Vitamin B3 (Niacin) - Nutrition

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What is Vitamin B3 (Niacin)?

Vitamin B3, also called niacin, is an essential water-soluble vitamin that participates as a cofactor in glucose, fatty acid and amino acid metabolism. The term niacin is used to describe a number of compounds that have biological activity associated with nicotinamide, including nicotinic acid, and a variety of pyridine nucleotide structures. Nicotinic acid and nicotinamide adenine dinucleotide (NAD) and nicotinamide adenine dinucleotide phosphate (NADP) are metabolized to nicotinamide within the intestinal lumen and absorbed across the intestinal mucosa by either carrier-mediated transport or passive diffusion. Once in the enterocyte nicotinamide is either released as free nicotinamide or converted to NAD for use by the cell. Niacin derivatives are filtered by the renal tubules, with some active reabsorption during periods of low intake[1].

Like most animals, dogs can synthesise a certain amount of niacin from the essential amino acid tryptophan. The tryptophan metabolite α-amino-β-carboxymuconic-ε-semialdahyde can be utilized in one of two pathways; it can be degraded by picolinic carboxylase to form acetyl-CoA and CO2 or it can be used to produce nicotinamide. Cats, unlike dogs, are unable to synthesise significant levels of niacin from tryptophan because they have very high activity of the enzyme picolinic carboxylase which results in rapid catabolism of trypophan to acetyl-CoA and CO2[2]. As such, cats require preformed niacin in the diet[3].

Why is it Important?

Niacin is used in oxidative-reduction reactions involving catabolism of glucose, fatty acids, ketone bodies, and amino acids. Chronic niacin deficiency results in a wide range of clinical signs from dermatitis and oral mucosa ulceration, to diarrhoea and death. This condition was originally called black-tongue in dogs and was used as a model to understand and prevent pellagra (i.e. niacin deficiency) in people.[4].

Roles in the Body

  1. Metabolic Function: The niacin derivatives, NAD and NADP, are required cofactors in dehydrogenase/reductase reactions. In general, NAD is used in catabolic reactions involving glucose, fatty acid, ketone, and amino acid metabolism while NADP is used in synthesis of lipids and cholesterol[1]. Both NAD and NADP also act as electron donors to the riboflavin-derivative flavin adenine dinucleotide (FAD) in the mitochondrial electron transport chain during adenosine triphosphate (ATP) production.
  2. Therapeutic Uses: High dose niacin supplementation has been shown to reduce low-density lipoprotein (LDL) and very low-density lipoprotein (VLDL) while increasing high-density lipoprotein (HDL) cholesterol concentrations in people.[5] Niacin supplementation has been suggested as a treatment to reduce hypercholesterolemia in dogs,[6] and has been shown to decrease VLDL synthesis in obese dogs.[7]

Consequences of Niacin Deficiency


Chronic niacin deficiency in puppy and adult dogs (also called “black-tongue”) causes anorexia, weight loss, erythema of the oral mucosa with progression to inflammation and ulceration, ptyalism, bloody diarrhoea, and eventually death.[2]


Cats and kittens fed niacin deficient diets develop anorexia, fever, erythema of oral mucosa and tongue with eventual ulceration, weight loss, and death within the 2-3 weeks.[8][9]

Niacin is prone to degradation with heat processing. Conditions associated with diuresis (e.g. chronic disease, such as renal disease or diabetes, or therapeutic intervention, such as intravenous fluids or increased water intake with management of lower urinary diseases) can result in increased loss of niacin and may increase daily requirements. Patients on chronic haemodialysis are at an increased risk of developing a deficiency.


There are no published studies evaluating niacin toxicity in cats. In dogs one study reported bloody diarrhoea in 2 dogs that were fed approximately x250 the adult requirement, and chronic exposure (11 days) resulted in death[10]. In humans, where it is used to help manage hypercholesterolemia, a high intake niacin (x25 the minimum requirement) can cause peripheral vasodilation (i.e. “flushing”)[5]. This side effect of therapeutic niacin has not been evaluated in dogs.

Dietary Sources

Niacin is naturally occurring in muscle and organ meats and pulses (i.e. legumes). Dietary niacin is typically found in the form of nicotinic acid in plant based materials, and as NAD or NADP in animal based materials. Certain whole grains such as corn and sorghum have a relatively high niacin content, but in these foods niacin is concentrated in the bran and germ layers and has poor bioavailability (i.e. highly bound within the cell), making them a poor source of dietary niacin. Niacin is also sensitive to degradation with heating and additional supplementation is required with commercial pet foods.

Diagnosing Niacin Deficiency

Diagnosis of niacin deficiency can be made using the nicotinamide loading test, which measures urine excretion of niacin metabolites;[11] though not routinely tested through veterinary reference laboratories. Diagnosis is also made on clinical signs consistent with deficiency and evaluation of diet.


  1. 1.0 1.1 McCormick DB. (2000) Niacin, Riboflavin, and Thiamin. In Biochemical and physiological aspects of human nutrition. 2000 Philadelphia, PA: WB Saunders Company p. 459-468.
  2. 2.0 2.1 National Research Council (NRC) (2006) Vitamins. In Nutrient Requirements for Dogs and Cats. 2006 Washington, DC: National Academies Press p.220-223.
  3. Morris, J.G. (2002) Idiosyncratic nutrient requirements of cats appear to be diet-induced evolutionary adaptations. Nutr Res Rev 2002;15; 153-168.
  4. Lanska DJ. (2012) The discovery of niacin, biotin, and pantothenic acid Ann Nutr Metab 2012;61:246-253.
  5. 5.0 5.1 Xenoulis PG and Steiner JM. (2010) Lipid metabolism and hyperlipidemia in dogs. Vet J 2010;183:12-21.
  6. Goldberg AC.(1998) Clinical trial experience with extended-release niacin (Niaspan): dose-escalation study. Am J Cardiol 1998;82:35U-38U
  7. Le Bloc’h J, et al.(2010) Nicotinic acid decreases apolipoprotein B100-containing lipoprotein levels by reducing hepatic very low density lipoprotein secretion through a possible diacylglycerol acyltransferase 2 inhibition in obese dogs. J Pharmacol Exp Ther 2010;334:583-589.
  8. Heath MK, et al. (1940) Feline pellagra. Science 1940;92:514;
  9. Da Silva AC, et al. (1952) The domestic cat as laboratory animal for experimental nutrition studies. II Niacin requirement and tryptophan metabolism. J Nutr 1952;1:26-32.
  10. Chen KK, et al. (1938) Toxicity of nicotinic acid. Proc Soc Exp Biol Med 1938; 38: 241-245.
  11. Carter EG. (1982) Quantitation of urinary niacin metabolites by reversed-phase liquid chromatography. Am J Clin Nutr 1982;36:926-30.

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