Page 128 - Small Animal Clinical Nutrition 5th Edition

Minerals and Vitamins 129

cervical spinal cord (Morris, 1996). Other signs included FUNCTION
Vitamin E functions as an antioxidant in the body and in
VetBooks.ir hypocalcemia, elevated PTH concentrations, posterior paraly- food. Of the vitamin E isomers, α-tocopherol is the most active
sis, ataxia and eventual quadriparesis.
biologic form in the body, whereas the γ-isomer is the most
Excessive intake of vitamin D is associated with increases in
25-OH-D , with the D form being more toxic than the D 2 active form in food. Mixed tocopherols, including γ-toco-
3
3
form. When circulating at very high concentrations, 25-OH- pherols, are widely used to prevent lipid oxidation in pet food
D can compete effectively with 1,25-(OH) -D for receptors products (Chapter 8).
3
3
2
in the intestine and bone. Therefore, during vitamin D toxico- Vitamin E works in conjunction with glutathione peroxidase
sis, 25-OH-D can induce actions usually attributed to 1,25- to protect cells against the adverse effects of reactive oxygen and
3
(OH) -D .Thus, 25-OH-D is believed to be the critical fac- other free radicals that initiate the oxidation of polyunsaturated
3
2
3
tor in vitamin D intoxication (NRC, 1987). Excessive vitamin membrane phospholipids. Vitamin E in cellular and subcellu-
D 3 supplementation below the toxic level decreases bone lar membranes is the first line of defense against peroxidation
remodeling and causes focal enlargement of the growth plate in of vital phospholipids. However, some peroxides are formed
growing puppies (Tryfonidou et al, 2003). Excessive vitamin D even when adequate levels of vitamin E are present.
concentrations may result in hypercalcemia, soft-tissue calcifi- Selenium, as part of the enzyme glutathione peroxidase, is a
cation and ultimately death (Morita et al, 1995; Nakamura et second line of defense that destroys peroxides before they dam-
al, 2004) (Case 6-6). age membranes. Therefore, selenium, vitamin E and sulfur-
The vitamin D maximum in the AAFCO (2007) dog and containing amino acids, through different biochemical mecha-
cat nutrient profiles is 5,000 IU/kg DM for dogs and 10,000 nisms, are capable of preventing some of the same nutritional
IU/kg DM for cats. The NRC (2006) proposed a safe upper diseases (McDowell, 1992). Vitamin E prevents fatty acid
limit of 80 µg cholecalciferol (3,200 IU)/kg DM for dogs and hydroperoxide formation, sulfur-containing amino acids are
750 µg cholecalciferol (30,000 IU)/kg DM for cats regardless precursors of glutathione peroxidase and selenium is a compo-
of lifestages. nent of glutathione peroxidase. In addition, vitamin E is impor-
tant for normal reproduction and is involved in modulating cel-
SOURCES lular signaling, regulating gene transcription, modulating
Marine fish and fish oils are the richest natural sources of immune function and inducing apoptosis (Brigelius-Flohe et
vitamin D in foodstuffs but they may pose a risk for toxicity. al, 2002).
One group of investigators found that moist foods generally
contained higher levels of vitamin D than extruded foods and METABOLISM
that some moist foods exceeded the AAFCO maximal recom- Vitamin E is absorbed from the small intestine by nonsat-
mended allowance of 10,000 IU/kg for cats (Morris, 1996). urable, passive diffusion, which depends on micellar solubiliza-
Other sources of vitamin D include fresh water fish and eggs tion. Whether presented as free alcohol or as esters, most vita-
(especially yolks). Beef, liver and dairy products contain small- min E is absorbed as the alcohol. Esters are largely hydrolyzed
er amounts of vitamin D. The most common synthetic sources in the gut wall before absorption, probably by a duodenal
of vitamin D in pet foods include cholecalciferol (D-activated mucosal esterase. The free alcohol enters the intestinal lacteals
animal sterol), vitamin D supplement, ergocalciferol (D-acti- and is transported via lymph to the general circulation.
3
vated plant sterol) and vitamin D supplement. The efficiency of vitamin E absorption is low and variable
2
(35 to 50%); the absorption efficiency is much lower than that
Vitamin E of vitamin A (Combs, 1998). Absorption of vitamin E is
Vitamin E is a term for a group of compounds with the biolog- enhanced by the simultaneous digestion and absorption of
ic activity of α-tocopherol. In nature, there are eight isomeric dietary lipids. Transfer of vitamin E across epithelial cells may
forms of vitamin E, four tocopherols (α, β, γ, δ) and four require several stages, most of them poorly understood. In
tocotrienols (α, β, γ, δ). Naturally occurring α-tocopherol (d-α- mammals, vitamin E is transported from the intestine to lym-
tocopherol) is now designated as RRR-α-tocopherol based on phatic capillaries in association with chylomicrons. Conversely,
RS or CIP system of chiral configuration. Synthetic α-toco- in birds, tocopherol is transported via the portal vein directly to
pherol (dl-α-tocopherol),a mixture of eight stereoisomers of α- the liver. Unlike cholesterol or vitamin A, α-tocopherol is not
tocopherol, is designated as all-rac (racemic)-α-tocopherol. re-esterified during the absorption process.
Vitamin E activity in pet food is generally expressed in interna- Vitamin E circulates in the lymph and blood bound to all
tional units. One IU of vitamin E equals 1 mg of all-rac-α- of the lipoproteins. There is a very high correlation between
tocopheryl acetate or 0.91 mg of all-rac-α-tocopherol. The tocopherol levels and the total lipid or cholesterol concentra-
most biopotent form of vitamin E is α-tocopherol.The relative tion in serum.
biopotencies of vitamin E isomers are as follows: α >β >δ >γ All tissues show linear increases in tocopherol concentrations
(McDowell, 1989). Also, tocopherols are generally more avail- with increases in tocopherol intake. This relationship differs
able than tocotrienols (Combs, 1998). Because some forms of from that of most other vitamins, which usually have distinct
vitamin E have little biologic activity, total vitamin E analysis is deposition thresholds in tissues other than the liver, and may
not a reliable means of determining vitamin E activity. provide an explanation for the pharmacologic effects of vitamin