|
 Technical Articles
/ Technical Articles' List
/
Back to Pets
|
| |
Zinc and copper nutriture in the cat |
 Send to a friend (2)
Who saw this article? New!
Author: ANDREA J. FASCETTI and JAMES G. MORRIS - University of California (Courtesy of Alltech Inc.)
Publication date: 03/22/2007
Twenty four minerals are known to be required by at least some animal species (McDowell, 1992). Mineral classification schemes aid in understanding their role in nutrition. Animals require macrominerals in percentage amounts in their diet. Trace minerals are distinguished from the major mineral elements, such as calcium, by the fact that they occur and function in living organisms in relatively small amounts or low concentrations – generally expressed as parts per million (ppm) or parts per billion (ppb), or as micrograms or nanograms (Underwood, 1981).
Much of the information about mineral needs of animals gained by trial and error throughout history was never recorded. Trace mineral nutrition was first developed in laboratory animals and in commercial livestock during the 1920s through the 1950s. Quantitative chemical analysis was not yet developed, but it was possible to make diets with determined amounts of trace elements, and hence to produce deficiency states (Solomons, 1995). It was only with the development of atomic absorption spectrophotometry that it first became feasible and practical to detect and quantify trace minerals in tissues and body fluids.
Despite the advances in our knowledge about trace mineral metabolism and companion animal nutrition, very little is known about trace mineral requirements and their bioavailability in the feline species. The cat is an obligate carnivore (Morris and Rogers, 1982), and in the wild was probably able to obtain all it required from its diet. However, with the domestication of the cat and the advent of commercially produced diets, trace mineral requirements need to be evaluated to ensure adequate dietary intake for all life stages. The aim of this paper is to briefly summarize current knowledge of copper and zinc nutrition in cats. Information on zinc and copper metabolism from other species is included, where relevant, to provide historical perspective and comparison.
Zinc
Zinc (Zn) is the most abundant intracellular trace element in animals; total body Zn approaches that of iron. However, within cells the concentration of free Zn is extremely low. The high intracellular concentration of Zn is maintained by binding sites with a high affinity for Zn and by the transport system. Zinc fulfills three different roles: catalytic, as an integral component of over 200 metalloenzymes; structural, in stabilizing membranes; and functional, in such roles as ‘zinc fingers’. Because of these different roles and the plethora of Zn-containing enzymes, the clinical signs of Zn deficiency frequently involve multiple organ systems, including growth, sexual maturation and immune function. Although a large number of Zn metalloenzymes have been characterized, in complex organisms unequivocal evidence of clinical signs linked to changes in an enzyme activity has not been forthcoming.
Zinc is presented to the enterocyte mainly in the form of Zn bound to such ligands as peptides, amino acids, nucleotides, and possibly free Zn, where the solubility of Zn would be an important determinant of uptake. Factors suggested as affecting Zn bioavailability fall into two categories, (1) chelating agents (e.g., phytic acid), and (2) metal ion interactions (e.g., copper, cadmium, iron) (Baker and Ammerman, 1995). It is apparent that the significance of some other dietary compounds, particularly calcium, depends on the animal species and the type of diet (Sandstrom and Lonnerdahl, 1989).
In dogs, the main absorption of Zn occurs in the duodenum and to a lesser extent from the ileum and jejunum (Naveh et al., 1988). Zinc absorption in the intestine involves a mediated (saturable) component and a nonmediated (nonsaturable) component that appear to be a function of the luminal Zn concentration (Cousins, 1989). At low luminal concentrations, the majority of Zn is absorbed through a carrier-mediated process. When low-Zn diets are fed to rats, kinetic evidence suggests that there is an increase in the transfer rate of Zn rather than a change in the affinity. The form in which Zn is absorbed is unclear, but evidence from pig brushborder vesicles suggests that Zn is absorbed as a Zn-peptide complex (Gly-Gly-His) that may use a peptide carrier system (Tacnet et al., 1993). Once inside the cell, Zn is bound to metallothionein and a cysteine-rich intestinal protein. Zinc absorption declines as metallothionein synthesis is elevated in response to dietary Zn intake (Coppen and Davies, 1987 and Hoadley et al., 1988). Zinc flux in the mucosal serosal direction is inversely related to the cellular concentration of metallothionein, and in the reverse direction directly related to metallothionein concentration.
In domestic animal nutrition, Zn first achieved prominence with the demonstration that the disease known as swine dermatitis or parakeratosis could be reversed by dietary supplements of 0.2% Zn carbonate (Tucker and Salmon, 1955). The diets fed to swine that produced this condition contained vegetable protein supplements (peanut meal, cottonseed meal, and soybean meal) and the incidence of the condition was significantly increased by the addition of 1.5% calcium carbonate or 2% bone meal to the ration. Thus, these rations contained high levels of calcium and plant products supplying phytates, both important factors later shown to reduce the bioavailability of Zn.
Subsequent to these observations, Roberston and Burns (1963) reported Zn deficiency in dogs given a high calcium diet. The study had three groups of dogs given a basal diet containing 3 g of calcium and 33 mg of Zn/kg of diet. One group of dogs was given the basal diet alone, another group was fed the basal diet plus 20 g calcium carbonate/kg diet, and the remaining group was given the basal diet plus 20 g calcium carbonate/kg diet and 200 mg Zn/kg diet. Dogs fed the basal diet with calcium carbonate developed Zn deficiency and had extremely poor weight gain. The dogs receiving the basal diet alone, or the basal diet plus calcium carbonate and 200 mg Zn/kg diet had no clinical signs of Zn deficiency and similar growth rates. These observations demonstrated that in dogs the calcium level of the diet is an important factor in Zn nutrition.
Zinc deficiency has been reported in dogs given generic dog foods (Sousa et al., 1988 and Huber et al., 1991). Generally these foods have been high in plant products (phytates) and inadequately supplemented with an available form of Zn. Dogs consuming these diets exhibited parakeratotic lesions. Dog foods commonly contain Zn oxide or Zn sulfate as supplemental sources of Zn.
There do not appear to be any reports of Zn deficiency in cats fed commercially prepared diets, and there is no published information on the bioavailability of Zn from various sources in cats.
The lower incidence of recorded Zn deficiency in cats may be a consequence of a lower proportion of plant proteins in cat foods compared to dog foods.
Cats, even when Zn deficient, do not exhibit the marked parakeratotic lesions that occur in dogs (Kane et al., 1981). Kittens given a low-Zn, purified diet following weaning exhibited reduced growth rates, parakeratotic lesions of the philtrum, reduced spermatogenesis, and poor haircoats.
Circumscribed, erythematous, raised areas on the ventral aspect of the abdomen similar to those of Zn deficiency in other species have been observed by one of the authors (Morris) in newborn kittens from queens given an expanded test diet (of similar formula to a commercial diet). These clinical signs resolved before weaning without a change in diet.
The National Research Council (NRC, 1986) recommends a minimum of 15 mg/kg diet for kittens fed diets containing a low quantity of compounds known to decrease Zn bioavailability, (e.g., phytate and fiber), under which conditions 50 mg/kg diet should suffice. The minimal requirement of Zn for gestation and lactation in cats has not been determined, although a high dietary Zn requirement (50-100 mg/kg diet) is known for several species for fetal development.
In dogs and cats, plasma Zn concentrations are responsive to dietary Zn intake. Brinkhaus et al. (1998) compared the ability of Zn propionate and Zn oxide to elevate the plasma Zn concentration of adult fasted dogs and concluded that Zn in the form of propionate had a higher availability. Wedekind and Lowry (1998) also compared the availability of Zn from Zn oxide and Zn propionate, but used growing puppies and diets with both 10 g and 15 g calcium/kg. They reported, using plasma Zn in a slope ratio method, that Zn propionate had a 60% to 80% higher bioavailability than Zn oxide. The bioavailability of both compounds was depressed by the addition of calcium to the diet, however that of Zn propionate was higher than Zn oxide.
Kuhlman and Rompala (1998) found that Beagle bitches fed organic forms of Zn (Zn proteinate), copper (copper proteinate) and manganese (manganese proteinate) had larger litters (7.3 pups, mean litter size) compared to bitches fed equal concentrations of these minerals supplied in their inorganic forms (6.2 pups, mean litter size). Lowe and Wiseman (1998) made comparisons of the bioavailability of Zn supplied as a Zn chelate (1 mole each of methionine, glycine and Zn), a Zn polysaccharide complex, and Zn oxide. These authors used adult dogs and a combination of hair growth and Zn content of hair as indices of bioavailability. They concluded that Zn from the chelate had a higher bioavailability than Zn oxide or polysaccharide complex. Wedekind and Lowry (1998) made the point that Zn in Zn sulfate is about twice as available as Zn supplied by the oxide, so both organic Zn sources and Zn sulfate are highly available in dogs. To the authors’ knowledge, there are no comparable studies in cats.
Copper
Copper (Cu), like Zn is an essential element for all living organisms, but in contrast to Zn, exhibits redox chemistry. The chemistry of Cu makes it particularly suited for releasing and accepting electrons, especially the direct transfer of electrons to molecular oxygen. Consequently, many Cucontaining enzymes such as cytochrome c oxidase, Cu/Zn superoxide dismutase, tyrosinase, and lysyl oxidase are involved in oxidation reactions. In humans and rats, Cu is absorbed primarily in the duodenum, though uptake may occur in other sections of the small intestine and perhaps even the colon. The efficiency of Cu absorption from normal foods can be quite high (55 to 75%), but declines to less than 10% with high concentrations in the diet.
Absorption of Cu from the gut (probably as Cu2+) is regarded as a two-step process: Cu entry at the brush border and its subsequent transfer across the basolateral membrane. Evidence suggests that uptake by the brush border is via nonmediated diffusion and an energy-dependent saturable carrier across the basolateral membrane, most likely a Ptype ATPase (Linder, 1991).
As in the case of Zn, entry of Cu into the enterocyte does not equate with transfer into the body. Copper may also be transported at the basolateral membrane by carriers used by other divalent ions, notably Zn and cadmium, which would explain the antagonism between these ions and Cu absorption. An alternative mechanism of antagonism is that these ions induce the production of metallothionein in mucosal cells, which reduces net Cu transfer. Metallothionein has a higher affinity for Cu than Zn. Binding of Cu to metallothionein and other proteins in the enterocyte results in trapping and subsequent loss when the mucosal cell is sloughed.
There is a dearth of reports of confirmed Cu deficiency in dogs given commercial diets, even though Cu was shown to be an essential dietary ingredient for dogs for the prevention of anemia many years ago (Linton, 1934 and Frost et al., 1939).
This may be because most dog foods contain adequate levels of available Cu, or that dogs have a relatively low Cu requirement as suggested by the NRC (1985). In contrast, there are a number of reports of Cu accumulation in certain breeds of dogs, particularly the terrier breeds, Bedlington, Skye, West Highland White and Kerry Blue (Brewer, 1998).
The Cu requirements of kittens for growth appear to be similar to those of other mammals (Doong et al., 1983), however the current NRC (1986) recommendation is marginal for optimal reproduction (Fascetti et al., 2000). Queens consuming purified diets with dietary Cu, supplied as Cu sulfate, at 10.8 mg/kg diet had higher conception rates (although not statistically significant) than queens consuming Cu sulfate at 4 and 5.8 mg Cu/kg diet. The concentration of dietary Cu affected the time interval (P=0.04) for queens to conceive after exposure to the tom (defined as the number of days from the introduction of a proven tom until conception). There was a significant difference between the queens consuming diets containing Cu at 4 and 10.8 mg/kg diet (P=0.05).
There was a negative linear relationship between dietary Cu concentration (x = Cu mg/kg diet) and the mean time (y = days) necessary for queens to conceive (y = 43.38 – 2.87x; R2 = 0.97). No significant differences among the dietary treatment groups in the number of kittens born per litter, birth defects, kitten mortality or birth weights were observed. Liver Cu concentrations were responsive to dietary Cu intake. However, plasma Cu concentrations, and the activities of superoxide dismutase, diamine oxidase and ceruloplasmin did not change over the range of 4 to 10.8 mg Cu/kg diet.
Problems of Cu availability have also been implicated in reproductive problems in cats. At the Feline Nutrition and Pet Care Center, University of California, Davis, reproductive failure in queens undergoing American Association of Feed Control Officials (AAFCO) protocol tests has been observed on three occasions with commercial diets.
Litters from queens given these diets were frequently stillborn or born prematurely; and kittens exhibited hypochromotrichia and collagen abnormalities evidenced by marked rotation and twisting of the limbs and curled tails. The common factor in these three diets was supplemental Cu in the form of Cu oxide. Commercial Cu oxide is mainly cupric oxide (Aoyagi and Baker, 1993), which has been shown to be unavailable to chickens and pigs (Baker et al., 1991 and Cromwell et al., 1989). Fascetti et al. (1998) gave four groups of queens purified diets containing either 10 mg Cu/kg diet as cupric oxide or Cu as cuprous sulfate at 3, 6 and 10 mg/kg diet. Lower conception rates (42 versus > 82%) and longer time intervals between exposure to the tom and conception occurred in queens given the Cu oxide diet. However, no kittens with skeletal or hair abnormalities were recovered. All but one of the queens consuming the Cu oxide diet ate her kittens at birth, which precluded their examination.
(Queens frequently eat kittens that are born dead or are defective at birth.) Cupric oxide does not supply a biologically available form of Cu for the cat and should not be used in any foods formulated for this species.
These studies demonstrate a major problem to further investigations of Cu metabolism in cats. Plasma Cu concentration was unresponsive to dietary Cu intake and did not reflect liver Cu concentrations, which markedly declined in cats consuming Cu-depletion diets or diets containing Cu supplied as Cu oxide. Furthermore, enzymes such as superoxide dismutase and diamine oxidase, and the cuproprotein ceruloplasmin were not responsive to dietary Cu intake (Fascetti et al., 2000).
Therefore it appears that studies on the bioavailability of Cu in diets intended for cats will either need to use isotopic methods or use other species, such as chicks, as test animals.
A suspected case of Cu deficiency has recently been described in a colony of kittens (Hendriks et al., 2001). The authors hypothesized it may have occurred secondary to the ingestion of Zn from galvanized iron cages used to house the cats. Clinical signs in the affected kittens ranged from weakening of the hind limbs, dysmetria to hind limb ataxia at 4- 5 months of age. Fading coat color, and broken and brittle tactile hairs were also observed before the first signs of ataxia were noted. A liver sample taken from 25% of the ataxic kittens for necropsy had a Cu concentration of 12.7 mg/kg (it was not reported if this was dry or wet weight). Histological lesions included Wallerian-type degeneration in the spinal cord, pons and medulla, and neuronal degeneration in the vestibular nuclei and ventral horns of the spinal cord. Analysis of the diet fed to the kittens at one time point showed a Cu concentration of 28 mg/kg diet and Zn concentrations of 78 mg/kg diet. The complete details concerning diet composition and analysis were not reported, but the authors believed the Cu to be bioavailable.
References
Aoyagi, S. and D.H. Baker. 1993. Bioavailability of copper in analytical-grade and feed-grade inorganic copper sources when fed to provide copper at levels below the chicks requirement. Poult. Sci. 72:1075-1083.
Baker, D.H., J. Odle, M.A. Funk and T.M. Wieland. 1991. Research Note: Bioavailability of copper in cupric oxide, cuprous oxide, and in a copper-lysine complex. Poult. Sci. 70:177-179.
Baker, D.H. and C.B. Ammerman. 1995. In: Bioavailability of Nutrients for Animals (C.B. Ammerman, D.H. Baker and A.J. Lewis, eds), Academic Press, New York, NY, pp. 372.
Brewer, G.J. 1998. Wilson disease and canine copper toxicosis. Am. J. Clin. Nutr. 67 (Suppl):1087S-1090S.
Brinkhaus, F., J. Mann, C. Zorich and J.A. Greaves. 1998. Bioavailability of zinc propionate in dogs. J. Nutr. 128:2596S-2597S.
Coppen, D.E. and N.T. Davies. 1987. Studies on the effect of dietary zinc dose on 65Zn absorption in vivo and on the effects of Zn status on 65Zn absorption and body loss in young rats. Br. J. Nutr. 57:35-44.
Cousins, R.J. 1989. Theoretical and practical aspects of zinc uptake and absorption. In: Mineral Absorption in the Monogastric GI Tract (J.A. Laslo and F.R. Dintzis, eds), Plenum, New York, NY., pp. 3-12.
Cromwell, G.L., T.S. Stahly and H.J. Monegue. 1989. Effects of source and level of copper on performance and liver copper stores in weanling pigs. J. Anim. Sci. 67:2996-3002.
Doong, G., C.L. Keen, Q.R. Rogers, J.G. Morris and R.B. Rucker. 1983. Selected features of copper metabolism in the cat. J. Nutr. 113:1963- 1971.
Fascetti, A.J., J.G. Morris and Q.R. Rogers. 1998. Dietary copper influences reproductive efficiency of queens. J. Nutr. 128:2590S-2592S.
Fascetti, A.J., Q.R. Rogers and J.G. Morris. 2000. Dietary copper influences reproduction in cats. J. Nutr. 130:1287-1290.
Frost, D.V., C.A. Elvehjem and E.B. Hart. 1939. The role of iron, copper, and cobalt in hemoglobin production in dogs on a milk diet. J. Biol. Chem. 128:xxxi.
Hendriks, W.H., F.J. Allan, M.F. Tarttelin, M.G. Collett and B.R. Jones. 2001. Suspected zincinduced copper deficiency in growing kittens exposed to galvanised iron. N. Z. Vet. J. 49(2):68- 72.
Hoadley, J.E., A.S. Leinart and R.J. Cousins. 1988. Relationship of 65Zn absorption kinetics to intestinal metallothionein in rats: Effect of zinc depletion and fasting. J. Nutr. 118:497-502.
Huber, T.L., D.P. Laflamme, L. Medleau, K.M. Comer and P.M. Rakich. 1991. Comparison of procedures for assessing adequacy of dog foods. J. Am. Vet. Med. Assoc. 199:731-734.
Kane, E., J.G. Morris, Q.R. Rogers, P.J. Ihrke and P.T. Cupps. 1981. Zinc deficiency in the cat. J. Nutr. 111:488-495.
Kuhlman, G. and R.E. Rompala. 1998. The influence of dietary sources of zinc, copper and manganese on canine reproduction performance and hair mineral content. J. Nutr. 128:2603S-2605S.
Linder, M.C. 1991. The Biochemistry of Copper. Plenum, New York, NY.
Linton, R.G. 1934. Canine Nutrition. In: Proc. 12th Int Vet Cong., New York, NY, p. 488.
Lowe, J.A. and J. Wiseman. 1998. A comparison of the bioavailability of three dietary zinc sources using four different physiologic parameters in dogs. J. Nutr. 128:2809S-2811S.
McDowell, L.R. 1992. Introduction. In: Minerals in Animal and Human Nutrition. Academic Press, New York, NY.
Morris, J.G. and Q.R. Rogers. 1982. Metabolic basis for some of the nutritional peculiarities of the cat. J. Sm. An. Pract. 23:599-613.
Naveh, Y., L. Bentur and E. Diamond. 1988. Site of zinc absorption in dog small intestine. J. Nutr. 118:61-64.
NRC. 1985. In: Nutrient Requirements of Dogs. 2nd rev. ed. Natl. Acad. Press, Washington, DC, p. 19.
NRC. 1986. In: Nutrient Requirements of Cats. 2nd rev. ed. Natl. Acad. Press, Washington, DC, pp. 17-18.
Robertson, B.T. and M.J. Burns. 1963. Zinc metabolism and zinc-deficiency syndrome in the dog. Am. J. Vet. Res. 24:997-1002.
Sandstrom, B. and B. Lonnerdahl. 1989. Promoters and antagonists of zinc absorption. In: Zinc in Human Biology (C.F. Mills, ed), Springer-Verlag, New York, NY, pp. 57-78.
Solomons, N.W. 1995. Trace element nutrition’s coming of age. Nutrition 11(1):47-48.
Sousa, C.A., A.A. Stannard, P.J. Ihrke, S.I. Reinke and L.P. Schmeitzel. 1988. Dermatosis associated with feeding generic dog foods: 13 cases (1981- 1982). J. Am. Vet. Med. Assoc. 192:670-680.
Tacnet, F., F. Lauthier and P. Ripoche. 1993. Mechanisms of zinc transport in the pig small intestine brush-border membrance vesicles. J. Physiol. 465:57-72.
Tucker, H.F. and W.D. Salmon. 1955. Parakeratosis or zinc deficiency disease in the pig. Proc Soc Exp. Biol. Med. 88:613-616.
Underwood, E.J. 1981. Trace metals in human and animal health. J. Hum. Nutr. 35:37-48.
Wedekind, K.J. and S.R. Lowry. 1998. Are organic zinc sources efficacious in puppies? J. Nutr. 128:2593S-2595S.
Authors: ANDREA J. FASCETTI and JAMES G. MORRIS
Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, CA, USA
Author: ANDREA J. FASCETTI and JAMES G. MORRIS - University of California (Courtesy of Alltech Inc.)
Publication date: 03/22/2007
Send to a friend (2)
Who saw this article? New!
MAKE A COMMENT ABOUT THIS ISSUE.
 
|
|
ENGOREART MAS 20081015
|
|
