Page 121 - Small Animal Clinical Nutrition 5th Edition
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122 Small Animal Clinical Nutrition
excretion of selenium is closely related to dietary intake in rats cose tolerance factor (GTF) that restored impaired glucose tol-
VetBooks.ir and people (Levander, 1986). A dietary threshold is reached at erance in rats (Schwarz and Mertz, 1959). Chromium was
identified as the active component. Chromium is ubiquitous in
low-selenium intakes, wherein excretion is shut down, thus con-
serving selenium. Urinary selenium increases proportionally at
water, soil and living matter; however, tissue levels in animals
higher selenium intakes. Fecal excretion, on the other hand, are very low because of limited uptake by plants and absorption
remains constant over a wide range of selenium intakes. by animals. Furthermore, many forms of chromium are poorly
Although selenium deficiency has been observed experimen- available. Therefore, supplementation with an available form
tally in dogs (Van Vleet, 1975), the incidence of selenium defi- may be warranted. Chromium in an organically bound form
ciency has not been reported for dogs and cats. Likewise, sele- (e.g., GTF) is absorbed better, has a different tissue distribution
nium toxicity has not been noted in dogs and cats, despite high and is more available to fetuses than inorganic chromium
concentrations (>4 mg selenium/kg food) in seafood and fish- (Mertz and Roginski, 1971).
containing cat foods. AAFCO (2007) selenium recommenda- Several studies in people and other animals have demonstrat-
tions are 0.11 mg/kg of food DM for dogs and 0.1 mg/kg of ed beneficial effects of chromium supplementation (in chromi-
food DM for cats. The NRC (2006) recommended allowance um deficiency or diabetics) including: 1) improved glucose tol-
is 0.35 and 0.30 mg DM selenium/kg diet for dogs and cats, erance, 2) reversed hyperglycemia and glycosuria, 3) decreased
respectively (growth and adult recommendations were not dif- circulating insulin concentrations, 4) decreased plasma lipid
ferent). This increase in minimum recommendations, relative concentrations, 5) decreased body fat, 6) increased protein
to previous NRC publications, takes into account potentially accretion, 7) improved immune response and 8) reduced corti-
low availability of selenium in pet food ingredients. sol production in response to heat and transport stress
Selenium availability is highly influenced by the chemical form (Anderson, 1987; Page et al, 1993; Moonsie-Shageer and
of selenium (supplied as a supplement or from foodstuffs). Mowat, 1993). Not all studies have shown improvements in
Furthermore, the requirement for selenium can be partially these variables. This lack of consistent response may be
replaced by vitamin E. Selenium in animal feeds is highly vari- accounted for by an adequate chromium nutriture for some
able primarily due to the variable selenium status of soils. Studies individuals or some factor other than chromium deficiency that
with pigs demonstrated that inorganic selenium (sodium selen- may have compromised the variable (impaired glucose toler-
ite) and organic selenium (selenium yeast) were equally effective ance, etc.). Few tests are available to specifically diagnose
in supporting glutathione peroxidase activity, but that selenium chromium status. The glucose tolerance test has been most
stores in tissues (liver and muscle) were greater when organic commonly used to evaluate chromium deficiency. Table 6-1
selenium was fed (Mahan, 1995). Selenium content in milk is lists signs of deficiency and excess.
also higher when selenium is supplied in the organic form.
Fish products are rich in selenium (1 to 6 mg selenium/kg), Boron
but selenium availability in these ingredients is low (Wedekind Boron indirectly influences PTH activity, thus it influences cal-
et al, 1997; Wedekind et al, 1998; Combs and Combs, 1986). cium, phosphorus, magnesium and cholecalciferol (vitamin
Selenium levels exceeding 2 mg selenium/kg of food DM have D ) metabolism. Investigators demonstrated that boron acts by
3
not been reported to be toxic for cats. Cats may be able to tol- at least three different mechanisms (Hunt et al, 1994): 1) it
erate higher selenium levels because the high-protein foods compensates for perturbations in energy substrate use induced
typically fed to cats are protective against high-selenium levels by vitamin D deficiency, 2) it enhances macromineral content
(Levander, 1986). in normal bone and 3) it enhances some indices of growth and
Current AAFCO (2007) guidelines set a maximum safe sele- cartilage maturation, independent of vitamin D. Boron has a
nium level for dogs at 2 mg/kg; however, NRC (2006) does not role in the control of urolithiasis. It decreases oxalate produc-
list a safe upper limit for cats. Neither NRC nor AAFCO has tion in women fed magnesium-deficient diets (Hunt et al,
listed a safe upper limit for selenium for cats. Fish, eggs and 1994a). Boron also decreases calcium loss and bone demineral-
liver are ingredients rich in selenium. Table 6-1 lists signs of ization in postmenopausal women (Nielsen et al, 1987). Table
deficiency and excess (Case 6-4).Typical selenium supplements 6-1 lists signs of deficiency and excess.
include sodium selenite and sodium selenite. See Chapter 29
for more information about selenium.
VITAMINS
Ultra-Trace Minerals
The minimum dietary requirements for ultra-trace elements in Definition
dogs and cats have not been determined. Based on research in The term “vitamine” was coined by Casmir Funk in 1912 when
other species, it is probable that supplemental micronutrients, he described a class of nitrogen-containing compounds that
such as chromium and boron, may be beneficial under certain were “vital-amines” (i.e., being vital to life).This term was later
physiologic and dietary circumstances. changed to vitamin when it was found that not all of these
compounds contained nitrogen. The discovery, isolation and
Chromium synthesis of vitamins have occurred in the last 100 years,
In 1957, investigators identified a compound they called glu- although the effects of vitamin deficiency, specifically scurvy,