Page 120 - Small Animal Clinical Nutrition 5th Edition
P. 120
Minerals and Vitamins 121
cells into the colloid space. Iodine then combines with tyrosine of iodine. Iodine supplements typically used in pet foods
VetBooks.ir residues associated with thyroglobulin protein to form include calcium iodate, potassium iodide and cuprous iodide.
Since the late 1970s, feline hyperthyroidism has become a
monoiodotyrosine (MIT) and diiodotyrosine (DIT). The oxi-
more frequently diagnosed condition. However, much remains
dation process proceeds further under the influence of the thy-
roid-peroxidase enzyme to couple MIT and DIT to form var- to be learned about this endocrinopathy (e.g., prevalence and
ious iodothyronines (e.g., T and T ). Finally, iodinated thy- cause). Hypothyroidism is a much more prevalent thyroid dis-
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roglobulin and thyroid hormones are reabsorbed into the thy- order in dogs. Both iodine excess and deficiency may result in
roid cells and exposed to proteolytic enzymes.Much of the pro- subclinical or overt thyroid dysfunction.
tein and iodinated tyrosines are lysed and returned as substrates Current AAFCO (2007) guidelines set a maximum safe level
to repeat the process. At the same time, some thyroid hormones for iodine for dogs at 50 mg/kg, whereas NRC (2006) recom-
are released into the circulation. Regulating the action of thy- mends 4 mg/kg as a safe upper limit. Neither NRC nor
roid hormones is a complex process involving interaction AAFCO sets a safe upper limit for iodine for cats. However,
among neurotransmitters, hormones and enzymes in the cen- estimates for establishing safe upper limits and/or lowest observ-
tral nervous system, the pituitary gland, the thyroid glands, the able adverse effect level for cats were determined in a recent
circulation and peripheral tissues. study (Wedekind et al, In press). In people, guidelines have been
Investigators have estimated the iodine requirement for established to define deficiency, adequacy and iodine excess
adult dogs to be 0.56 mg/kg DM (Belshaw et al, 1975). (Laurberg et al,2001) based upon urinary iodine concentrations.
AAFCO (2007) recommends an iodine level of 1.5 mg/kg When these guidelines are applied to cats (corrected for meta-
0.67
DM for dogs. This margin of safety is prudent in practical bolic equivalent basis; BW ), dietary intakes between 0.46 and
foods to overcome potential effects of goitrogens and negative 3.5 mg/kg were considered optimal, whereas dietary intakes
mineral antagonisms. exceeding 3.5 mg/kg were defined as excessive. In addition, cats
A recent study (Wedekind et al, In press) estimated the fed the highest dietary iodine intake (8.8 to 9.2 mg/kg iodine)
iodine requirement for adult cats to be 0.46 mg/kg DM. This for one year had significantly reduced FT and numerically
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estimate was based upon three measurements of iodine status: lowered TT and TT at 12 months.Thus, these findings sug-
3
4
regression of Tc 99m thyroid:salivary ratio (scintigraphy), gest 3.5 mg/kg as a no observable adverse effect level or safe
iodine balance and urinary iodine excretion after iodine intake. upper level and intakes of 8.8 mg/kg as a lowest observable
These estimates agreed closely with the iodine requirement adverse effect level. Table 6-1 lists signs of iodine deficiency and
determined for dogs (Belshaw et al, 1975) and people (DRI, excess. See Chapter 29 for more information about iodine.
2001). This estimate is higher than current AAFCO (2007)
minimum iodine recommendations for adult cats (i.e., 0.35 Selenium
mg/kg DM iodine), but is much lower than the NRC (2006) Selenium is an essential constituent of glutathione peroxidase,
recommended iodine allowance (1.4 mg iodine/kg diet). Note which helps protect cellular and subcellular membranes from
that the NRC (2006) recommendation does not agree closely oxidative damage. Glutathione peroxidase and vitamin E work
with current AAFCO recommendations and was based upon synergistically to reduce the destructive effects of peroxidative
data derived from two studies (Scott et al, 1961; Ranz et al, reactions on living cells. Selenium spares vitamin E in at least
2002). Unfortunately, these studies should not have been used three ways: 1) preserves the integrity of the pancreas, which
as a basis for establishing the iodine requirement of cats. The allows normal fat digestion, and thus normal vitamin E absorp-
Scott (1961) study used a nutritionally incomplete or imbal- tion, 2) reduces the amount of vitamin E required to maintain
anced diet (i.e., the diet used was an all meat diet [beef hearts], integrity of lipid membranes via glutathione peroxidase and 3)
which was grossly deficient in calcium).The Ranz (2002) study aids retention of vitamin E in the blood plasma in some
was of short duration (i.e., 54 days total with only a seven-day unknown way.
period for each iodine level). In this study, the minimum iodine Vitamin E reduces the selenium requirement in at least two
level evaluated, approximately 4.1 mg/kg iodine, was not low ways: 1) maintains body selenium in an active form, or prevents
enough to yield a valid iodine requirement estimate. losses from the body and 2) prevents destruction of lipids with-
Interestingly, the previous NRC (1986) did not cite the Scott in membranes, thereby inhibiting production of hydroperoxides
(1961) reference. and reducing the amount of the selenium-dependent enzyme
The iodine requirement is influenced by physiologic state needed to destroy peroxides formed in cells (Scott et al, 1982).
and diet. Lactating animals require more dietary iodine because Selenium also has a vital role in maintaining normal thyroid
about 10% of the iodine intake is normally excreted in milk hormone and iodine metabolism, particularly through the con-
(McDowell, 1992). Likewise, the presence of goitrogenic sub- trol of deiodinase enzymes that regulate conversion of T to T 3
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stances and nutrient excesses of certain minerals (e.g., arsenic, (Arthur, 1993).
bromide, fluoride, cobalt, manganese, calcium and potassium) The duodenum is the main site of selenium absorption.There
may increase the need for iodine (NRC, 2005). Potential is no homeostatic control of selenium absorption regardless of
sources of goitrogens in pet foods include peas, peanuts, soy- the dietary selenium concentration. Likewise, selenium status
beans and flaxseed. Fish, eggs and iodized salt are rich sources also appears to have little effect on selenium uptake. Excretion
of iodine, whereas most animal proteins are moderate sources of selenium, however, is homeostatically regulated. Urinary