by Larry L. Berger, Ph.D.
Professor, Animal Sciences
University of Illinois
The role of chromium as an essential trace element in human and laboratory animal nutrition is well recognized (Anderson, 1987; Offenbacher and Pi-Sunyer, 1988). The purpose of this article is to review the increasing body of evidence which suggests that chromium may also be an essential trace element for livestock and poultry.
Schwarz and Mertz in 1959 were the first to identify chromium as the active constituent of the glucose tolerance factor (GTF). Although the exact structure of GTF is unknown, it is thought to be a nicotinic acid-trivalent chromium-nicotinic acid axis with ligands of glutamic acid, glycine and cysteine (Mertz et al., 1974). Chromium may have several biological functions, including activating certain enzymes and maintaining structural integrity of nucleic acids, but its main role is as the key component of the GTF which enhances the action of insulin.
In general, GTF chromium has been shown to be more biologically active than an equal amount of inorganic trivalent chromium. However, there have been cases where trivalent chromium (CrCl3) has improved animal performance. For example, Rosebrough and Steele (1981) reported that adding 20 ppm chromium from CrCl3 increased (P<.05) weight gains of turkey poults fed diets that were protein deficient. Turkeys fed the supplemental chromium had higher liver glycogen levels as a result of increasing the activity of the enzyme glycogen synthetase. In addition, chromium increased glucose transport by increasing insulin activity. The reason why the chromium response occurred only in the protein deficient state is uncertain.
Similar responses have been observed with protein-deficient rats (Mertz and Roginski, 1963). Rats fed 10% crude protein diets supplemented with 2 ppm chromium from CrCl3 had less of a weight gain depression than rats fed the same diet without supplemental chromium. When additional stress was applied through controlled exercise or blood loss, rats fed chromium deficient diets had poorer performance and survival. Differences in performance were not due to increased water content, but reflected changes in the amount of carcass protein. More recent research (Anderson, et al., 1988) with humans and mice has shown that stress increases the urinary excretion of chromium.
Newly received feedlot calves frequently are heavily stressed and are susceptible to shipping fever. Chang and Mowat (1992) evaluated the effects of supplemental chromium, from high-chromium yeast, on the performance and health of stressed calves with or without long-acting oxytetracycline. During the first 28 days, feeding 0.4 ppm chromium increased averaged daily gains by 30% (1.34 vs 1.74 lbs/day) and gains per unit of dry matter intake by 27% (0.123 vs 0.156) in calves not receiving oxytetracycline. In contrast, chromium supplementation had no affect on the performance of calves receiving the antibiotic. Calves in this trial were stressed in that they were transported by truck for 18 hours, rested, and offered hay and water for 10 hours, and then transported for an additional 26 hours before arrival. It is likely that this level of stress increased urinary chromium excretion and depleted body chromium stores. Stress often causes increased glucose metabolism which results in increased mobilization of chromium from body stores. Once the chromium is mobilized, very little is reabsorbed and most is excreted in the urine.
Chromium supplementation may also affect the excretion of other minerals during stress. Increased urinary excretion of zinc and copper has been reported with calves after market-transit stress, fasting, and infectious bovine rhinotracheitis infection. However, stress-induced losses of zinc, copper, iron, and manganese were reduced in mice fed supplemental chromium (Schrauzer et al., 1986).
Since several trace elements are required for maximum immune response, chromium supplementation may have allowed the stressed calves to more effectively ward off infectious organisms. The fact that chromium had no additive response with the oxytetracycline, suggest that both agents may have the same outcome, but different modes of action. The chromium may have had its effect by allowing the calves' immune system to be more responsive in attacking the pathogens, while the antibiotic kills the invading organism itself.
For chromium to have its maximum effect, it appears that it is beneficial to get the chromium into the calves prior to, or very early in the stress period. Mowat and Chang (1992) reported that when chelated chromium was fed early in the stress period, morbidity was reduced to one-third of that of the control cattle and rate of gain was improved by 43% during the initial 21 days. In previous trials, chromium was supplied after the calves had experienced significant stress and did not affect morbidity. Again, the use of chromium and long-acting oxytetracycline in combination did not have an additive effect. In addition, during days 21-35 post arrival, compensatory gain occurred in the morbid and antibiotic-treated calves. Nevetheless, these data are interpreted to suggest that chromium supplementation of stress feeder calves may reduce the need for antibiotic therapy.
The exact mechanism by which chromium enhances the immune system is not known. However, one of the consistent results of these Canadian studies was that chromium supplementation reduced serum cortisol levels. Glucocorticoids, which includes cortisol, are known to suppress the immune system. This may explain why steers receiving supplemental chromium and soybean meal had higher immunoglobin levels in the first trial.
The form of chromium supplementation may be critical to obtaining a response. For example, in the Chang and Mowat (1992) trial, the basal diet contained 12.1 ppm of chromium. It is doubtful that adding 0.4 ppm chromium in this case would give a significant response. Recent work by Anderson (1988) showed that only 0.4-3% of the inorganic trivalent chromium was absorbed. In addition, the conversion of CrCl3 to GTF chromium may be very slow or entirely lacking in some species. Consequently, dietary chromium by itself, may have little or no relationship to the amount of biologically active chromium.
However, the importance of the form of chromium may vary with specie and the trait being evaluate within a specie. For example, Page et al., (1993) compared chromium picolinate with inorganic chromium (CrCl3) in the diets of growing and finishing pigs. Feed efficiency was improved 6.4% (P<.05) by the addition of 200 ppb of chromium from CrCl3 while the same concentration of chromium from chromium picolinate had no effect on feed efficiency. In contrast, 100 and 200 ppb of chromium from chromium picolinate improved feed intake (P<.06), backfat (P<.01) and percent muscling in the carcass (P<.01), while CrCl3 had no effect.
In another trial, Page et al., (1993) compared the performance of growing-finishing pigs fed 0, 25, 50, 100, 200 ppb of chromium from chromium picolinate. Average daily gain was increased by 50 and 200 ppb of chromium, but reduced by the 100 ppb level. The reason for this inconsistent response is unknown. Serum cholesterol levels were decreased linearly (P<.01) with increasing chromium supplementation. Carcass parameters were not affected in this study.
Page et al., conducted a third study to look at higher levels of chromium supplementation. Growing-finishing pigs were fed 0, 100, 200, 400, and 800 ppb of chromium from chromium picolinate. This study suggest that excess chromium can impair performance in that feed intake and rate of gain were reduced linearly (P<.05). Serum growth hormone was increased as supplemental chromium increased from 0 to 400 ppb and decreased from 400 to 800 ppb of chromium. Carcass composition was improved (P<.01) with all levels of supplemental chromium. Chromium has been shown to affect nuclear protein and RNA synthesis. Further research is needed to clarify whether this is the mechanism by which chromium can influence carcass composition in pigs.
Lactating Holstein cows may also benefit from chromium supplementation. Burton (1993) fed 19 cows (11 multiparous and 8 primiparous) 0.5 ppm of chelated chromium for 6 weeks prior to calving. Control cows (13 multiparous and 8 primiparous) were fed the same diet without supplemental chromium. When milk production was averaged across parity, there were no significant differences. However, multiparous cows gave 13.4% more fat-corrected milk (P<.05) when fed chromium compared to the unsupplemented controls during the first 16 weeks of lactation.
In addition, lymphocytes from cows fed supplemental chromium had higher con A-stimulated blastogenic responses than from control at 2 weeks prepartum, at calving and 4 weeks postpartum. The treated cows also had consistently higher anti-OVA antibody response profiles than unsupplemented controls. Blood insulin and IGF-I concentrations did not appear to be different between treatment groups, but growth hormone concentrations tended to be lower in the chromium supplemented cows.
The reason for the effects of parity on the response to chromium are difficult to explain. However, the results are interpreted to suggest that chromium is playing a role which deserves further investigation in the lactating cow.
In summary, there is a growing body of evidence which suggest that chromium may be an essential trace element for livestock and poultry. The nutritional requirement for chromium may vary with different specie and physiological state within a specie. If additional research verifies chromium as an essential nutrient, trace mineralized salt would be the ideal delivery mechanism. However, it should be emphasized, that currently the FDA has not approved any chromium source for use in animal nutrition.
Literature Cited
Anderson, R.A. 1988. Chromium. In:K.T.Smith (Ed.) Trace minerals in Foods. p. 231. Marcel Dekker In. New York.
[Burton, J.L. 1993. Supplemental chromium - its benefit to the bovine immune system, P. 34. Proc. of the 29th Nutrition conference for Feed Manufacturers. University of Guelph, Ontario, Canada.]
Chang, X., and D.N. Mowat. 1992. Supplemental chromium for stressed and growing feeder calves. J. Anim. Sci. 70:559.
Mertz, W., and E.E. Roginski. 1963. The effect of trivalent chromium on galactose entry in rat epididymal fat tissues. J. Biol. Chem. 238:868.
Mertz, W., E.W. Toepfer, E.E. Roginski and M.M. Polansky. 1974. Present knowledge of the role of chromium. Fed. Proc. 33:2275.
Mowat, D.N., and X. Chang. 1992. Chromium and immunity of stressed feeder calves. In: Proc. of the University of Guelph Nutrition Conf. April 28, 1992.
Offenbacher, E.G. and G.X. Pi-Sunyer. 1988. Chromium in human nutrition. Ann. RE. Nutr. 8:543.
Page, T.G., L.L. Southern, T.L. Ward, and D.L. Thompson, Jr., 1993. Effect of chromium picolinate on growth and serum and carcass traits of growing-finishing pigs. J. Anim. Sci. 71:656.
Rosebrough, R.W., and N.C. Steele. 1981. Effect of supplemental chromium or nicotinic acid on carbohydrate metabolism during basal, starvation, and refeeding periods in poults. Poultry. Sci. 60:407.
Schrauzer, G.N., K.P. Shrestha, T.B. Molenaar, and S. Mead. 1986. Effects of chromium supplementation on food energy utilization and the trace element composition in the liver and heart of glucose-exposed young mice. Biol. Trace. Elem. Res. 9:79.
Schwarz, K. and W. Mertz. 1959. Chromium (III) and the glucose tolerance factor. Arch. Biochem. Biophys. 85:292.
© Salt Institute, 1993
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