Page 129 - Small Animal Clinical Nutrition 5th Edition

130 Small Animal Clinical Nutrition

E. Vitamin E levels in tissues vary markedly with no consistent min E levels may be beneficial (Morris and Rogers, 1994). A
VetBooks.ir relationship to lipid parameters. The vitamin is most concen- number of inflammatory dermatoses in animals have been
treated with oral vitamin (Chapter 32). People have been given
trated in membrane-rich cell fractions such as mitochondria
and microsomes.
much higher dietary concentrations of vitamin E without
Vitamin E undergoes very little metabolism. Usually less than adverse clinical signs (Combs, 1998).
1% of orally ingested vitamin E is excreted in urine (Combs,
1998). The major route of excretion is fecal elimination. SOURCES
The need for vitamin E in the diet is markedly influenced by Only plants synthesize vitamin E.The richest sources of vita-
dietary composition.The requirement increases with increasing min E are vegetable oils and, to a lesser extent, seeds and cereal
levels of polyunsaturated fatty acids (PUFA), oxidizing agents, grains. Tocopherol concentrations are highest in green leaves.
vitamin A, carotenoids and trace minerals and decreases with Tocotrienols are not found in green leaves, but instead are found
increasing levels of fat-soluble antioxidants, sulfur-containing in the bran and germ fractions of certain plants. Animal tissues
amino acids and selenium. Various researchers have recom- tend to be low in vitamin E, with the highest levels occurring in
mended up to 60 mg of α-tocopherol per g of PUFA; howev- fatty tissues. Common vitamin E supplements used in pet foods
er, there is no consensus among experts about the quantitation include α-tocopherol and α-tocopherol acetate.
of this relationship (Combs, 1998).
Vitamin K
REQUIREMENTS Like other fat-soluble vitamins, vitamin K is a generic descrip-
The AAFCO (2007) recommended allowance for vitamin E tor for a group of compounds exhibiting the antihemorrhagic
is 50 IU/kg DM for dogs and 30 IU/kg DM for cats, irrespec- activity of phylloquinone. Phylloquinone (vitamin K ) and
1
tive of the lifestage. For cat foods containing fish oils, AAFCO menaquinone (vitamin K ) are the two major naturally occur-
2
recommends an additional 10 IU vitamin E/g of fish oil/kg of ring forms of vitamin K. Green leafy vegetables are the primary
food above the allowance. The vitamin E allowance recom- sources of vitamin K whereas vitamin K is produced from
1
2
mended by NRC (2006) is 30 mg α-tocopherol (33 IU)/kg actinomycete bacteria found in normal intestinal microflora.
DM for dogs for all lifestages. For cats, the vitamin E allowance Vitamin K is now called menaquinone-7 (MK-7) in recogni-
2
is 38 mg α-tocopherol (42 IU)/kg DM for growth and main- tion of the seven-isoprenoid units. Menadione or vitamin K 3
tenance and 31 mg α-tocopherol (34 IU)/kg DM for gestation (2-methyl-1,4-napthoquinone) is the parent compound of the
and lactation. vitamin K series. When used in pet food, it is usually added in
a complex form such as menadione sodium bisulfate complex
DEFICIENCY AND TOXICITY (MSBC) or menadione dimethylpyrimidinol bisulfate (MPB),
The clinical manifestations of vitamin E deficiency vary as the bioactive form of vitamin K.
markedly between species. In general, however, the neuromus-
cular, vascular and reproductive systems are affected most com- FUNCTION
monly. Signs of vitamin E deficiency are mostly attributed to Vitamin K plays a major role in the carboxylation of proteins
membrane dysfunction as a result of the oxidative degradation (factors II, VII, IX, X and proteins C and S) to convert pro-
of polyunsaturated membrane phospholipids and disruption of thrombin to thrombin for normal blood clotting. Vitamin K is
other critical cellular processes. Clinical findings of vitamin E also involved in the synthesis of osteocalcin, a protein that reg-
deficiency in dogs include degenerative skeletal muscle disease ulates the incorporation of calcium phosphates in growing bone
associated with muscle weakness, degeneration of testicular (Combs, 1998).
germinal epithelium and impaired spermatogenesis, failure of
gestation, brown pigmentation (lipofuscinosis) of intestinal METABOLISM
smooth muscle and decreased plasma tocopherol concentra- The absorption of natural vitamin K in food is between 40
tions. In cats, deficiency signs include steatitis, focal interstitial and 70% (Combs, 1998). Ingested phylloquinone is absorbed
myocarditis, focal myositis of skeletal muscle and periportal from the proximal small intestine into the lymphatic system by
mononuclear infiltration in the liver (Case 6-7). an energy-dependent process. Menaquinone is absorbed from
Vitamin E is one of the least toxic fat-soluble vitamins. the small intestine by a passive noncarrier-mediated process.
Animals and people apparently tolerate high levels without Conditions that impair lipid absorption also adversely affect
adverse effects. However, at very high doses, antagonism with vitamin K absorption. Upon absorption, vitamin K is transport-
other fat-soluble vitamins may occur, resulting in impaired ed to the liver in chylomicrons. The vitamin is rapidly concen-
bone mineralization, reduced hepatic storage of vitamin A and trated in the liver, but in contrast to other fat-soluble vitamins,
coagulopathies as a result of decreasing absorption of vitamins vitamin K has a very rapid turnover in this organ. No specific
D, A and K, respectively. A maximum of 1,000 IU/kg DM was carriers have been identified for any of the K vitamers.
recommended by AAFCO for dogs; however, AAFCO (2007) Although phylloquinones and menaquinones are ingested,
set no maximum for cats. There is no evidence of vitamin E much of the vitamin K in tissues is from bacterial origin.
toxicity in dogs and very limited information when vitamin E Menadione is rapidly excreted in urine as the phosphate, sulfate
is given orally to cats. In certain conditions, higher dietary vita- or glucuronide form of menadiol. However, catabolism of phyl-