The role of trace minerals in immunity and lipid metabolism in cattle

race minerals exist in cells and tissues of the animal body in a variety of functional and chemical combinations and in characteristic concentrations that vary with the mineral and tissue (McDowell, 1992; Underwood and Suttle, 1999). The concentrations of trace minerals must usually be maintained within quite narrow limits if the functional and structural integrity of the tissue is to be maintained and the growth, health and productivity of the animal are to remain unimpaired (McDowell, 1992; Underwood and Suttle, 1999).

Ingestion of diets that are deficient, imbalanced or excessively high in trace minerals induces changes in the form or concentration of that trace mineral in the body tissues and fluids such that it falls below, or rises above, the tolerable limits. In such cases, biochemical lesions develop, physiological functions are adversely affected and structural disorders may arise in ways that vary with the mineral, the degree and duration of the dietary deficiency or toxicity, and the age, sex, or species of animal involved (McDowell, 1992; Underwood and Suttle, 1999).

Certain homeostatic mechanisms in the body can be activated which delay or minimize the onset of such diet-induced changes. Ultimate prevention of the changes requires that the animal be supplied with a diet that is palatable and non-toxic and which contains the required minerals, as well as other nutrients, in adequate amounts, proper proportions and available forms (Underwood, 1971; Combs, 1998; Underwood and Suttle, 1999).

Mineral deficiencies, toxicities, and imbalances require the animal to metabolically compensate for the nutrient deviation. In doing so, certain metabolic diseases can manifest and energy metabolism and immune function can be depressed, thus decreasing overall animal performance and health.

The intent of the first part of this review is to discuss the function of trace minerals in health and immunity. The second portion of this review is focused on the role of copper in lipid metabolism in cattle.

The immune system

The immune system is a remarkably adaptive defense system that has evolved in vertebrates to protect them from invading pathogenic microorganisms. It is able to generate an enormous variety of cells and molecules capable of specifically recognizing and eliminating an apparently limitless variety of foreign invaders. These cells and molecules act together in an adaptable dynamic network to protect the host (Kuby, 1994).

Immunity is the ability to resist infection. Immunity can be classified into nonspecific and specific components. Innate or nonspecific immunity refers to the basic resistance to disease that a species or individual possesses.

Innate immunity can be described as comprising four types of defensive barriers: 1) anatomic (skin), 2) physiologic (temperature, pH, oxygen tension), 3) phagocytic (ingestion of macromolecules by macrophages and neutrophils), and 4) inflammatory (vasodilatation and capillary permeability; Kuby, 1994). Acquired or specific immunity is immunity induced by exposure to an antigen either naturally or via vaccination (Kuby, 1994). Acquired or specific immunity can be further divided into two subcategories: humoral and cell-mediated immunity. The humoral branch of the immune system involves the interaction of B cells with extracellular antigen and their subsequent proliferation and differentiation into antibody-secreting cells that are specific for a certain antigen. Antibodies secreted by B cells function as the effector of the humoral immune response by binding to an extracellular antigen and neutralizing and/or facilitating its elimination. Cell-mediated immunity involves the interaction of T cells and their associated cytokines to eliminate intracellular pathogens (Galyean et al., 1999).

Functionally, an immune response can be divided into two interrelated activities; recognition and response. The immune system is able to recognize subtle chemical differences that distinguish one foreign pathogen from another (Kuby, 1994). At the same time, the system is able to discriminate between foreign molecules and the body’s own cells and proteins. Once a foreign protein is recognized, the immune system enlists the participation of a variety of cells and molecules to mount an appropriate response known as the effector response, which is uniquely suited to eliminate a specific type of pathogen (Kuby, 1994). Later exposure to the same foreign organism induces a memory response, characterized by a heightened immune response that serves to eliminate the pathogen and prevent disease. Overall, the basic function of the immune system in eukaroytes is to distinguish self from nonself and thus prevent disease.


Trace minerals

Trace minerals function primarily as catalysts in enzyme systems within cells. The roles that trace minerals play in enzymatic reactions range from weak, ionic strength effects to highly specific associations known as metalloenzymes (Underwood, 1971). Deficiencies and or imbalances of trace minerals can alter the activities of certain enzymes and functions of specific organs thus impairing specific metabolic pathways as well as overall immune response. For an in-depth review of the effects of micronutrients on immunity see Galyean et al. (1999) and Spears (2000).


ZINC

Zinc is an essential component of numerous enzymes and is part of the structure of many proteins. Zinc-containing enzymes are found in all major metabolic pathways involved in carbohydrate, lipid, protein and nucleic acid metabolism, epithelial tissue integrity, cell repair and division, and vitamin A transport and utilization (Kaneko, 1989).

Numerous experiments with humans and laboratory animals have indicated that zinc deficiency reduces immune response and disease resistance (Chesters, 1997). However, there is little research in ruminants examining the influence of zinc deficiency on immune function and disease resistance.

Lambs fed a semi-purified diet severely deficient in zinc showed a reduced blastogenic response to PHA (a T-cell mitogen), but an increased response to PWM, a T-dependent B-cell mitogen (Droke and Spears, 1993). Zinc deficient lambs also had a lower percentage of lymphocytes and a higher percentage of neutrophils in blood. Inflammatory response to PHA was also similar in zinc-adequate and zinc-deficient lambs. Furthermore, zincdeficient cattle showed similar cell-mediated and humoral immune responses as zinc adequate cattle (Spears and Kegley, unpublished data). However, Engle et al. (1997) reported a greater skin swelling response in zinc-adequate calves when compared to marginally zinc-deficient calves.

Although the data are both limited and variable on the effects of marginal zinc deficiency on immune function, Galyean et al. (1995) reported that increasing the level of supplemental zinc from 30 to 100 mg/kg diet tended to reduce morbidity from respiratory diseases in newly weaned stressed (by transport) calves.


COPPER

Animals require copper for a number of enzymes (cytochrome oxidase, lysyl oxidase, superoxide dismutase, dopamine-ß-hydroxylase, tyrosinase and ceruloplasmin) that are involved in an array of important body functions such as cellular respiration, bone formation, proper cardiac function, tissue development, myelination of the spinal cord, keratinization, tissue pigmentation and lipid metabolism. Understanding how copper functions in the aforementioned enzymes can help to explain the clinical signs observed during a copper deficiency.

Prohaska and Failla (1993) have conducted several studies in rats and mice that indicate that both cell mediated and humoral immunity are greatly depressed by copper deficiency. However, studies in domestic livestock have failed to show consistent effects of copper deficiency on either cellmediated or humoral immune response.

Severe copper deficiency induced by feeding a semi-purified diet low in copper did not affect in vitro mitogen-induced lymphocyte blastogenesis (Stabel et al., 1993; Ward et al., 1997). Furthermore, the addition of 5 mg Mo/kg to the semi-purified diet to produce a more severe copper deficiency did not reduce lymphocyte blastogenic response to PHA or PWM (Ward et al. 1997). However, in a recent study by Wright et al. (2000) low copper status was associated with a reduced response of peripheral-blood lymphocytes to stimulation with T cell-mitogens following weaning and IBRV challenge.

From the more basic molecular immune research it is clear that copper plays an important role in the immune response. The variable responses of copper supplementation on immune responses in research with domesticated livestock species may lie in the numerous factors that affect an animal’s response to copper supplementation. These include duration and concentration of copper supplementation, the absence or presence of dietary copper antagonists (sulfur, iron and molybdenum), environmental factors and breed differences in copper metabolism. Future research is warranted to determine the effects of copper and copper antagonists on immune response and disease resistance in domesticated livestock species.


SELENIUM

Selenium was first identified in the 1930s as a toxic element to some plants and animals. However, selenium is now known to be required by laboratory animals, food animals and humans (McDowell, 1992). Selenium is necessary for growth and fertility in animals and for the prevention of a variety of disease conditions. In 1973, Rotruck et al. reported that selenium functions as a component of glutathione peroxidase, an enzyme that inactivates oxygen radicals such as hydrogen peroxide and prevents them from causing cellular damage.

Since the discovery by Rotruck et al. (1973) selenium has been shown to affect specific components of the immune system (Mulhern et al., 1985).

Earlier research by Reffett et al. (1988) reported lower serum IgM (an antibody produced by B cells) concentrations and anti-IBRV titers in selenium-deficient calves challenged with infectious bovine rhinotracheitis virus (IBRV) compared to selenium-adequate calves. Polymorphonuclear leukocyte function was reduced in goats (Aziz et al., 1984) and cattle (Gyang et al., 1984) fed selenium-deficient diets compared with controls receiving selenium-adequate diets. Some studies have shown increased T-lymphocyte blastogenesis following in vitro stimulation with mitogen, but others have not (Spears, 2000). Recently, bovine mammary endothelial cells growing in selenium-deficient cell culture media were found to exhibit enhanced neutrophil adherence when stimulated with cytokines (Maddox et al., 1999; Spears, 2000). These findings may indicate that selenium could affect neutrophil migration into tissues and subsequent inflammation.


CHROMIUM

Chromium (Cr) was first shown to be essential for mammals by Schwarz and Mertz (1959). Since then, trivalent chromium has been shown to influence carbohydrate metabolism (Mertz, 1993), lipid metabolism (Abraham et al., 1991), and protein absorption and metabolism (Okada et al., 1983: Kornegay et al., 1997).

Highly variable responses to chromium supplementation have made it difficult to determine the specific effect of chromium on the immune system (Spears, 2000). Burton et al. (1994) reported that in newly weaned stressed feedlot calves, chromium supplementation at 0.5 mg Cr/kg diet for 30 days post-transit to the feedlot increased the magnitude of peak antibody titer response to IBR vaccination but had no effect on antibody titers to IP-3 vaccination. Dairy cows supplemented with 0.5 mg Cr/kg diet had greater primary and secondary antibody responses to immunization of an ovalbumin antigen than control cows, but had similar antibody responses to human erythrocyte antigen immunization (Burton et al., 1993). It is unclear why the chromium response was observed with one antigen and not the other.

Furthermore, the addition of 0.4 mg Cr/kg diet did not affect antibody titer responses to porcine erythrocyte immunization in stressed cattle (Kegley et al., 1997). Inconsistent immune responses to chromium supplementation have also been observed in swine (van Heugten and Spears, 1997) and sheep (Gentry et al., 1999).

The reason for the variable responses to chromium supplementation on immune responses in domestic livestock species is unclear. Factors that may contribute to the inconsistent findings among studies may include: 1) the initial chromium status of the animals; 2) the amount of available chromium in the basal diet; 3) the form of chromium supplemented; and 4) the type or degree of stress imposed on the animals (Spears, 2000).


SUMMARY: TRACE MINERALS AND IMMUNITY

The interactions between trace mineral status, immunology and disease resistance are extremely complex. From basic research it is clear that micronutrients have an important role in immune response. Despite the apparent involvement of certain trace minerals in the immune system, deficiencies of trace minerals have not always increased the susceptibility of domestic animals to natural or experimentally-induced infections (Spears, 2000). There are many factors that could affect an animal’s response to trace mineral supplementation such as the duration and concentration of trace mineral supplementation, the absence or presence of dietary antagonists, environmental factors and breed differences in trace mineral metabolism. Future research is warranted to determine the effects of trace mineral supplementation on immune response and disease resistance in domesticated livestock species.


Copper and lipid metabolism in cattle

RUMINANT AND NONRUMINANT FATTY ACID METABOLISM DIFFER

In contrast to nonruminants, ruminant diets are typically low (2-5%) in fat (Bauman, 1976). The extensive hydrogenation of unsaturated fatty acids by rumen microorganisms results in primarily saturated fatty acids being absorbed from the small intestine and incorporated into adipose tissue regardless of the diet (Dawson and Kemp, 1970). Therefore, the fatty acid composition of adipose tissue in ruminant animals is generally not affected by the fatty acid composition of the diet (Bauman, 1976). Microbes that pass out of the rumen are digested in the abomasum and their fatty acids are released. Microbial fatty acids synthesized de novo consist mainly of 16:0 and 18:0 with small amounts of mono- and polyunsaturated fatty acids present (Hartfoot, 1978). However, ruminant adipose tissue does contain unsaturated fatty acids. The unsaturated fatty acids in adipose tissue are primarily produced by an active desaturase enzyme that can desaturate both stearate and fatty acids arising from de novo synthesis (Pothoven et al., 1974). Payne and Masters (1971) reported higher desaturase activity in sheep adipose tissue than in rat adipose tissue and suggested that this was an adaptation to the greater percentage of saturated fatty acids absorbed by ruminants.

There are marked species differences in the tissues principally responsible for lipogenesis (O’Hea and Leveille, 1969). Adipose tissue is the predominant site of excess energy conversion to fatty acids in ruminants whereas liver and adipose tissue can synthesize fatty acids in rats (Ingle et al., 1973).

The primary carbon source for fatty acid synthesis in nonruminants is glucose derived from dietary carbohydrates. In ruminants the carbon source is primarily acetate (Ingle et al., 1973). Incubations with mesenteric adipose, liver and mammary tissue have indicated that these tissues from mature ruminants have a limited ability to incorporate glucose into fatty acids with acetate being the predominant carbon source for lipogenesis (Hanson and Ballard, 1967). The reason for the difference in fatty acid carbon source between ruminants and nonruminants is because little dietary carbohydrate leaves the rumen due to microbial degradation, and activities of ATP citratelyase and NADP-malate dehydrogenase in adipose tissue in ruminants are relatively low (Ingle et al., 1972).

The source of reducing equivalents to support fatty acid synthesis in ruminant animals also differs from that of nonruminants. In ruminant adipose tissue, it has been estimated that approximately 75-85% of NADPH is generated by the pentose phosphate cycle. High concentrations of cytosolic NADP-isocitrate dehydrogenase in ruminant adipose tissue produce approximately 15-25 % of the reducing equivalents needed for fatty acid synthesis (Yang and Baldwin, 1973).


ROLE OF COPPER

Dietary copper (Cu), when fed at physiological concentrations, has been shown to alter lipid metabolism in rats (Klevay, 1973; Petering et al., 1977).

Moreover, feeding pharmacological concentrations of copper (250 mg Cu/ kg DM) decreased plasma and breast muscle cholesterol concentrations in poultry (Pesti and Bakalli, 1996) and increased unsaturated and decreased saturated fatty acids in backfat of finishing pigs (Amer and Elliot, 1973a,b).

Limited research suggests that dietary copper at physiological concentrations may affect lipid metabolism in ruminants. Copper supplementation (from copper oxide needles) to copper-deficient sheep led to increased adipose cell volume and increased in vitro lipolytic rates in adipose tissue (Sinnett-Smith and Woolliams, 1987). Ward and Spears (1997) first reported that supplemental copper reduced backfat in steers. In this experiment, Angus steers were fed diets with or without supplemental copper for a total of 274 days. Copper was supplemented at 7.5 ppm during a 29- day receiving phase and at 5.0 ppm during the growing and finishing phases.

Half the steers in each copper treatment were also supplemented with 5 ppm of molybdenum, a copper antagonist. Copper supplementation decreased backfat, regardless of whether molybdenum was supplemented, and tended to increase longissimus muscle area. Liver copper concentrations in biopsy samples obtained toward the end of the study were much higher in coppersupplemented steers; and molybdenum addition to the diet reduced liver copper as expected. Plasma copper concentrations were reduced only in steers supplemented with molybdenum and not receiving supplemental copper.

A more recent series of studies (Engle et al., 2000a,b; Engle and Spears, 2000) have confirmed that dietary copper affects backfat and have examined in more detail the effects of dietary copper on lipid and cholesterol metabolism in feedlot cattle. In the first experiment, Angus and Angus x Hereford steers were fed a corn silage-based diet for 56 days followed by a high concentrate finishing diet for 101 or 121 days. Copper was supplemented as copper sulfate to provide 0, 20 or 40 ppm Cu. In addition, a number of other copper sources (citrate, proteinate and tribasic copper chloride) were evaluated when supplemented at 20 ppm Cu. Copper supplementation reduced backfat without affecting marbling. Increasing the level of supplemental copper from 20 to 40 ppm did not further reduce backfat. The copper sources did not differ in their ability to alter backfat. Cholesterol content of longissimus muscle tended (P<0.11) to be reduced by supplemental copper. Serum cholesterol concentrations were lower in copper-supplemented steers by day 84 of the finishing phase. The fatty acid composition of longissimus muscle was also affected by copper with polyunsaturated fatty acids (linoleic and linolenic acid) being higher in coppersupplemented steers. The ratio of unsaturated to saturated fatty acids tended (P<0.11) to be higher in copper-supplemented steers. Liver and plasma copper concentrations were lower in control steers at the end of the study; however, liver and plasma copper concentrations in control steers were above concentrations considered indicative of copper deficiency.

In a second experiment, copper was supplemented from copper sulfate at 0, 10 or 20 ppm only during the finishing phase (Engle and Spears, 2000).

This study indicated that 10 ppm supplemental copper was sufficient to reduce backfat and alter muscle fatty acid profile. Similar to the earlier study, the reduction in backfat occurred without a decrease in marbling.

The ratio of unsaturated:saturated fatty acids in longissimus muscle and the proportion of total fatty acids as polyunsaturated fatty acids were higher in steers supplemented with copper. The increase in muscle polyunsaturated fatty acids in steers supplemented with copper may relate to copper affecting ruminal biohydrogenation of dietary unsaturated fatty acids or the fatty acyl desaturase system. The reduced backfat in copper supplemented steers may result from copper altering catecholamine metabolism (Engle et al., 2000b).


COPPER AND CHOLESTEROL METABOLISM

A potential mechanism for the observed reduction in serum and tissue cholesterol concentrations in copper-supplemented animals may be due in part to elevated liver copper concentrations. Kim et al. (1992) have shown that copper deficiency in rats causes hypercholesterolemia by increasing hepatic reduced glutathione (GSH) concentrations, which increases the activity of 3-hydroxy-3-methyl-glutaryl coenzyme A (HMG-CoA) reductase, the rate limiting enzyme in cholesterol synthesis. High concentrations of liver Cu may regulate cholesterol biosynthesis indirectly by decreasing the reduced form of glutathione (GSH) and increasing the oxidized form of glutathione (GSSG) (Kim et al., 1992; Bakalli et al., 1995). The decrease in cellular GSH may protect hepatic cells from the harmful free radical-forming toxic effects of high copper. As copper enters the liver cells, it is rapidly complexed by GSH and then transferred to metallothionein, the form in which it is stored (Freedman et al., 1989). Increasing cellular GSSG concentrations has been shown to decrease the activity of HMG-CoA reductase (Gilbert and Stewart, 1981; Roitelman and Schechter, 1984; Ziegler, 1985; Gilbert, 1990). With a decrease in HMG-CoA reductase activity, carbon flux through the mevalonate pathway would be reduced, thus decreasing cholesterol synthesis.

In most mammals, the primary site of endogenous cholesterol synthesis is the liver (Siperstein, 1970). However, in ruminants the primary site of cholesterol synthesis is the small intestine and adipose tissue, with the liver producing a small proportion of the total endogenous cholesterol (Liepa et al., 1978). The absorption of copper from the intestinal lumen into the enterocyte is thought to require similar mechanisms as described for hepatocytes. Therefore, it is hypothesized that supplemental copper may reduce cholesterol synthesis in both the liver and intestine (via similar mechanisms) resulting in an overall reduction in serum cholesterol in ruminants (Engle et al., 2000a).


COPPER AND UNSATURATED FATTY ACIDS

A potential mechanism for the observed increase in unsaturated fatty acids in longissimus muscle of copper-supplemented steers may be due to an increase in the activity of the fatty acyl desaturase system as indicated previously. Feeding pharmacological concentrations of copper increased estimated desaturase activity in pigs (Thompson et al., 1973). Ho and Elliot (1974) reported that pigs supplemented with 250 mg Cu/kg DM from copper sulfate had decreased proportions of stearic and palmitic acids with concomitant increases in the medium chain myristic acid as well as those of the major long-chain fatty acids in the depot fat. Increases in the capacities of hepatic and adipose microsomes to desaturate 1-14C-oleate and 1-14Cpalmitoyl- CoA relative to the controls (adequate in copper) were also observed. This suggests that supplemental dietary copper enhances the specific activities of the fatty acyl desaturase system, and that this enhancement contributes to the observed changes in fatty acid composition of the depot fat. In calves fed 1000 mg Cu/liter of milk replacer, apparent delta-9-desaturase enzyme activity in calf liver and heart was greater than in control calves fed 10 mg Cu/L of milk replacer (Jenkins and Kramer, 1989). Findings by Jenkins and Kramer (1989) are consistent with reports of high dietary copper promoting delta-9-desaturase activity in rat and swine liver (Cunnane, 1982).

Another possible mechanism for the increased unsaturated fatty acid composition in longissimus muscle of copper-supplemented cattle may be due to effects on ruminal biohydrogenation of unsaturated fatty acids.

Biohydrogenation of C18:2 initiates with the isomerization of the cis-9, cis- 12 molecule into cis-9 trans-11 C18:2 (a conjugated linoleic acid) as the first intermediate (Kepler et al., 1966). The subsequent step is a reduction of the cis-9 double bond, resulting in trans C18:1 (n-7) as the second intermediate. This step involves a reductase using electron donors. The final step is another reduction, resulting in C18:0. Copper may inhibit biohydrogenation of C18:2 by interfering with the formation of an electronegative center involved in the hydrogen transfer in the isomerization of C18:2 (Kepler et al., 1971).

A recent study (Engle and Spears, 2000) suggested that dietary copper may affect microbial biohydrogenation of fatty acids in the rumen. Adding 20 or 40 ppm Cu to growing and finishing cattle diets increased polyunsaturated fatty acid proportions of total fat in longissimus muscle.

The C18:1 trans isomer, an intermediate of biohydrogenation (Kepler et al., 1966; Christie, 1981), was reduced in longissimus muscle of supplemented steers, suggesting an effect of copper on biohydrogenation. Further research is needed to determine the effect of copper levels on ruminal biohydrogenation of unsaturated fatty acids.


COPPER AND CATECHOLAMINE SYNTHESIS

Catecholamines are derived from tyrosine (Figure 1, Gilman, 1980). Research investigating the role of copper in catecholamine synthesis has primarily compared copper-deficient animals to copper-adequate controls. An early in vivo study showed that the conversion of dopamine to norepinephrine was impaired in copper-deficient rats (Missala et al., 1967). Later research indicated that copper deficiency decreases the concentrations of norepinephrine in the brains of rats (Prohaska and Wells, 1974) and sheep (O’Dell et al., 1976). These findings suggest that the dopamine ßhydroxylase- catalyzed conversion of dopamine to norepinephrine is the ratelimiting step in copper deficiency.




Figure 1. Formation of catecholamines from tyrosine (Gilman, 1980).


Dopamine ß-hydroxylase (DBH) is a tetrameric glycoprotein that contains eight copper atoms when fully saturated (Ash et al., 1984). Copper deficient cattle fed a semi-purified diet deficient in copper (1.32 ppm Cu) for 355 days had lower norepinephrine concentrations in adrenal tissue homogenates and tended to have lower DBH enzyme activity relative to controls (Hesketh, 1981). Prohaska et al. (1990) observed a 60% decrease in mice and rat plasma and heart norepinephrine concentrations with a concurrent increase (approximately 5-fold) in dopamine concentrations relative to the controls.

These findings are consistent with the concept that copper deficiency depresses DBH activity. However, copper-deficient mice and rats excreted twice as much dopamine and norepinephrine in the urine as the controls.

Furthermore, Gross and Prohaska (1990) observed that urinary output of norepinephrine and dopamine were higher in mice during copper deficiency, whereas output of creatinine and epinephrine were unchanged. Calculated turnover rates of norepinephrine were higher in heart tissue of deficient mice than those from copper-adequate mice. They suggested that the smaller norepinephrine pool observed in the organs of copper-deficient mice may have resulted from lower synthesis due to limiting DBH activity and to higher turnover.

Research investigating the effects of copper supplementation above animal requirements on catecholamine synthesis is limited. Lin et al. (1995) reported that copper supplementation of genetically obese mice at 50 ppm increased dopamine, norepinephrine and epinephrine concentrations by 14, 50 and 31%, respectively in the plasma relative to mice receiving 4 ppm Cu (Lin et al., 1995). Furthermore, copper supplementation of genetically lean control mice tended to increase plasma dopamine, norepinephrine and epinephrine concentrations by 3, 14, and 9%, respectively, relative to the nonsupplemented lean mice. This is the first evidence indicating that copper supplementation above requirements may increase circulating levels of catecholamines. In a recent study, copper supplementation of feedlot steers reduced backfat depth and tended (P<0.14) to increase circulating concentrations of norepinephrine relative to unsupplemented controls (Engle et al., 2000b). The slight increase in circulating catecholamine concentrations may have increased lipolysis of adipose tissue (stored as backfat); ultimately decreasing backfat depth in supplemented steers.


Summary

Studies in broilers and laying hens indicate that supplementing copper in excess of nutritional requirements substantially reduces the cholesterol content of breast muscle and eggs. In finishing cattle, adding copper at concentrations at or slightly above requirements has reduced backfat and increased the polyunsaturated fatty acid content of muscle. Decreasing cholesterol and increasing polyunsaturated fatty acids in animal products produced for human consumption has potential human health benefits. The reduction in backfat seen in cattle would decrease the amount of trim required at processing and ultimately reduce wastage. In addition, reduced backfat could slightly reduce the fat content of edible beef tissues.

by Terry E. Engle - Animal Sciences Dept. of Colorado State University