J. Anim. Sci. 2005. 83:2762-2774
© 2005 American Society of Animal Science
Effects of dietary zinc and iron supplementation on mineral excretion, body composition, and mineral status of nursery pigs1,2
M. J. Rincker,
G. M. Hill3,
J. E. Link,
A. M. Meyer and
J. E. Rowntree4
Department of Animal Science, Michigan State University, East Lansing 48824
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Abstract
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Two experiments were conducted to evaluate the effects of dietary Zn and Fe supplementation on mineral excretion, body composition, and mineral status of nursery pigs. In Exp. 1 (n = 24; 6.5 kg; 16 to 20 d of age) and 2 (n = 24; 7.2 kg; 19 to 21 d of age), littermate crossbred barrows were weaned and allotted randomly by BW, within litter, to dietary treatments and housed individually in stainless steel pens. In Exp. 1, Phases 1 (d 0 to 7) and 2 (d 7 to 14) diets (as-fed basis) were: 1) NC (negative control, no added Zn source); 2) ZnO (NC + 2,000 mg/kg as Zn oxide); and 3) ZnM (NC + 2,000 mg/kg as Zn Met). In Exp. 2, diets for each phase (Phase 1 = d 0 to 7; Phase 2 = d 7 to 21; Phase 3 = d 21 to 35) were the basal diet supplemented with 0, 25, 50, 100, and 150 mg/kg Fe (as-fed basis) as ferrous sulfate. Orts, feces, and urine were collected daily in Exp. 1; whereas pigs had a 4-d adjustment period followed by a 3-d total collection period (Period 1 = d 5 to 7; Period 2 = d 12 to 14; Period 3 = d 26 to 28) during each phase in Exp. 2. Blood samples were obtained from pigs on d 0, 7, and 14 in Exp. 1 and d 0, 7, 21, and 35 in Exp. 2 to determine hemoglobin (Hb), hematocrit (Hct), and plasma Cu, (PCu), Fe (PFe), and Zn (PZn). Pigs in Exp. 1 were killed at d 14 (mean BW = 8.7 kg) to determine whole-body, liver, and kidney mineral concentrations. There were no differences in growth performance in Exp. 1 or 2. In Exp. 1, pigs fed ZnO or ZnM diets had greater (P < 0.001) dietary Zn intake during the 14-d study and greater fecal Zn excretion during Phase 2 compared with pigs fed the NC diet. Pigs fed 2,000 mg/kg, regardless of Zn source, had greater (P < 0.010) PZn on d 7 and 14 than pigs fed the NC diet. Whole-body Zn, liver Fe and Zn, and kidney Cu concentrations were greater (P < 0.010), whereas kidney Fe and Zn concentrations were less (P < 0.010) in pigs fed pharmacological Zn diets than pigs fed the NC diet. In Exp. 2, dietary Fe supplementation tended to increase (linear, P = 0.075) dietary DMI, resulting in a linear increase (P < 0.050) in dietary Fe, Cu, Mg, Mn, P, and Zn intake. Subsequently, a linear increase (P < 0.010) in fecal Fe and Zn excretion was observed. Increasing dietary Fe resulted in a linear increase in Hb, Hct, and PFe on d 21 (P < 0.050) and 35 (P < 0.010). Results suggest that dietary Zn or Fe additions increase mineral status of nursery pigs. Once tissue mineral stores are loaded, dietary minerals in excess of the body’s requirement are excreted.
Key Words: Iron • Nursery Pig • Nutrient Balance • Whole Body • Zinc
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Introduction
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Nutrient management plans focus primarily on P and N with little regard to other nutrients; yet, the accumulation of Zn in soil can hinder crop production (Takkar and Mann, 1978
). Swine manure volume and its nutrient content have been estimated based on standard values reported by ASAE (1988); however, current values representing today’s genetics and management practices are needed by producers to accurately estimate the swine manure volume and its nutrient content.
The addition of 2,000 to 3,000 mg of Zn/kg of diet as Zn oxide to nursery pig diets is a common practice in the swine industry because of the reported improvements in growth performance (Smith et al., 1997; Hill et al., 2000). However, feeding pharmacological Zn to nursery pigs can result in a significant increase in the total quantity of Zn excreted during a pig’s entire production cycle (Meyer et al., 2002). This is a particular concern in today’s swine industry, where intensive production units have increased the volume of manure produced in facilities that may have limited access to land for application.
The analyzed Fe concentration of most nursery diets is in excess of the NRC (1998) postweaning dietary Fe requirement, 80 mg/kg, which occurs because many feed ingredients have a high Fe concentration, including dicalcium phosphate, limestone, and blood meal. Nonetheless, the availability of Fe from different sources varies greatly (Deming and Czarnecki-Maulden, 1989). Similar to Zn, environmental concerns exist because of the high dietary Fe concentrations and variability in the Fe availability of feedstuffs.
The objectives of this research were to determine the effects of dietary Zn and Fe supplementation on mineral excretion, nutrient balance, and mineral status of nursery pigs. Experiment 1 compared an organic (Zn Met) vs. inorganic (Zn oxide) Zn form immediately (14 d) after weaning, whereas Exp. 2 evaluated increasing concentrations of supplemental dietary Fe as ferrous sulfate.
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Materials and Methods
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Animal Use and Care
These experiments were conducted at the Michigan State University Swine Teaching and Research Facility. Use of animals in these experiments was approved by the All-University Committee on Animal Use and Care (Exp. 1: 12/99-159-00; Exp. 2: 12/02-164-00).
Experiment 1
Animals and Treatments.
Eight sets of three littermate barrows (Duroc x Landrace–Yorkshire) were weaned at 16 to 20 d and individually housed in metabolism pens during a 14-d feeding experiment. Pigs were allotted randomly, within litter, on the basis of initial BW (mean = 6.5 kg) to one of three dietary treatments in a randomized complete block design. There were eight pigs per treatment.
Dietary treatments (Table 1; as-fed basis) consisted of: 1) NC (negative control, no added Zn source); 2) ZnO (NC + 2,000 mg of Zn/kg of diet as Zn oxide); and 3) ZnM (NC + 2,000 mg of Zn/kg of diet as Zn Met). Complexity of the diets changed with phases (Phase 1 = d 0 to 7; Phase 2 = d 7 to 14) to meet or exceed NRC (1998) nutrient recommendations, excluding Zn, and to satisfy changes in digestive capabilities of the weanling pig. Experimental Zn concentrations were obtained by replacing an appropriate amount of corn, soybean meal, dicalcium phosphate, and limestone with the respective Zn source. Additionally, dietary ingredients were adjusted to maintain equal Lys, Ca, and P concentrations. The Zn oxide source used was a feed-grade source. To equalize the Met concentration in the diets, supplemental Met was decreased in the ZnM diet by the amount calculated to be present in the Zn Met source. Diets were fed in meal form.
Housing and Fecal, Urine, and Orts Collection.
Pigs were housed in metabolism pens located in a temperature-controlled room. Initial room temperature was maintained at 29°C and decreased by 1°C weekly. Each metabolism pen was constructed of stainless steel, provided 0.81 m2 of total space, and contained a stainless steel feeder and nipple waterer that allowed for access to feed and water throughout the experiment. Pigs were fed to appetite twice daily. Although water samples were not collected in this experiment, we have collected water samples for previous experiments and analyzed them for mineral concentrations, and they were minimal or undetectable. Additionally, each pen was designed to allow for the total but separate collection of urine, feces, and orts. Fecal material was collected daily during the 14-d experiment by removing a screen (1-mm openings) located directly beneath the entire floor space of the pen. Fecal samples were collected, placed in plastic bags, and stored at –20°C until analysis. Below the fecal collection screen was a stainless-steel pan that was angled toward a 10-mm hole on one end. A 3.8-L capacity polypropylene container was located at the end of the pan to collect all urine at the same time fecal samples were collected. Total urine volume was recorded daily, and a 50-mL subsample was retained in a polypropylene tube and stored at –20°C until analysis. Orts were collected daily at the same time as urine and fecal samples, oven-dried (Fisher Isotemp, Fisher Scientific, Hampton, NH), and used in the determination of ADFI.
Performance, Blood, Tissue, and Whole-Body Collection.
Pigs were weighed and bled on d 0, 7, and 14. Pig weights were used to calculate ADG. Blood samples were drawn by jugular venipuncture into 10-mL heparinized (143 USP units of sodium heparin per tube) Vacutainer (Becton Dickinson, Franklin Lakes, NJ) tubes with 21-gauge, 3.81-cm needles and then centrifuged at 2,000 x g for 10 min at 4°C (GS-6KR; Beckman, Palo Alto, CA). Plasma was collected into polypropylene tubes and stored at –80°C until minerals were analyzed.
At the conclusion of the experiment, pigs (mean BW = 8.7 kg; 32 ± 2 d of age) were fasted for 8 h and then killed via cardiac injection of sodium pentobarbital (87 mg/kg of BW). Liver and kidney samples were excised and stored in Whirl-Pak bags (Nasco, Fort Atkinson, WI) at –80°C until mineral analysis. The remaining whole-body of each pig was processed as previously described by Rincker et al. (2004). Additionally, six pigs from the original contemporary group (mean BW = 6.1 kg; 18 ± 2 d) were killed before the initiation of the balance study. Whole-body samples were collected in a similar manner to that previously described to establish baseline (BL) measurements of mineral concentrations.
Experiment 2
Animals and Treatments.
Four sets of six littermate barrows (n = 24; Duroc x Landrace–Yorkshire), with an initial mean BW of 7.2 kg, were weaned at 19 to 21 d for this 35-d feeding experiment. Five barrows from each litter were allotted randomly, within litter, based on initial BW to one of five dietary treatments. To formulate a diet similar to those used in the commercial industry yet minimize Fe contributions by ingredients, we analyzed potential feedstuffs for minerals of interest (Table 2). To limit the Fe concentration in the basal diets, the base mineral mix used in this experiment contained minimal Fe (729 mg/kg, as-fed basis) compared with typical commercial base mineral mixes that contain 15,000 to 20,000 mg of Fe/kg. Dietary treatments were obtained by supplementing the basal diets (Table 3) with 0, 25, 50, 100, or 150 mg of Fe/kg of diet as ferrous sulfate monohydrate (FeSO4·H2O). The remaining barrow from each litter was allotted to the basal diet supplemented with 0 mg of Fe/kg of diet. Eight pigs were fed the basal diet, and four pigs per treatment were fed the basal diet supplemented with 25, 50, 100, or 150 mg of Fe/kg of diet.
Complexity of the diet changed by phase to meet or exceed NRC (1998) nutrient recommendations, excluding Fe. Phase 1 (d 0 to 7) and Phase 2 (d 7 to 21) diets were fed in pelleted form, whereas Phase 3 (d 21 to 35) diets were fed in meal form.
Housing and Fecal, Urine, and Orts Collection.
Pigs were housed in the same metabolism pens used in Exp. 1. Pigs were fed their assigned diets and given a 4-d adjustment period followed by a 3-d collection period in which urine, feces, and orts were collected (Period 1 = d 5 to 7; Period 2 = d 12 to 14; Period 3 = d 26 to 28). During each dietary collection period, feces and urine samples were collected daily, processed, and stored as described in Exp. 1. Because Phase 1 and 2 diets were fed in pelleted form, a marker was not used to signify the beginning and end of the collection period. Instead, the collection period began at 0600 and a daily collection was 24 h in length.
Before analysis, daily fecal samples collected in each dietary period (3 d) were combined, mixed, and a composite sample was obtained for each period. A composite urine sample for each pig was obtained by thawing and mixing the daily 50-mL subsamples for each period. A percentage of each daily subsample corresponding to that sample’s percentage of the total urine output for that period was used to obtain the composite sample for each period.
Performance, Blood, and Tissue Collection.
Pigs were weighed at the end of each dietary phase to calculate ADG. Additionally, pigs were bled on d 0, 7, 21, and 35 via jugular venipuncture as described in Exp. 1. An aliquot of whole blood was transferred into a polypropylene tube and stored on ice for hemoglobin (Hb) and hematocrit (Hct) determinations. The remaining whole blood was processed as described in Exp. 1 to collect plasma for mineral analyses.
Laboratory Analyses
In Exp. 1, daily fecal and urine samples were analyzed individually, whereas composite fecal and urine samples for each dietary period were analyzed in Exp. 2. Fecal samples were oven-dried and then ground in a Cyclotec mill (1093 Sample Mill, Foss, Eden Prairie, MN) equipped with a 1-mm screen. Urine samples were prepared for mineral analysis by centrifugation (500 x g at 4°C for 10 min), and the supernatant fraction was transferred to a clean polypropylene tube. Feed, fecal, urine, liver, kidney, and whole-body samples were analyzed for minerals (Ca, Cu, Fe, Mg, Mn, P, and Zn) by flame atomic absorption or colorimetric spectrophotometry as described previously (Rincker et al., 2004). Analysis of plasma Cu, Fe, and Zn (PCu, PFe, and PZn, respectively), whole-body (protein), and blood (Hb and Hct) samples was performed as described previously (Rincker et al., 2004). All analyses were performed in duplicate. Feed, fecal, and whole-body mineral concentrations are reported on a DM basis, whereas liver and kidney mineral concentrations are reported on a wet basis.
Statistical Analyses
Performance (ADG), tissue, and whole-body data were analyzed as a randomized complete block design using the MIXED procedures of SAS (SAS Inst., Inc., Cary, NC). The model included the effects of litter (replication), treatment, and litter x treatment (error), with litter considered a random effect. Pig was the experimental unit for analysis of data. Additionally, blood measurements and nutrient balance data were analyzed using the MIXED model methodology of SAS for analysis of repeated measure data. The subject for the repeated measures was individual pig nested within treatment, and d 0 Hb, Hct, PCu, PFe, and PZn were used as covariates for their respective individual analyses. Statistical analysis of Zn balance data was performed on loge-transformed least squares means. Thus, data presented are back-transformed means with error bars for corresponding 95% confidence intervals. In Exp. 1, two preplanned orthogonal comparisons were made: 1) NC vs. Zn (2,000 mg of Zn/kg of diet as ZnO or ZnM); and 2) ZnO vs. ZnM. In Exp. 2, the effects of increasing dietary concentrations of supplemental Fe were partitioned into linear and quadratic components using orthogonal polynomial contrasts. Due to unequally spaced dietary concentrations of supplemental Fe, coefficients were derived using the integrative matrix language (PROC IML) procedures of SAS. Differences were considered significant at an 
level of P < 0.050 and highly significant at the level of P < 0.010.
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Results and Discussion
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Experiment 1
Growth performance response to pharmacological dietary Zn is variable. Feeding pharmacological Zn concentrations (1,500 to 3,000 mg of Zn/kg of diet) to nursery pigs has been shown to improve growth performance (Carlson et al., 1999; Hill et al., 2000, 2001); however, other research (Tokach et al., 1992) has reported no benefits due to pharmacological Zn concentrations (3,000 mg of Zn/kg of diet as ZnO). In the present experiment, no differences were observed in ADG (178.6, 170.9, and 113.6 g for NC, ZnO, and ZnM, respectively). Nursery pigs in an isolated and clean environment and fed diets containing carbadox did not respond to pharmacological Zn (Meyer et al., 2002). Our pigs were individually housed in stainless steel metabolism pens, whereas Meyer et al. (2002) fed two pigs per pen. Pigs in Exp. 1 originated from a herd with a high health status, and scouring was not observed during the 14-d experiment. Reports suggest that pharmacological Zn improves growth performance via an improvement in gut morphology (Carlson et al., 1999) and a decrease in scouring (Poulsen, 1995).
Pigs fed the NC diet had greater daily dietary DMI during Phases 1 (P = 0.041) and 2 (P = 0.044) and overall (P = 0.043) than pigs fed ZnO or ZnM diets (Table 4). The increase in dietary DMI by NC fed pigs may have prevented any observed growth differences; however, dietary Zn intake by pigs fed the NC diet during Phase 1 (38 mg of Zn/d) and 2 (10 mg of Zn/d) was less than the NRC (1998) recommendation for a 5- to 10-kg pig (50 mg of Zn/d). No clinical signs of Zn deficiency were observed. Other researchers (Hill et al., 1986; Wedekind et al., 1994) have reported adequate growth performance by nursery pigs when dietary Zn concentrations (24 to 33 mg of Zn/kg of diet) were less than the NRC (1998) recommendation.
Pigs fed pharmacological Zn concentrations as either ZnO or ZnM had greater (P < 0.001) daily Zn intake than pigs fed the NC diet throughout the 14-d experiment (Figure 1A). Consequently, these pigs had greater (P < 0.001) fecal Zn excretion than pigs fed the NC diet during Phase 2 (Figure 1B). After weaning, voluntary feed intake is generally insufficient to meet maintenance requirements (Bark et al., 1986). Pluske et al. (1995) estimated that the energy requirement for maintenance was not met until d 5 after weaning when pigs were weaned at 21 d of age. Although dietary DMI during Phase 1 was comparable to values previously reported in group-housed pigs (Rincker et al., 2004), the DMI, along with feeding a highly digestible diet, yielded a low fecal mass and subsequent fecal Zn during Phase 1 (Figure 1B). As pigs became more adapted to the environment (diet, pen, etc.), DMI increased, and subsequent fecal mass was increased during Phase 2.
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Figure 1. Effects of dietary Zn supplementation in Exp. 1 on nursery pigs: A) dietary Zn intake, mg/d (treatment; P < 0.001); B) fecal Zn excretion, mg/d (treatment x day; P = 0.003); and C) urinary Zn excretion, mg/d (treatment; P < 0.001). Statistical analysis of data (n = 8 per treatment; initial mean BW = 6.5 kg; initial age = 16 to 20 d) was performed on loge-transformed least squares means. Data presented are back-transformed means with error bars for corresponding 95% confidence intervals. Treatments were: NC (negative control, no added Zn source); ZnO (NC + 2,000 mg of Zn/kg of diet as Zn oxide); and ZnM (NC + 2,000 mg of Zn/kg of diet as Zn Met). Preplanned orthogonal comparisons were: 1) NC vs. Zn (ZnO plus ZnM); and 2) ZnO vs. ZnM.
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Because dietary Zn intake of pigs fed the NC diet was less than the NRC (1998) recommendation, pigs fed that diet had negligible fecal Zn excretion throughout the 14-d experiment (Figure 1B
). Retention rate of dietary Zn increases when the dietary concentration is below the body’s requirement. Thus, the fecal Zn excretion of pigs fed the NC diet was assumed to be of endogenous origin. Endogenous fecal Zn excretion represents an inevitable and constant metabolic loss, as well as homeostatic mechanisms excreting Zn absorbed in excess of the body’s requirements (Weigand and Kirchgessner, 1980). These authors reported that fecal Zn excretion in rats fed diets containing 5.6 or 10.6 mg of Zn/kg of diet was completely of endogenous origin. The Zn present in most plant protein sources is poorly available because it forms an insoluble complex with phytate (Oberleas et al., 1962).
The major route of Zn excretion in pigs is the feces. Feeding 2,000 mg of Zn/kg of diet as ZnO and ZnM resulted in 12.9- and 9.2-fold increases, respectively, in the overall quantity of fecal Zn excreted compared with pigs fed the NC diet (202.5 vs. 2,615.9 and 1,863.1 mg). The greatest increase in fecal Zn excretion occurred during Phase 2, when fecal Zn excretion increased 13-and 57-fold in pigs fed ZnO and ZnM diets, respectively, from d 7 to 14 (Figure 1B). Following a 10-d period of feeding pharmacological Zn diets, Case and Carlson (2002) reported a similar increase (15-fold) in fecal Zn excretion between pigs fed 3,000 vs. 250 mg of Zn/kg of diet as ZnO. Because they did not measure Zn balance during the loading phase (d 0 to 10), Zn balance was negative (–109.0 mg/d) for d 10 to 15. We determined daily Zn balance from weaning until 14 d after weaning. Pigs fed pharmacological ZnO or ZnM diets were in positive Zn balance throughout Phase 1 (d 0 to 7) and did not approach a negative Zn balance until d 13 to 14, when they became Zn loaded, and homeostatic mechanisms increased fecal Zn excretion. Meyer et al. (2002) reported that fecal Zn excretion increased (20-fold) and percentage Zn absorbed decreased as dietary Zn concentration increased (0 to 3,000 mg of Zn/kg of diet as ZnO); however, pigs were not in a negative Zn balance after 21 d.
During Phase 2, pigs fed diets containing 2,000 mg of Zn/kg of diet as ZnM had greater (P < 0.001) urinary Zn excretion than pigs fed ZnO or NC diets (Figure 1C). In lambs, Spears (1989) reported that urinary Zn excretion tended to be less with ZnM than with ZnO and suggested that the disparity in urinary Zn excretion between sources might represent differences in postabsorptive metabolism of Zn. It has been shown in piglets that 48 h after a Met load, the dose is fully catabolized and excreted as urinary S products (Hou et al., 2003). Although all diets in Exp. 1 were formulated to contain equal concentrations of Met, the organic Zn source has Zn bound to Met, which may result in a greater portion of absorbed Zn being metabolized and excreted via the renal system.
Pigs fed pharmacological ZnO diets had greater (P = 0.043) dietary Cu intake than pigs fed pharmacological ZnM diets (Table 5). Because dietary Cu concentrations were similar, this was due to the slightly greater dietary DMI by pigs fed pharmacological ZnO vs. ZnM diets. Pigs fed pharmacological ZnO or ZnM diets had greater (P = 0.003) dietary Fe intake and fecal Fe excretion than pigs fed the NC diet (Table 5). Pharmacological ZnO and ZnM diets had greater dietary Fe concentrations (Table 1). Meyer et al. (2002) also reported an increase in fecal Fe excretion in pigs fed pharmacological ZnO (2,000 to 3,000 mg of Zn/kg of diet) for 21 d; however, they noted an increase in dietary Fe concentrations because of the Fe in the commercial Zn oxide source.
In pigs, the normal range for PZn concentration is 0.8 to 1.2 mg/L (Underwood and Suttle, 1999). In Exp. 1, the initial (d 0) mean PZn concentration was 1.05 mg/L (Table 6). Pigs fed pharmacological ZnO or ZnM diets had a greater PZn concentration on d 7 (P = 0.018) and 14 (P = 0.001) than pigs fed the NC diet; however, no differences in PZn concentration were observed in pigs fed the two Zn sources at pharmacological concentrations. Other research has shown that pigs fed 2,000 mg of Zn/kg of diet as ZnM had greater PZn concentration on d 14 than pigs fed 2,000 mg of Zn/kg of diet as ZnO (Schell and Kornegay, 1996). Hahn and Baker (1993) reported that ZnO had a lower uptake from the gut, resulting in a lower PZn concentration in contrast to other Zn sources in which Zn was bound to sulfate, Lys, or Met. Using a broken-line plot of PZn concentration as a function of supplemental ZnO intake, Hahn and Baker (1993) suggested that PZn concentration was unresponsive when supplemental ZnO intake was less than 1,300 mg/d. Our data suggest otherwise; dietary Zn intake by pigs fed the NC, ZnO, and ZnM diets were 38.2, 296.6, and 190.9 mg/d during Phase 1, and 10.1, 528.4, and 440.6 mg/d during Phase 2, respectively. This result is similar to that of Wedekind et al. (1994), who evaluated another inorganic Zn source, Zn-sulfate, at lower dietary concentrations (27 mg of Zn/kg of basal diet to 47 mg of added Zn/kg of basal diet) and observed a linear response in PZn concentration.
Hill and Matrone (1970) reported that the trace minerals Cu, Fe, and Zn are transition metals, which have similar chemical and physical properties (i.e., similar electronic structure). Thus, an imbalance in one mineral can have an antagonistic effect on the concentration of another mineral. In rats, Murthy et al. (1974) reported that a negative correlation existed between PCu and PZn concentration; this is thought to occur via metallothionein, which has a greater affinity for Cu than for Zn (Hall et al., 1979). In our study (Table 6), no differences in PCu and PFe concentrations were observed between experimental treatments, even though PZn concentration was increased in pigs fed pharmacological Zn compared with those fed the NC diet.
Pigs fed pharmacological ZnO or ZnM diets had greater liver Fe (P = 0.006) and Zn (P = 0.001) concentrations than pigs fed the NC diet (Table 7). Although no differences (P = 0.633) in liver Zn concentration were observed between Zn sources in our experiment, Schell and Kornegay (1996) reported that pigs fed 2,000 mg of Zn/kg of diet as ZnM had greater liver Zn concentration than pigs fed 2,000 mg of Zn/kg of diet as ZnO. Excess Zn is known to induce a Cu deficiency, including anemia and decreased ceruloplasmin activity (Magee and Matrone, 1960). Ceruloplasmin, a key Cu-containing enzyme, is required for binding of Fe to transferrin via its ferroxidase activity (Osaki and Johnson, 1969). Consequently, an accumulation of Fe may occur due to a decrease in ceruloplasmin activity (Lee et al., 1968); however, no differences in liver Cu concentration were observed in this study. Pigs fed the NC diet did have a lower (P = 0.002) kidney Cu concentration and greater kidney Fe (P = 0.002) and Zn (P = 0.001) concentrations than pigs fed pharmacological ZnO or ZnM diets (Table 7). The greater kidney Zn concentration and lower urinary Zn excretion in pigs fed the NC diet suggest that these pigs tenaciously retained Zn in renal tissue by minimizing urinary Zn loss to compensate for low available Zn in the diet. Thus, renal Cu and Fe were altered because of the three-way interaction among Cu, Fe, and Zn, as previously reported by Hill et al. (1983). These results also agree with those of Schell and Kornegay (1996), who reported higher Fe and lower Cu concentration in kidney of pigs fed the control diet (105 mg of Zn/kg of diet) than in pigs fed 3,000 mg of Zn/kg of diet.
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Table 7. Effects of dietary Zn supplementation on nursery pig liver and kidney mineral concentrations (wet basis) in Exp. 1a
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Information regarding the whole-body mineral composition of today’s swine genetics, which is necessary for nutrient management plans, is limited. Whole-body mineral concentrations of nursery pigs in Exp. 1 are shown in Table 8. Pigs fed pharmacological ZnO or ZnM diets had a greater (P = 0.001) whole-body Zn concentration than pigs fed the NC diet. No difference (P = 0.713) was observed between Zn sources. We previously reported that pigs fed pharmacological ZnO during Phases 1 (d 0 to 7) and 2 (d 7 to 21) and then adequate Zn (107.5 mg of Zn/kg of diet) during Phase 3 (d 21 to 35) had a mean whole-body Zn concentration of 72.3 mg/kg (Rincker et al., 2004). In Exp. 1, whole-body Zn concentration of pigs fed the NC diet was 62.3 mg/kg (similar to the previous publication), whereas that of pigs fed pharmacological Zn for 14 d was increased 5-fold (346.3 mg/kg). Because pigs from both studies were of similar genetics fed in the same facilities, this suggests that when pharmacological Zn is removed from the diet, homeostatic mechanisms decrease the excess tissue Zn accumulated during earlier phases.
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Table 8. Effects of dietary Zn supplementation on nursery pig whole-body mineral concentration (DM basis) and percentage of protein in Exp. 1a
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No differences were observed in the percentage of protein and whole-body Cu, Fe, Mg, Mn, Ca, and P concentrations between pigs fed pharmacological ZnO or ZnM diets and pigs fed the NC diet (Table 8). However, pigs fed the ZnO diet had greater (P < 0.010) whole-body Mg and P concentrations than pigs fed the ZnM diet. The decreased whole-body Mg and P concentrations in pigs fed pharmacological ZnM may be attributed to a slightly lower dietary DMI. Mahan and Shields (1998) evaluated the macro- and micromineral concentrations of pigs at various intervals from birth to 145 kg of BW. They reported that macromineral concentrations generally reflected the metabolic need for soft and/or hard tissue development, whereas trace elements, except for Fe and Zn, maintained a constant concentration from weaning to 145 kg of BW. Increases in the concentration of Fe and Zn paralleled increases in pig weights, reflecting tissue expansion and a corresponding increase in heme compounds and epidermal tissue, respectively. Wiseman et al. (2003) reported that pigs with greater lean gain potential had greater body concentrations of minerals (Zn, Cu, S, and K), particularly those associated with lean tissue deposition.
Experiment 2
The basal diets contained 189.00, 223.80, and 97.80 mg of Fe/kg of diet (as-fed basis) for Phase 1, 2, and 3, respectively (Table 3); however, basal diets were formulated to contain 50 to 60 mg of Fe/kg of diet. We suspect that the excess dietary Fe was in the ferric oxide form, which is a poorly absorbed form and ineffective in meeting the pigs Fe requirement (Ammerman and Miller, 1972). We previously reported that pigs of similar genetics fed the same dietary treatments used in the current experiment had liver Fe concentrations ranging from 35 to 113 mg/kg (0 to 150 mg of supplemental Fe/kg of diet), which suggests that the excess dietary Fe was not absorbed and stored in the primary Fe storage organ.
In Exp. 2, increasing concentrations of supplemental Fe did not affect ADG (0.36, 0.40, 0.42, 0.39, and 0.40 kg for 0, 25, 50, 100, and 150 mg of supplemental Fe/kg of diet, respectively). Amine et al. (1972) suggested that BW gain is not a sensitive indicator of Fe adequacy because a decrease in growth is one of the last signs of an iron disorder following the development of hypochromic-microcytic anemia. Studies by Dove and Haydon (1991), Yu et al. (2000), and Rincker et al. (2004) also reported no effect on growth performance due to decreased dietary Fe concentration.
The improvements in dietary DMI during Periods 2 (linear; P = 0.002) and 3 (quadratic; P = 0.025) were of sufficient magnitude that dietary DMI tended to increase (linear; P = 0.075) during the 35-d experiment (Table 9). A similar response to treatments was observed in fecal DM excretion during Periods 2 (linear; P = 0.003) and 3 (quadratic; P = 0.055); however, no differences were observed in overall fecal DM excretion. Additionally, a decrease (linear; P < 0.05) in urine volume due to dietary treatments was noted in each period and for the overall experiment, but this response in urine volume may be confounded by some water wastage accumulating in the urine collection containers.
Increasing the dietary concentration of supplemental Fe resulted in a linear increase in (P = 0.001) dietary Fe intake and fecal Fe excretion (Table 10). When expressed as a percentage of intake, however, there were no differences in the percentage of Fe retained between experimental treatments.
Increasing dietary Fe concentration resulted in a linear increase in dietary Zn (P = 0.003), Cu (P = 0.014), Mn (P = 0.010), P (P = 0.070), and Mg (P = 0.065) intake (Table 10). Because diets were formulated to contain equal mineral concentrations, the increases in dietary mineral intake resulted from an increase in dietary DMI. Pigs had increased fecal Zn (linear; P = 0.020) excretion and decreased urinary Zn (quadratic; P = 0.010), Mn (linear; P = 0.007), Ca (linear; P = 0.031), and Mg (linear; P = 0.015) excretion in response to increasing dietary Fe. The decreases in urinary mineral excretion are the result of a decrease in overall urine volume for the 35-d experiment. The increases in dietary mineral intake combined with the decreases in urinary mineral excretion resulted in a linear increase in Cu (P = 0.013), Mn (P = 0.021), Ca (P = 0.034), P (P = 0.024), and Mg (P = 0.014) retained. No differences were observed among dietary treatments, however, in the percentage of Cu, Fe, Mn, Zn, Ca, and P retained in Exp. 2.
Hemoglobin and Hct are commonly used to assess Fe status because of their ease of measurement. These indicators of Fe status decrease after the depletion of liver, kidney, and spleen Fe stores. There were no differences in blood measurements at the start of Exp. 2 (Table 11). Following completion of Phase 2 (d 21), increasing dietary Fe concentration resulted in a linear increase (P = 0.001) in Hb concentration and Hct percent that was maintained until the study ended (d 35). A whole blood Hb concentration of 100 g/L is considered adequate, whereas 80 g/L suggests borderline anemia, and 70 g/L or less indicates anemia (Zimmerman, 1980). During the 35-d experiment, mean Hb concentration of all experimental treatment groups remained above the adequate concentration. A linear increase in PFe concentration was observed in response to experimental diets on d 7 (P = 0.034), 21 (P = 0.054), and 35 (P = 0.011). Results for blood measurements in Exp. 2 are consistent with previous results from our laboratory using a larger number of pigs (Rincker et al., 2004).
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Table 11. Effects of dietary Fe supplementation on nursery pig hematological status and plasma mineral concentrations in Exp. 2a
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As previously mentioned, an interrelationship exists between Cu, Fe, and Zn because of their similar chemical and physical properties (Hill and Matrone, 1970). On d 35, a linear increase (P = 0.045) in PZn concentration was observed in response to the increase in dietary Fe concentration (Table 11). Even though PZn concentration was affected by dietary treatments, plasma mineral concentrations were within normal ranges (PZn = 0.8 to 1.2 mg/L; PCu = 1.0 to 1.3 mg/L) reported by Underwood and Suttle (1999).
In conclusion, feeding pharmacological concentrations of Zn to nursery pigs increased Zn stores, but fecal Zn excretion was increased only after 9 to 10 d of supplementation. Results indicate that nursery pigs load Zn in tissues for approximately 9 to 10 d, and then excrete large quantities of Zn, resulting in a negative Zn balance after d 13 to 14. In Exp. 2, indicators of hematological status were increased due to supplemental Fe. Additionally, increasing the dietary Fe concentration increased dietary mineral intake via an increase in dietary DMI. Subsequently, fecal Fe and Zn excretion were increased. The current experiments provide useful data to swine producers regarding whole-body mineral composition, as well as fecal and urinary mineral excretion values for current genetics.
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Implications
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Manure management in intensive production units will continue to challenge the swine industry. Consequently, there is a need to continue to evaluate nutritional strategies that maximize animal performance, while minimizing environmental concerns. Feeding pharmacological concentrations of zinc to nursery pigs for 9 to 10 d has the potential to maintain rapid growth performance without large amounts of fecal zinc being excreted. When pharmacological concentrations of zinc are fed for a longer duration, tissues become loaded and homeostatic mechanisms excrete excess zinc. Homeostatic mechanisms also regulate the tissue loading of other minerals, such that when diets contain more than is required by the body, excess mineral quantities are excreted.
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Footnotes
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1 Partially funded by Six-State Consortium on Animal Waste Management of the EPA and USDA, CSREES Initiative for Future Agriculture and Food Systems grants. 
2 Appreciation is expressed to APC, Inc. (Ankeny, IA), International Ingredient Corp. (St. Louis, MO), The Solae Co. (St. Louis, MO), and Akey (Lewisburg, OH) for their donation of ingredients.
4 Current address: 107 J. B. Francioni Hall, Louisiana State Univ., Baton Rouge 70803.
3 Correspondence: 2209 Anthony Hall (phone: 517-355-9676; fax: 517-432-0190; e-mail: hillgre{at}msu.edu).
Received for publication November 22, 2004.
Accepted for publication August 4, 2005.
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Literature Cited
|
|---|
Amine, E. K., R. Neff, and D. M. Hegsted. 1972. Biological estimation of available iron using chicks or rats. J. Agric. Food Chem. 20:246–251.[Medline]
Ammerman, C. B., and S. M. Miller. 1972. Biological availability of minor mineral ions: A review. J. Anim. Sci. 35:681–694.
ASAE. 1988. Manure Production and Characteristics. ASAE Data D384, American Society of Agricultural Engineers, St. Joseph, MI.
Bark, L. J., T. D. Crenshaw, and V. D. Leibbrandt. 1986. The effect of meal intervals and weaning on feed intake of early weaned pigs. J. Anim. Sci. 62:1233–1239.
Carlson, M. S., G. M. Hill, and J. E. Link. 1999. Early- and traditionally weaned nursery pigs benefit from phase-feeding pharmacological concentrations of zinc oxide: Effect on metallothionein and mineral concentrations. J. Anim. Sci. 77:1199–1207.[Abstract/Free Full Text]
Case, C. L., and M. S. Carlson. 2002. Effect of feeding organic and inorganic sources of additional zinc on growth performance and zinc balance in nursery pigs. J. Anim. Sci. 80:1917–1924.[Abstract/Free Full Text]
Deming, J. G., and G. L. Czarnecki-Maulden. 1989. Iron bioavailability in calcium and phosphorus sources. J. Anim. Sci. 67(Suppl. 1):253. (Abstr.)
Dove, C. R., and K. D. Haydon. 1991. The effect of copper addition to diets with various iron levels on the performance and hematology of weanling swine. J. Anim. Sci. 69:2013–2019.[Abstract]
Hahn, J. D., and D. H. Baker. 1993. Growth and plasma zinc responses of young pigs fed pharmacologic levels of zinc. J. Anim. Sci. 71:3020–3024.[Abstract]
Hall, A. C., B. W. Young, and I. Bremner. 1979. Intestinal metallothionein and the mutual antagonism between copper and zinc in the rat. J. Inorg. Biochem. 11:57–66.[Medline]
Hill, C. H., and G. Matrone. 1970. Chemical parameters in the study of in vivo and in vitro interactions of transition elements. Fed. Proc. 29:1474–1481.[Medline]
Hill, D. A., E. R. Peo, Jr., A. J. Lewis, and J. D. Crenshaw. 1986. Zinc-amino acid complexes for swine. J. Anim. Sci. 63:121–130.
Hill, G. M., G. L. Cromwell, T. D. Crenshaw, C. R. Dove, R. C. Ewan, D. A. Knabe, A. J. Lewis, G. W. Libal, D. C. Mahan, G. C. Shurson, L. L. Southern, and T. L. Veum. 2000. Growth promotion effects and plasma changes from feeding high dietary concentrations of zinc and copper to weanling pigs (regional study). J. Anim. Sci. 78:1010–1016.[Abstract/Free Full Text]
Hill, G. M., D. C. Mahan, S. D. Carter, G. L. Cromwell, R. C. Ewan, R. L. Harrold, A. J. Lewis, P. S. Miller, G. C. Shurson, and T. L. Veum. 2001. Effect of pharmacological concentrations of zinc oxide with or without the inclusion of an antibacterial agent on nursery pig performance. J. Anim. Sci. 79:934–941.[Abstract/Free Full Text]
Hill, G. M., E. R. Miller, P. A. Whetter, and D. E. Ullrey. 1983. Concentration of minerals in tissues of pigs from dams fed different levels of dietary zinc. J. Anim. Sci. 57:130–138.
Hou, C., L. J. Wykes, and L. J. Hoffer. 2003. Urinary sulfur excretion and the nitrogen/sulfur balance ratio reveal nonprotein sulfur amino acid retention in piglets. J. Nutr. 133:766–772.[Abstract/Free Full Text]
Lee, G. R., S. Nacht, J. N. Lukens, and G. E. Cartwright. 1968. Iron metabolism in copper-deficient swine. J. Clin. Invest. 47:2058–2069.
Magee, A. C., and G. Matrone. 1960. Studies on growth, copper metabolism of rats fed high levels of zinc. J. Nutr. 72:233–242.
Mahan, D. C., and R. G. Shields, Jr. 1998. Macro- and micromineral composition of pigs from birth to 145 kilograms of body weight. J. Anim. Sci. 76:506–512.[Abstract/Free Full Text]
Meyer, T. A., M. D. Lindemann, G. L. Cromwell, H. J. Monegue, and N. Inocencio. 2002. Effects of pharmacological levels of zinc as zinc oxide on fecal zinc and mineral excretion in weanling pigs. Prof. Anim. Sci. 18:162–168.[Abstract/Free Full Text]
Murthy, L., L. M. Klevay, and H. G. Petering. 1974. Interrelationships of zinc and copper nutriture in the rat. J. Nutr. 104:1458–1465.
NRC. 1998. Nutrient Requirements of Swine. 10th ed. Natl. Acad. Press, Washington, DC.
Oberleas, D., M. E. Muhrer, and B. L. O’Dell. 1962. Effects of phytic acid on zinc availability and parakeratosis in swine. J. Anim. Sci. 21:57–61.[Abstract/Free Full Text]
Osaki, S., and D. A. Johnson. 1969. Mobilization of liver iron by ferroxidase (ceruloplasmin). J. Biol. Chem. 244:5757–5758.[Abstract/Free Full Text]
Pluske, J. R., I. H. Williams, and F. X. Aherne. 1995. Nutrition of the neonatal pig. Pages 187–235 in The Neonatal Pig, Development and Survival. M. A. Varley, ed. CAB Int., Wallingford, UK.
Poulsen, H. D. 1995. Zinc oxide for weanling piglets. Acta Agric. Scand. Anim. Sci. 45:159–167.
Rincker, M. J., G. M. Hill, J. E. Link, and J. E. Rowntree. 2004. Effects of dietary iron supplementation on growth performance, hematological status, and whole-body mineral concentrations of nursery pigs. J. Anim. Sci. 82:3189–3197.[Abstract/Free Full Text]
Schell, T. C., and E. T. Kornegay. 1996. Zinc concentration in tissues and performance of weanling pigs fed pharmacological levels of zinc from ZnO, Zn-methionine, Zn-lysine, or ZnSO4. J. Anim. Sci. 74:1584–1593.[Abstract]
Smith, J. W., M. D. Tokach, R. D. Goodband, J. L. Nelssen, and B. T. Richert. 1997. Effects of the interrelationship between zinc oxide and copper sulfate on growth performance of early-weaned pigs. J. Anim. Sci. 75:1861–1866.[Abstract/Free Full Text]
Spears, J. W. 1989. Zinc methionine for ruminants: relative bioavailability of zinc in lambs and effects of growth and performance of growing heifers. J. Anim. Sci. 67:835–843.
Takkar, P. N., and M. S. Mann. 1978. Toxic levels of soil and plant zinc for maize and wheat. Plant Soil 49:667–669.
Tokach, L. M., M. D. Tokach, R. D. Goodband, J. L. Nelssen, S. C. Henry, and T. A. Marsteller. 1992. Influence of zinc oxide in starter diets on pig performance. Page 41 in Proc. Am. Assoc. Swine Practitioners, Perry, IA.
Underwood, E. J., and N. F. Suttle. 1999. The Mineral Nutrition of Livestock. 3rd ed. CABI Publishing, New York, NY.
Wedekind, K. J., A. J. Lewis, M. A. Giesemann, and P. S. Miller. 1994. Bioavailability of zinc from inorganic and organic sources for pigs fed corn-soybean meal diets. J. Anim. Sci. 72:2681–2689.[Abstract]
Weigand, E., and M. Kirchgessner. 1980. Total true efficiency of zinc utilization: determination and homeostatic dependence upon the zinc supply status in young rats. J. Nutr. 110:469–480.
Wiseman, T. G., D. C. Mahan, J. C. Peters, N. D. Fastinger, S. Ching, and Y. Y. Kim. 2003. Body mineral composition of gilts and barrows from two genotypes of pigs from 18 to 127 kg body weight. J. Anim. Sci. 81(Suppl. 2):83. (Abstr.)
Yu, B., W. Huang, and P. W. Chiou. 2000. Bioavailability of iron from amino acid complex in weanling pigs. Anim. Feed Sci. Technol. 86:39–52.
Zimmerman, D. R. 1980. Iron in swine nutrition. Pages 1–56 in National Feed Ingredient Association Literature Review on Iron in Animal and Poultry Nutrition. Natl. Feed Ingred. Assoc., Des Moines, IA.
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Abstract
Introduction
