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==What is Vitamin E (α-Tocopherol)?==

==What is Vitamin E (α-Tocopherol)?==

Vitamin E is a category of '''essential fat-soluble vitamins referred to as tocopherols'''. There are four stereoisomers of tocopherols found in nature (α, β, γ, and δ). Of these, '''α-tocopherol has the highest biological activity'''. Similar to other fat-soluble vitamins, vitamin E is incorporated into mixed micelles along with dietary fat and absorbed by diffusion across the mucosal surface of the small intestine. Absorbed vitamin E is then incorporated into chylomicrons and released into the lymphatics for transport to the liver, though some absorption into the portal circulation occurs as well. Within the liver selective α-tocopherol-binding proteins will incorporate α-tocopherol into very low density lipoproteins (VLDLs); α-tocopherol-binding proteins have only limiting binding of β-, γ-, or δ-isomers<ref name="Chow">Chow CK. Vitamin E. In Biochemical and physiological aspects of human nutrition. 2000 Philadelphia, PA: WB Saunders Company p.584-598.</ref>. The resultant α-tocopherol laden VLDLs transport α-tocopherol throughout the body. Vitamin E is primarily excreted through bile in faeces, though significant amounts of the metabolite α-tocopheric acid can also lost through urine<ref name="NRC">National Research Council (NRC). Vitamins. In Nutrient Requirements for Dogs and Cats. 2006 Washington, DC: National Academies Press p.205-210.</ref>.  

Vitamin E is a category of '''essential fat-soluble vitamins referred to as tocopherols'''. There are four stereoisomers of tocopherols found in nature (α, β, γ, and δ). Of these, '''α-tocopherol has the highest biological activity'''. Similar to other fat-soluble vitamins, vitamin E is incorporated into mixed micelles along with dietary fat and absorbed by diffusion across the mucosal surface of the [[Small Intestine Overview - Anatomy & Physiology|small intestine]]. Absorbed vitamin E is then incorporated into chylomicrons and released into the [[Lymphatic System Overview - Anatomy & Physiology|lymphatics]] for transport to the [[Liver - Anatomy & Physiology|liver]], though some absorption into the portal circulation occurs as well. Within the liver selective α-tocopherol-binding proteins will incorporate α-tocopherol into very low density lipoproteins (VLDLs); α-tocopherol-binding proteins have only limiting binding of β-, γ-, or δ-isomers<ref name="Chow">Chow CK. Vitamin E. In Biochemical and physiological aspects of human nutrition. 2000 Philadelphia, PA: WB Saunders Company p.584-598.</ref>. The resultant α-tocopherol laden VLDLs transport α-tocopherol throughout the body. Vitamin E is primarily excreted through [[Bile acids|bile]] in faeces, though significant amounts of the metabolite α-tocopheric acid can also lost through urine<ref name="NRC">National Research Council (NRC). Vitamins. In Nutrient Requirements for Dogs and Cats. 2006 Washington, DC: National Academies Press p.205-210.</ref>.  

==Why is it Important?==

==Why is it Important?==

Vitamin E is an antioxidant that protects cellular membranes lipid peroxidation by free radicals.  

Vitamin E is an antioxidant that protects cellular membranes lipid peroxidation by free radicals.  

Roles in the body

 

#'''Antioxidant''': Reactive oxygen species (e.g., peroxide, superoxide, and nitric oxide radicals) are formed during normal cellular respiration. These free radicals can cause damage to membrane-bound polyunsaturated fatty acids (PUFAs) as well as deoxyribonucleic acid (DNA). Membrane and intracellular vitamin E is able to donate a hydrogen electron to help prevent or stop propagation of this cellular damage. Oxidized α-tocopherols can be regenerated within the cell by other antioxidant systems, such as glutathione and vitamin C<ref name="Chow"/>.

==Roles in the Body==

#'''Cell Signalling''': Aside from its role as an antioxidant, α-tocopherol is also an inhibitor of protein kinase C in platelets. The presence of high concentrations of α-tocopherol in endothelial cells also down-regulates the intracellular and vascular cell adhesion molecules. The combination of these two effects can result in inhibition of platelet aggregation<ref name="Brigelius">Brigelius-Flohe R and Traber MG. Vitamin E: function and metabolism. FASEB 1999;13:1145-1155.</ref>.

#'''Antioxidant''': Reactive oxygen species (e.g., peroxide, superoxide, and nitric oxide radicals) are formed during normal cellular respiration. These free radicals can cause damage to membrane-bound polyunsaturated fatty acids (PUFAs) as well as [[DNA|deoxyribonucleic acid (DNA)]]. Membrane and intracellular vitamin E is able to donate a hydrogen electron to help prevent or stop propagation of this cellular damage. Oxidized α-tocopherols can be regenerated within the cell by other antioxidant systems, such as glutathione and vitamin C<ref name="Chow"/>.

#'''Cell Signalling''': Aside from its role as an antioxidant, α-tocopherol is also an inhibitor of protein kinase C in [[platelets]]. The presence of high concentrations of α-tocopherol in endothelial cells also down-regulates the intracellular and vascular cell adhesion molecules. The combination of these two effects can result in inhibition of platelet aggregation<ref name="Brigelius">Brigelius-Flohe R and Traber MG. Vitamin E: function and metabolism. FASEB 1999;13:1145-1155.</ref>.

== Consequences of Vitamin E Deficiency ==

== Consequences of Vitamin E Deficiency ==

====Dogs:====  

====Dogs:====  

Vitamin E deficiency in dogs can develop anorexia, reproductive failure, skeletal and endocardial muscle degeneration, retinal degeneration, dermatitis, and subcutaneous oedema<ref>Elvehjem CA, et al. The effect of vitamin E on reproduction of dogs on milk diets. J Pediatr 1944;24:436-441.</ref><ref>Van Vleet JF. Experimentally induced vitamin E-selenium deficiency in the growing dog. JAVMA 1975; 166:769-774.</ref><ref name="Davidson">Davidson MG, et al. Retinal degeneration associated with vitamin E deficiency in hunting dogs. JAVMA 1998;213:645-651.</ref>. Dogs with concurrent intestinal disease affecting absorption of dietary fat (i.e., a protein-losing enteropathy) as well as dogs with liver disease are at a higher risk of developing relative α-tocopherol deficiencies despite adequate dietary intake.

Vitamin E deficiency in dogs can develop anorexia, reproductive failure, skeletal and endocardial muscle degeneration, retinal degeneration, dermatitis, and subcutaneous [[oedema]]<ref>Elvehjem CA, et al. The effect of vitamin E on reproduction of dogs on milk diets. J Pediatr 1944;24:436-441.</ref><ref>Van Vleet JF. Experimentally induced vitamin E-selenium deficiency in the growing dog. JAVMA 1975; 166:769-774.</ref><ref name="Davidson">Davidson MG, et al. Retinal degeneration associated with vitamin E deficiency in hunting dogs. JAVMA 1998;213:645-651.</ref>. Dogs with concurrent intestinal disease affecting absorption of dietary fat (i.e., a [[Protein Losing Enteropathy|protein-losing enteropathy]]) as well as dogs with liver disease are at a higher risk of developing relative α-tocopherol deficiencies despite adequate dietary intake.

====Cats:====  

====Cats:====  

Clinical signs of vitamin E deficiency in cats and kittens include anorexia, depression, myopathy, and pansteatitis (i.e., painful nodular inflammation of adipose tissue)<ref>Gershoff SN and Norkin SA. Vitamin E deficiency in cats. J Nutr 1962;77:303-308.</ref><ref>Dennis JM and Alexander RW. Nutritional myopathy in a cat. Vet Rec 1982;111:195-196.</ref><ref name="Niza">Niza MM, et al. Feline pansteatitis revisited: hazards of unbalanced home-made diets. J Feline Med Surg 2003;5:271-277.</ref>. The level of vitamin E required to prevent clinical sign of deficiency is directly related to the level of dietary PUFAs.

Clinical signs of vitamin E deficiency in cats and kittens include anorexia, depression, myopathy, and pansteatitis (i.e., painful nodular inflammation of adipose tissue)<ref>Gershoff SN and Norkin SA. Vitamin E deficiency in cats. J Nutr 1962;77:303-308.</ref><ref>Dennis JM and Alexander RW. Nutritional myopathy in a cat. Vet Rec 1982;111:195-196.</ref><ref name="Niza">Niza MM, et al. Feline pansteatitis revisited: hazards of unbalanced home-made diets. J Feline Med Surg 2003;5:271-277.</ref>. The level of vitamin E required to prevent clinical sign of deficiency is directly related to the level of dietary PUFAs.

====Influence of Diet:====  

====Influence of Diet:====  

The metabolic requirement for vitamin E is dependent on the PUFA concentration in the diet as well as the degree of peroxidation that occurs during processing and storage<ref name="Chow"/><ref name="NRC"/>. Diets high in fat and specifically high in long-chain omega-3 PUFAs will increase the tocopherol requirements in the diet<ref name="Davidson"/><ref name="Niza"/><ref>Hendricks WH, et al. Vitamin E requirement of adult cats increased slightly with high dietary intake of polyunsaturated fatty acids. J Nutr 2002;132:1613S-1615S.</ref>. Recycling of α-tocopherol is also impaired with concurrent high intakes of vitamin C (a water-soluble vitamin that is not a dietary required for dogs and cats); supplementation with vitamin C may increase vitamin E requirements<ref>Chen LH. Interaction of vitamin E and ascorbic acid (review). In Vivo 1989;3:199-209.</ref>.

The metabolic requirement for vitamin E is dependent on the PUFA concentration in the diet as well as the degree of peroxidation that occurs during processing and storage<ref name="Chow"/><ref name="NRC"/>. '''Diets high in fat and specifically high in long-chain omega-3 PUFAs will increase the tocopherol requirements in the diet'''<ref name="Davidson"/><ref name="Niza"/><ref>Hendricks WH, et al. Vitamin E requirement of adult cats increased slightly with high dietary intake of polyunsaturated fatty acids. J Nutr 2002;132:1613S-1615S.</ref>. Recycling of α-tocopherol is also impaired with concurrent high intakes of vitamin C (a water-soluble vitamin that is not a dietary requirement for dogs and cats); supplementation with vitamin C may increase vitamin E requirements<ref>Chen LH. Interaction of vitamin E and ascorbic acid (review). In Vivo 1989;3:199-209.</ref>.

==Toxicity==

==Toxicity==

There are no published reports of vitamin E toxicity in dogs, though in cats high levels of dietary vitamin E can resulting in prolonged bleeding times<ref>Strieker MJ, et al. Vitamin K deficiency in cats fed commercial fish-based diets. J Small Anim Prac 1996;37:322-326.</ref>. High dosage of vitamin E supplementation in people has also been associated with increased risk of mortality<ref>Bjelakovic G, et al. Mortality in randomized trials of antioxidant supplements for primary and secondary prevention systematic review and meta-analysis. JAMA 2007;297:842-857.</ref>, though this effect has not been studied in dogs and cats.

There are no published reports of vitamin E toxicity in dogs, though in cats high levels of dietary vitamin E can result in prolonged bleeding times<ref>Strieker MJ, et al. Vitamin K deficiency in cats fed commercial fish-based diets. J Small Anim Prac 1996;37:322-326.</ref>. High dosage of vitamin E supplementation in people has also been associated with increased risk of mortality<ref>Bjelakovic G, et al. Mortality in randomized trials of antioxidant supplements for primary and secondary prevention systematic review and meta-analysis. JAMA 2007;297:842-857.</ref>, though this effect has not been studied in dogs and cats.

==Dietary Sources==

==Dietary Sources==

==Diagnosing Vitamin E Deficiency==

==Diagnosing Vitamin E Deficiency==

Confirmation of Vitamin E deficiency is made by measuring plasma α-tocopherol concentration, although this is not routinely available in most veterinary reference laboratories. Physical examination may reveal consist skin lesions and a diagnosis may be confirmed via biopsy of nodules.  

Confirmation of Vitamin E deficiency is made by measuring plasma α-tocopherol concentration, although this is not routinely available in most veterinary reference laboratories. Physical examination may reveal skin lesions and a diagnosis may be confirmed via biopsy of nodules.  

A suspicion of a deficiency may arise when there is a presence of clinical signs consistent with deficiency and evaluation of diet demonstrates a deficiency.  

A suspicion of a deficiency may arise when there is a presence of clinical signs consistent with deficiency and evaluation of diet demonstrates a deficiency.  

[[Category:Vitamins]]

[[Category:Vitamins]]

[[Category:To Do - Nutrition]]

[[Category:To Do - Nutrition]]

[[Category:To Do - Nutrition GGP]]

[[Category:To Do - Nutrition preMars]]