Vitamin E (α-Tocopherol) - Nutrition

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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[1]. 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[2].

Why is it Important?

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

Roles in the Body

  1. 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[1].
  2. 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[3].

Consequences of Vitamin E Deficiency

Dogs:

Vitamin E deficiency in dogs can develop anorexia, reproductive failure, skeletal and endocardial muscle degeneration, retinal degeneration, dermatitis, and subcutaneous oedema[4][5][6]. 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.

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)[7][8][9]. The level of vitamin E required to prevent clinical sign of deficiency is directly related to the level of dietary PUFAs.

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[1][2]. Diets high in fat and specifically high in long-chain omega-3 PUFAs will increase the tocopherol requirements in the diet[6][9][10]. 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[11].

Toxicity

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[12]. High dosage of vitamin E supplementation in people has also been associated with increased risk of mortality[13], though this effect has not been studied in dogs and cats.

Dietary Sources

Nuts, seeds and seed oils have high concentration of α-tocopherol. Mixed-tocopherols (i.e. combination of δ- and α-tocopherol) are used in commercial pet foods due to increased stability with processing and storage compared to α-tocopherol alone. The concentration of the biologically active α-tocopherol in mixed-tocopherol can range from 10-40% of the total vitamin E content. Mixed-tocopherols are effective at preventing lipid oxidation that occurs during the processing and storage of foods, but depending on the source may not provide adequate concentrations of α-tocopherol to the diet.

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 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.

References

  1. 1.0 1.1 1.2 Chow CK. Vitamin E. In Biochemical and physiological aspects of human nutrition. 2000 Philadelphia, PA: WB Saunders Company p.584-598.
  2. 2.0 2.1 National Research Council (NRC). Vitamins. In Nutrient Requirements for Dogs and Cats. 2006 Washington, DC: National Academies Press p.205-210.
  3. Brigelius-Flohe R and Traber MG. Vitamin E: function and metabolism. FASEB 1999;13:1145-1155.
  4. Elvehjem CA, et al. The effect of vitamin E on reproduction of dogs on milk diets. J Pediatr 1944;24:436-441.
  5. Van Vleet JF. Experimentally induced vitamin E-selenium deficiency in the growing dog. JAVMA 1975; 166:769-774.
  6. 6.0 6.1 Davidson MG, et al. Retinal degeneration associated with vitamin E deficiency in hunting dogs. JAVMA 1998;213:645-651.
  7. Gershoff SN and Norkin SA. Vitamin E deficiency in cats. J Nutr 1962;77:303-308.
  8. Dennis JM and Alexander RW. Nutritional myopathy in a cat. Vet Rec 1982;111:195-196.
  9. 9.0 9.1 Niza MM, et al. Feline pansteatitis revisited: hazards of unbalanced home-made diets. J Feline Med Surg 2003;5:271-277.
  10. 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.
  11. Chen LH. Interaction of vitamin E and ascorbic acid (review). In Vivo 1989;3:199-209.
  12. Strieker MJ, et al. Vitamin K deficiency in cats fed commercial fish-based diets. J Small Anim Prac 1996;37:322-326.
  13. 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.



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