Page 120 - Small Animal Clinical Nutrition 5th Edition
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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-
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                  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
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