Multitrial analysis of the effects of copper level and source on performance in nursery pigs.

A multitrial analysis was conducted to evaluate the effect of different levels of Cu from either Cu(2-hydroxy-4-(methylthio)butanoic acid [HMTBa])2 or CuSO4 on growth performance in nursery pigs. Six nursery trials were conducted from 2007 to 2012 under the same commercial conditions with initial BW of 5.75 ± 0.41 kg at 21 ± 3 d of age; the trials lasted for 42 d with a 3-phase feeding program (7 d in Phase I, 14 d in Phase II, and 21 d in Phase III). Diets were medicated with antibiotics and supplemented with 3,000 mg/kg Zn as ZnO during phases I and/or II. Treatments included a basal diet without added Cu or according to the NRC (1998) and supplemental levels of Cu (50 to 250 mg Cu/kg diet) from either Cu(HMTBa)2 or CuSO4; HMTBa was supplemented to make diets isomethionine. Treatments from each trial included 6 or 9 replicate pens/treatment with 22 to 25 piglets/pen. Mixed model analysis was conducted in which trial was considered a random effect, Cu level was considered a continuous fixed effect, and Cu source was a fixed effect. The basal diet within trial and statistical tests of the intercept between sources were not different, resulting in fitting a common intercept mixed model to the overall responses across phases. Cumulative ADG and ADFI quadratically responded (P < 0.05) with increasing Cu supplementation; predicted optimal ADG and ADFI occurred at 174 and 119 mg/kg, respectively. Increasing Cu supplementation linearly improved G:F (P = 0.054). No differences between sources were observed in ADG or ADFI. Numerically, pigs fed Cu(HMTBa)2 had higher ADG and lower ADFI compared to pigs fed CuSO4, resulting in better G:F for pigs supplemented with Cu(HMTBa)2 compared to pigs supplemented with CuSO4 (P < 0.01). The linear slope for increasing Cu supplementation on G:F was 2.1-fold higher for Cu(HMTBa)2 than that of CuSO4, with larger differences occurring in Phase II. In conclusion, Cu supplementation in nursery diets resulted in improved performance and Cu(HMTBa)2 is more effective than CuSO4 in improving feed efficiency.

The feline iodine requirement is lower than the 2006 NRC recommended allowance.

The purpose of this study was to determine the iodine (I) requirement in adult cats. Forty-two healthy euthyroid cats (1.6-13.6 years old) were utilized in a randomized complete block design. Cats were fed a dry basal diet (0.23 mg/kg I) for a minimum of 1 month (pre-test) then switched to a different basal diet supplemented with seven levels of KI for 1 year (experimental period). Analysed I concentrations were 0.17, 0.23, 0.47, 1.1, 3.1, 6.9 and 8.8 mg I/kg diet [dry matter (DM) basis] and used to construct a response curve. Response variables included I concentrations in serum, urine and faeces, urinary I:creatinine ratio, I balance, technetium(99m) pertechnetate (Tc(99m)) thyroid:salivary ratio, complete blood count and serum chemistries as well as serum thyroid hormone profiles. No significant changes in food intake, weight gain or clinical signs were noted. Serum I, daily urinary I, daily faecal I and urinary I:creatinine ratio were linear functions of iodine intake. An estimate of the I requirement (i.e. breakpoint) was determined from regression of Tc(99m) thyroid:salivary ratio (scintigraphy) on I intake at 12 months [0.46 mg I/kg diet (DM basis) as well as 9 months I balance (0.44 mg I/kg diet (DM)]. The I requirement estimate determined in our study at 12 months for adult cats (0.46 mg I/kg) was higher than current Association of American Feed Control Officials (AAFCO) recommendations (e.g. 0.35 mg I/kg), but was lower than the 2006 National Research Council (NRC) I recommended allowance (e.g. 1.4 mg I/kg).

Primary hair growth in dogs depends on dietary selenium concentrations.

Selenium (Se) plays an important role in hair growth. The objective of this study was to investigate the effect of dietary selenium concentration on hair growth in dogs. Thirty-six beagles were stratified into six groups based on age, gender and body condition score. The dogs were fed a torula yeast-based canned food for 3 weeks. Then the dogs were fed varying amounts of selenium supplied as selenomethionine for an additional 24 weeks. Analysed selenium concentrations in the experimental foods for the six groups were 0.04, 0.09, 0.12, 0.54, 1.03 and 5.04 mg/kg dry matter respectively. Body weight and food intake were not affected by the selenium treatments. Serum selenium concentration was similar initially but was significantly different at the end of the study among groups. Dietary selenium concentration below 0.12 mg/kg diet may be marginal for an adult dog. Dietary treatment had no effect on serum total thyroxine (TT(4)), free thyroxine (FT(4)), and free 3,3',5-triiodothyronine (FT(3)). There was a significant diet and time interaction (p = 0.038) for total 3,3',5 triiodothyronine (TT(3)). Hair growth was similar among groups initially but significantly reduced in dogs fed diets containing 0.04, 0.09 or 5.04 mg Se/kg when compared with 0.12, 0.54 and 1.03 mg Se/kg at week 11 (p < 0.05) and week 22 (p = 0.061). These results demonstrated that both low and high selenium diets reduce hair growth in adult dogs.

The selenium requirement of the puppy.

Current selenium (Se) recommendations for the puppy are based on extrapolation from other species (0.11 mg Se/kg diet). The purpose of this study was to experimentally determine the Se requirement in puppies. Thirty beagle puppies (average = 8.8 weeks old) were utilized in a randomized complete block design with age, litter and gender used as blocking criteria. Puppies were fed a low Se (0.04 mg Se/kg diet) torula yeast-based diet for 14 days (pre-test period) after which this same diet was supplemented with five levels of Na2SeO3 for 21 days (experimental period) to construct a response curve (0, 0.13, 0.26, 0.39 or 0.52 mg Se/kg diet). Response variables included Se concentrations and Se-dependent glutathione peroxidase activities (GSHpx) in serum as well as serum total triiodothyronine (TT3), serum total thyroxine (TT4) and serum free T4 (FT4). No significant changes in food intake and body weight gain occurred, and no clinical signs of Se deficiency were observed. A breakpoint for serum GSHpx could not be determined in our study due to analytical difficulties. A broken-line, two-slope response in serum Se occurred with a breakpoint at 0.17 mg Se/kg diet. When Se from the basal diet was added to this estimate, the breakpoint for serum Se equated to 0.21 mg Se/kg diet. TT3 increased linearly with increasing Se intake, whereas TT4 was unchanged. However, the ratio of TT4 : TT3 decreased linearly in response to supplemental Se. In summary, although we estimated the selenium requirement for the puppy based on serum Se, our 0.21 mg Se/kg diet estimate is higher than that seen for adult dogs, kittens, rats or poultry (0.13, 0.15, 0.15 and 0.15 mg Se/kg diet respectively). This difference may be due to the fact that GSHpx was used as the biomarker of Se status.

Determination of the selenium requirement in kittens.

The purpose of this study was to determine the selenium (Se) requirement in kittens. Thirty-six specific-pathogen-free kittens (9.8 weeks old) were utilized in a randomized complete block design to determine the Se requirement in cats with gender and weight used as blocking criteria. Kittens were fed a low Se (0.02 mg/kg Se) torula yeast-based diet for 5 weeks (pre-test) after which an amino acid-based diet (0.027 mg Se/kg diet) was fed for 8 weeks (experimental period). Six levels of Se (0, 0.05, 0.075, 0.10, 0.20 and 0.30 mg Se/kg diet) as Na2SeO3 were added to the diet and were used to construct a response curve. Response variables included Se concentrations and Se-dependent glutathione peroxidase activities (GSHpx) in plasma and red blood cells (RBC) as well as plasma total T3 (TT3) and total T4 (TT4). No significant changes in food intake, weight gain or clinical signs of Se deficiency were noted. Estimates of the kitten's Se requirement (i.e. breakpoints) were determined for RBC and plasma GSHpx (0.12 and 0.15 mg Se/kg diet, respectively), but no definitive breakpoint was determined for plasma Se. Plasma TT3 increased linearly, whereas plasma TT4 and the ratio of TT4 : TT3 decreased in a quadratic fashion to dietary Se concentration. The requirement estimate determined in this study (0.15 mg Se/kg) for kittens is in close agreement with other species. As pet foods for cats contain a high proportion of animal protein with a Se bioavailability of 30%, it is recommended that commercial diets for cats contain 0.5 mg Se/kg DM.

A low-selenium diet increases thyroxine and decreases 3,5,3'triiodothyronine in the plasma of kittens.

The effect of a low-selenium diet on thyroid hormone metabolism was investigated in growing kittens. Twelve specific-pathogen-free kittens with ages ranging from 16 to 18 weeks were divided into two groups of equal number with equal sex distribution in each group. One group was fed a yeast-based low-selenium diet (0.02 mg Se/kg diet) while the other group was fed the same diet supplemented with Na2SeO3 at 0.4 mg Se/kg diet for 8 weeks. Food intake, body weight and body weight gain were not affected by the low-Se diet during the study period. However, kittens given the low-Se diet had significantly reduced plasma selenium concentration and glutathione peroxidase activity. Plasma total thyroxine (T4) increased and total 3,5,3'triiodothyronine (T3) decreased significantly in kittens fed the low-Se diet at the end of the study. These results suggest that type I deiodinase in cats is a selenoprotein- or a selenium-dependent enzyme.

Effect of increasing dietary antioxidants on concentrations of vitamin E and total alkenals in serum of dogs and cats.

Oxidative damage to DNA, proteins, and lipids has been implicated as a contributor to aging and various chronic diseases. The presence of total alkenals (malondialdehyde and 4-hydroxyalkenals) in blood or tissues is an indicator of lipid peroxidation, which may be a result of in vivo oxidative reactions. Vitamin E functions as a chain-breaking antioxidant that prevents propagation of free radical damage in biologic membranes. This 6-week dose-titration study was conducted to assess the effect of selected dietary vitamin E levels on byproducts of in vivo oxidative reactions in dogs and cats. Forty healthy adult dogs and 40 healthy adult cats were assigned to four equal groups per species in a complete random block design. A control group for both dogs and cats was fed dry food containing 153 and 98 IU vitamin E/kg of food (as fed), respectively. Canine and feline treatment groups were fed the same basal dry food with vitamin E added at three different concentrations. The total analyzed dietary vitamin E levels for the canine treatment groups were 293, 445, and 598 IU vitamin E/kg of food, as fed. The total analyzed dietary vitamin E levels for the feline treatment groups were 248, 384, and 540 IU vitamin E/kg of food, as fed. Increasing levels of dietary vitamin E in dog and cat foods caused significant increases in serum vitamin E levels compared with baseline values. Although all treatments increased concentrations of vitamin E in serum, all were not effective at decreasing serum alkenal levels. The thresholds for significant reduction of serum alkenal concentrations in dogs and cats were 445 and 540 IU vitamin E/kg of food, respectively, on an as-fed basis. The results of this study show that normal dogs and cats experience oxidative damage and that increased dietary levels of antioxidants may decrease in vivo measures of oxidative damage.

Bioavailability of zinc from inorganic and organic sources for pigs fed corn-soybean meal diets.

Two experiments were conducted with pigs 1) to determine the effect of supplemental Zn on growth performance, bone Zn, and plasma Zn in pigs fed Zn-unsupplemented, corn-soybean meal diets and 2) to assess bioavailability of Zn from inorganic and organic Zn sources. In both experiments, weanling pigs were fed a diet with no supplemental Zn for 5 wk to deplete their Zn stores. In Exp. 1, 192 pigs were fed a corn-soybean meal diet (growing diet, 32 mg/kg of Zn; finishing diet, 27 mg/kg of Zn) supplemented with feed-grade ZnSO4.H2O to provide 0, 5, 10, 20, 40, and 80 mg/kg of supplemental Zn. Supplemental Zn did not affect weight gain, feed intake, or gain/feed during either the growing or the finishing period (P > .05). However, bone and plasma Zn concentrations increased linearly (P < .01) in response to supplemental Zn at dietary Zn levels between 27 mg/kg (basal) and 47 mg/kg (breakpoint). In Exp. 2, three levels of supplemental Zn from ZnSO4.H2O (0, 7.5, and 15 mg/kg of supplemental Zn) were used to construct a standard curve (metacarpal, coccygeal vertebrae, and plasma Zn concentrations regressed on supplemental Zn intake; R2 = .93, .89, and .82, respectively). From the standard curve, the bone and plasma Zn concentrations obtained from pigs fed 15 mg/kg of supplemental Zn from ZnO and 7.5 mg/kg of supplemental Zn from Zn-methionine (ZnMET) and Zn-lysine (ZnLYS) were used to calculate bioavailable Zn via multiple linear regression, slope-ratio analysis. The estimates of Zn bioavailability differed depending on which variable was used. Overall trends indicated the following rankings: ZnSO4.H2O > ZnMet > ZnO > ZnLys.

Methodology for assessing zinc bioavailability: efficacy estimates for zinc-methionine, zinc sulfate, and zinc oxide.

The bioavailability of zinc-methionine (ZnMET) was compared to that of feed-grade ZnSO4.H2O using three different diets: purified (crystalline amino acid [AA]), semipurified (soy isolate), and complex (corn-soybean [C-SBM]) diet. With the Zn-deficient purified or semipurified diet, weight gain and tibia Zn responded linearly to both ZnSO4.H2O and ZnMET supplementation. Common-intercept, multiple linear regression indicated differences in Zn bioavailability between ZnMET and ZnSO4.H2O for both diets as indicated by bone Zn. With the ZnSO4.H2O standard set at 100%, bioavailability of Zn from ZnMET was 117% (P less than .05) in the AA diet and 177% (P less than .01) in the soy isolate diet. The ZnMET was also compared to ZnSO4.H2O in a C-SBM diet containing 117 mg of Zn/kg. When high levels of Zn were added to this diet (0, 250, 500, and 750 mg/kg of supplemental Zn), consistent tissue Zn responses did not occur beyond the first increment. Addition of lower levels of supplemental Zn (0, 5, 10, 20, 30, 40 and 50 mg/kg) to a Zn-unsupplemented C-SBM basal diet (45 mg/kg of Zn), however, resulted in a broken-line, two-slope response in tibia Zn for both ZnMET and ZnSO4.H2O. Inflection points occurred at 60 and 54 mg of Zn/kg of diet for ZnSO4.H2O and ZnMET, respectively. The ratio of slopes (ZnMET:ZnSO4.H2O) below the inflection points was 206% (P less than .01), indicating that Zn was considerably more bioavailable in ZnMET than in ZnSO4.H2O for chicks consuming C-SBM diets. When feed-grade ZnO was compared to feed-grade ZnSO4.H2O in chicks consuming C-SBM diets, bone Zn slopes below the respective inflection points indicated that Zn was 61% bioavailable in ZnO relative to ZnSO4.H2O.

Phosphorus, but not calcium, affects manganese absorption and turnover in chicks.

Two balance studies with growing chicks were conducted to evaluate the effects of excess Ca or excess P on endogenous fecal Mn excretion and true Mn absorption. An isotope-dilution technique was used to estimate endogenous manganese in excreta. Supplements were added to a corn-soybean diet containing 1% Ca, 0.7% P (0.5% available P) and 37 mg Mn/kg. In Experiment 1, supplemental Ca levels of 0, 0.5 and 1.0% from feedgrade limestone were compared. True absorption of Mn was not affected by Ca level (P greater than 0.10) and averaged 2.8% for birds fed the Mn-unsupplemented diet. In Experiment 2, a 2 x 3 factorial arrangement of treatments included: 100 and 1000 mg/kg supplemental Mn (from MnSO4.H2O) and 0, 0.4 and 0.8% added P supplied by dicalcium phosphate. Excess P significantly decreased true absorption of Mn (P less than 0.01). In birds fed 100 mg/kg supplemental Mn, absorption of Mn decreased 22% as excess P increased from 0 to 0.8%, whereas in birds fed 1000 mg/kg supplemental Mn, Mn absorption decreased 59% as a result of 0.8% P supplementation. These results confirm that the antagonism of Mn by inorganic P is due to reduced gut absorption of Mn.

Manganese turnover in chicks as affected by excess phosphorus consumption.

A repletion-depletion assay was conducted to evaluate the effect of Mn status and excess dietary P provided as dicalcium phosphate on Mn excretion and turnover. Chicks were fed either Mn-adequate (30 mg Mn/kg) or high Mn (1000 mg Mn/kg) casein-dextrose diets for 7 d. Following this loading period, the chicks were fed a Mn-deficient casein-dextrose diet (1.4 mg Mn/kg) with or without 0.5% excess P supplied from dicalcium phosphate. Whole body (without feathers) and selected body tissues (liver, kidney, gut, tibia and feathers) were assayed for Mn content at 0, 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 10, 15 and 20 d after initiation of the Mn-deficient diet. Excess P had little effect on Mn turnover. All tissues showed significantly reduced biological half-lives (P less than 0.05) as a result of loading chicks with a high level of Mn (1000 mg/kg) during the 7-d loading period. However, there was wide variation in Mn turnover rates among tissues. Liver, kidney and whole body contained readily exchangeable manganese in much higher proportions than did bone.

Effect of varying calcium and phosphorus level on manganese utilization.

Two experiments were conducted to evaluate the effect of varying levels of excess Ca and P on manganese (Mn) utilization. The criterion used to study the Mn-antagonizing effects of excess Ca and P was the regression of total tibia Mn on supplemental Mn intake. In Experiment 1, high supplemental levels of Mn were fed (0, 500, and 1,000 mg Mn per kg); in Experiment 2, lower Mn levels were fed (0, 50, and 100 mg Mn per kg). Supplements were added to a corn-soybean meal diet containing 1.1% Ca, .7% (.5% available) P, and 37 mg Mn per kg. In Experiment 1, a 3 x 3 x 3 factorial arrangement of treatments (four replicates) was used. Treatments were as follows: 0, .5, and 1.0% excess Ca as feed-grade ground limestone; 0, .4, and .8% excess P as KH2PO4; and 0, 500, and 1,000 mg Mn per kg as MnSO4.H2O. Total tibia Mn was depressed by P (P less than .0001) but not by Ca (P greater than .05). Compared with the standard (no added P), .4% P reduced Mn utilization by 22%, whereas .8% P reduced it by 38%. Manganese supplementation was found to ameliorate the growth-depressing effect of .8% supplemental P. Results of Experiment 2 agreed with the results in Experiment 1, providing evidence that bioavailability estimates obtained from experiments containing high levels of Mn can be extrapolated to diets containing lower levels. Results from Experiment 2 indicated that, relative to the standard (no added P), .22, .44 and .88% excess P reduced Mn utilization by 16, 22 and 31%, respectively.

Manganese utilization in chicks as affected by excess calcium and phosphorus ingestion.

Three experiments were conducted to assess Mn utilization in the presence or absence of excess Ca and P from various sources. Supplements were added to a corn-soybean meal diet containing 1% Ca, .7% (.5% available) P and 37 mg of Mn per kg. Three percentages of supplemental Mn from MnSO4.H2O (0, 500, and 1,000 mg of Mn per kg) were used to construct a standard curve of tibia Mn regressed on the 14-day supplemental Mn intake (r averaged .96 for the three experiments). From this, the tibia Mn values obtained from chicks fed diets containing 1,000 mg of supplemental Mn per kg of diet plus 1% added Ca from various sources, were used to calculate bioavailable Mn via standard-curve methodology. In Experiment 1, analytical-grade (AG) CaCO3, feed-grade (FG) oyster shell and FG dicalcium phosphate decreased Mn utilization by 20, 15 and 53%, respectively, but FG limestone was without effect. Experiments 2 and 3 were conducted to determine how different combinations of Ca and P, as well as different cationic forms of P, affected Mn utilization. The results from these experiments indicated that feeding .88% of excess inorganic P, regardless of source and whether fed alone or in combination with excess Ca, reduced Mn utilization by 50 to 65%. Among the Ca sources, only oyster shell caused a reduction in Mn utilization. It is evident that excess dietary P is more antagonistic to Mn than is excess Ca.

Zinc bioavailability in feed-grade sources of zinc.

Chick bioassays were used to assess bioavailability of zinc (Zn) from inorganic Zn sources. A soy isolate-dextrose diet containing 13 mg Zn/kg diet was supplemented with feed-grade sources of ZnSO4.H2O (ZnSO4) or ZnO and fed for 2 wk after a 7-d Zn-depletion protest period. Bioavailability of Zn in ZnO relative to ZnSO4 (set at 100%) was determined by multiple regression slope-ratio methodology, using both growth and tibia Zn accumulation in chicks fed graded levels of ZnO and ZnSO4. Linear responses for gain and tibia Zn occurred at dietary Zn levels (ZnSO4.7H2O) between 13 mg/kg (basal) and 33 mg/kg (gain) or 53 mg/kg (total tibia Zn). Therefore, two bioavailability assays were conducted using supplemental Zn levels of 0, 7.5 and 15 mg/kg from each Zn source. When weight gain was regressed on supplemental Zn intake, bioavailability of Zn in ZnO was only 61.2% (P less than .01) that of ZnSO4. When total tibia Zn was regressed on supplemental Zn intake, bioavailability of Zn compared with ZnSO4 (set at 100.0%) was 44.1% (P less than .001) for ZnO. With chicks fed soy-based diets, bioavailability of Zn from ZnO was less than that of ZnSO4.