Difference between revisions of "Vitamin B6 (Pyridoxine) - Nutrition"
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==Roles in the Body== | ==Roles in the Body== | ||
| − | Vitamin B<sub>6</sub> as PLP is an essential cofactor for glycogen phosphorylase during gluconeogenesis. It is also a cofactor in serine palmitoyl transferase used sphingolipid synthesis, a cofactor in γ-aminolevulinic acid synthentase, the first and rate-limiting step in | + | Vitamin B<sub>6</sub> as PLP is an essential cofactor for glycogen phosphorylase during gluconeogenesis. It is also a cofactor in serine palmitoyl transferase used sphingolipid synthesis, a cofactor in γ-aminolevulinic acid synthentase, the first and rate-limiting step in heme synthesis. PLP is also required for synthesis of [[Taurine - Nutrition|taurine]], dopamine, histamine, and norepinephrine, and is involved in multiple steps in the conversion of [[Tryptophan - Nutrition|tryptophan]] to [[Vitamin B3 (Niacin) - Nutrition|niacin]]<ref>Shane B. Folic Acid, Vitamin B12, and Vitamin B6. In Biochemical and physiological aspects of human nutrition. 2000 Philadelphia, PA: WB Saunders Company p. 511-518.</ref>. |
==Consequences of Vitamin B<sub>6</sub> Deficiency== | ==Consequences of Vitamin B<sub>6</sub> Deficiency== | ||
====Dogs:==== | ====Dogs:==== | ||
| − | Induced vitamin B<sub>6</sub> deficiency has been reported to cause anorexia, weight loss, and microcytic hypo chromic [[Regenerative and Non-Regenerative Anaemias|anaemia]] in puppies, and if left untreated could result in death. Ataxia, hematochezia, | + | Induced vitamin B<sub>6</sub> deficiency has been reported to cause anorexia, weight loss, and microcytic hypo chromic [[Regenerative and Non-Regenerative Anaemias|anaemia]] in puppies, and if left untreated could result in death. Ataxia, hematochezia, seizures, muscle fasciculations, cardiac dilation and hypertrophy of both the left and right auricles and ventricles (with more pronounced changes to the right), and demyelination of peripheral nerves have also been described in adult dogs fed Vitamin B<sub>6</sub> deficient diets<ref>National Research Council (NRC). Vitamins. In Nutrient Requirements for Dogs and Cats. 2006 Washington, DC: National Academies Press p.218-220.</ref><ref>Street HR, et al. Observations on vitamin B6 deficiency in the dog. J Nutr 1941;21:275-290</ref>. |
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====Cats:==== | ====Cats:==== | ||
| − | Induced vitamin B<sub>6</sub> deficiency in kittens was reported to result in poor growth rate, microcytic hypochromic anaemia, and [[Urolithiasis#Calcium oxalate|calcium oxalate | + | Induced vitamin B<sub>6</sub> deficiency in kittens was reported to result in poor growth rate, microcytic hypochromic anaemia, and [[Urolithiasis#Calcium oxalate|calcium oxalate]] crystalluria<ref>Bai SC, et al. Vitamin B6 deficiency in kittens. J Nutr 1989;119: 1020-1027.</ref>. Increased dietary intake of [[Protein Overview - Nutrition|protein]] has also been show to increase Vitamin B<sub>6</sub> requirement in cats<ref>Bai SC, et al. The level of dietary protein affects the vitamin B-6 requirement of cats. J Nutr 1991 121;1054-1061.</ref>. |
| − | Vitamin B<sub>6</sub> is '''light sensitive and prone to degradation with heat processing'''. Conditions associated with diuresis (e.g. chronic disease, such as | + | Vitamin B<sub>6</sub> is '''light sensitive and prone to degradation with heat processing'''. Conditions associated with diuresis (e.g., chronic disease, such as renal disease or [[Diabetes Insipidus|diabetes]], or therapeutic intervention, such as intravenous fluids or increased water intake with management of [[Cystitis|lower urinary diseases]]) can result in increased loss of Vitamin B<sub>6</sub> and may increase daily requirements. Patients on chronic haemodialysis are at an increased risk for development of deficiency. |
==Toxicity== | ==Toxicity== | ||
| − | There are no published toxicity reports in cats, but chronic high intake (i.e. >100x the requirement) of Vitamin B<sub>6</sub> can result in ataxia and tonic convulsions in dogs within 1 week of daily administration<ref>Hoover DM, et al. Ultrastructural Lesions of Pyridoxine Toxicity in Beagle Dogs. Vet Pathol 1981;18: 769-777.</ref><ref>Montpetit VJ, et al. Alteration of neuronal cytoskeletal organization in dorsal root ganglia associated with pyridoxine neurotoxicity. Acta Neuropathol 1988;76:71-81.</ref>. | + | There are no published toxicity reports in cats, but chronic high intake (i.e., >100x the requirement) of Vitamin B<sub>6</sub> can result in ataxia and tonic convulsions in dogs within 1 week of daily administration<ref>Hoover DM, et al. Ultrastructural Lesions of Pyridoxine Toxicity in Beagle Dogs. Vet Pathol 1981;18: 769-777.</ref><ref>Montpetit VJ, et al. Alteration of neuronal cytoskeletal organization in dorsal root ganglia associated with pyridoxine neurotoxicity. Acta Neuropathol 1988;76:71-81.</ref>. |
==Dietary Sources== | ==Dietary Sources== | ||
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==References== | ==References== | ||
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[[Category:Vitamins]] | [[Category:Vitamins]] | ||
| + | [[Category:To Do - Nutrition]] | ||
| + | [[Category:To Do - Nutrition preMars]] | ||
Revision as of 09:23, 22 May 2015
What is Vitamin B6 (Pyridoxine)?
Vitamin B6, also commonly called pyridoxine, is an essential water-soluble vitamin used as a cofactor in a number of enzymatic reactions. Vitamin B6 in the diet is found as pyridoxine, pyridoxal, and pyridoxamine all of which are hydrolysed by a phosphatase before absorption across the intestinal mucosa by passive diffusion. Once within the enterocyte the hydrolysed vitamin B6 derivative is phosphorylated by pyridoxine kinase and transported to the liver for continued metabolism to its active form, pyridoxal-5-phosphate (PLP). In the liver PLP is bound to albumin and then transported to target tissues. Large concentrations of pyridoxine are found in muscle, but this depot is not available during periods of Vitamin B6 deficiency and is only released during muscle catabolism. Vitamin B6 derivatives are freely filtered by the renal tubules.
Why is it Important?
The active form of Vitamin B6, PLP, participates in a number of reactions involving amino acid metabolism (e.g. aminotransferases, decarboxylases, racemizations) as well as various synthetic pathways and gluconeogenesis.
Roles in the Body
Vitamin B6 as PLP is an essential cofactor for glycogen phosphorylase during gluconeogenesis. It is also a cofactor in serine palmitoyl transferase used sphingolipid synthesis, a cofactor in γ-aminolevulinic acid synthentase, the first and rate-limiting step in heme synthesis. PLP is also required for synthesis of taurine, dopamine, histamine, and norepinephrine, and is involved in multiple steps in the conversion of tryptophan to niacin[1].
Consequences of Vitamin B6 Deficiency
Dogs:
Induced vitamin B6 deficiency has been reported to cause anorexia, weight loss, and microcytic hypo chromic anaemia in puppies, and if left untreated could result in death. Ataxia, hematochezia, seizures, muscle fasciculations, cardiac dilation and hypertrophy of both the left and right auricles and ventricles (with more pronounced changes to the right), and demyelination of peripheral nerves have also been described in adult dogs fed Vitamin B6 deficient diets[2][3].
Cats:
Induced vitamin B6 deficiency in kittens was reported to result in poor growth rate, microcytic hypochromic anaemia, and calcium oxalate crystalluria[4]. Increased dietary intake of protein has also been show to increase Vitamin B6 requirement in cats[5]. Vitamin B6 is light sensitive and 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 Vitamin B6 and may increase daily requirements. Patients on chronic haemodialysis are at an increased risk for development of deficiency.
Toxicity
There are no published toxicity reports in cats, but chronic high intake (i.e., >100x the requirement) of Vitamin B6 can result in ataxia and tonic convulsions in dogs within 1 week of daily administration[6][7].
Dietary Sources
Vitamin B6 is naturally occurring in muscle and organ meats, eggs, dairy, and vegetables. Vitamin B6 is also supplemented into all commercially-prepared complete and balanced dog and cat foods.
Diagnosing Pyridoxine Deficiency
Diagnosis of pyridoxine deficiency is based on presence of microcytic hypochromic anaemia, potential presence of calcium oxalate crystals in urine sediment evaluation, and measurement of increased plasma tyrosine concentration. Diagnosis is also made on clinical signs consistent with deficiency and direct measurement pyridoxine levels of diet.
References
- ↑ Shane B. Folic Acid, Vitamin B12, and Vitamin B6. In Biochemical and physiological aspects of human nutrition. 2000 Philadelphia, PA: WB Saunders Company p. 511-518.
- ↑ National Research Council (NRC). Vitamins. In Nutrient Requirements for Dogs and Cats. 2006 Washington, DC: National Academies Press p.218-220.
- ↑ Street HR, et al. Observations on vitamin B6 deficiency in the dog. J Nutr 1941;21:275-290
- ↑ Bai SC, et al. Vitamin B6 deficiency in kittens. J Nutr 1989;119: 1020-1027.
- ↑ Bai SC, et al. The level of dietary protein affects the vitamin B-6 requirement of cats. J Nutr 1991 121;1054-1061.
- ↑ Hoover DM, et al. Ultrastructural Lesions of Pyridoxine Toxicity in Beagle Dogs. Vet Pathol 1981;18: 769-777.
- ↑ Montpetit VJ, et al. Alteration of neuronal cytoskeletal organization in dorsal root ganglia associated with pyridoxine neurotoxicity. Acta Neuropathol 1988;76:71-81.