The products of vitamin B metabolism are
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blood have been reported for dogs and cats (Table 6-5), but excreted in the urine; pyridoxic acid is the predominant meta-
these values generally have not been useful markers of deficien- bolic product. Different from other species, cats excrete little
cy in other species (Baker et al, 1986; Jacob and Swendseid, pyridoxic acid in urine even after a large oral dose of pyridox-
1996). No niacin toxicity information in cats is available. ine hydrochloride (Coburn and Mahuren, 1987). The main
However, excessive ingestion of nicotinic acid causes bloody metabolites of vitamin B in cat urine are pyridoxine 3-sulfate,
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stool, convulsions and even death (Chen et al, 1938). pyridoxal 3-sulfate and N-methylpyridoxine.

SOURCES REQUIREMENTS
Niacin is a very stable vitamin found in a variety of food- The AAFCO (2007) recommended allowance for pyridox-
stuffs. The greatest amounts of niacin are found in yeast, ani- ine is 1 mg/kg DM for dogs and 4 mg/kg DM for cats for all
mal/fish by-products, cereals, legumes and oilseeds. Niacin lifestages. The NRC (2006) recommended allowance for