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A total of 126 gilts and sows (PIC 1050) and their litters were used to determine the effects of dietary vitamin E concentration and source on sow plasma, milk, and pig concentrations of α-tocopherol. Additionally, we estimated the bioavailability of D-α-tocopheryl acetate (D-α-TAc) relative to DL-α-tocopheryl acetate (DL-α-TAc) when fed in diets containing dried distillers grains with solubles (DDGS). The 6 dietary treatments included DL-α-TAc at 44 and 66 mg/kg and D-α-TAc at 11, 22, 33, and 44 mg/kg. From breeding to d 69 of gestation, sows were fed 2.0 kg/d of a diet containing 40% DDGS, 0.30 mg/kg added Se, and no added vitamin E. Vitamin E treatments were fed from d 70 of gestation through weaning. Plasma was collected from sows on d 69 and 100 of gestation, at farrowing, and at weaning. Colostrum and milk samples were also collected. Plasma from 3 pigs per litter and heart and liver samples from 1 pig per litter were collected at weaning. Plasma, milk, and tissues from 6 litters per treatment were analyzed for α-tocopherol. Although tissue, plasma, and milk concentrations of α-tocopherol were the primary response criteria of interest, sow and litter performance were measured. As expected, treatment effects were not observed for lactation feed intake, sow BW, or backfat measurements. A trend (P = 0.085) for a treatment effect on average pig BW at weaning was detected, with pigs nursing sows fed 44 mg/kg DL-α-TAc weighing less because of a younger weaning age. No other differences in litter performance were observed. As D-α-TAc increased in the diet, sow plasma, colostrum, and milk, pig plasma, and pig heart concentrations of α-tocopherol increased (linear, P < 0.03). Sows fed diets with 44 mg/kg D-α-TAc had increased (P < 0.03) plasma and colostrum and pig plasma concentrations of α-tocopherol compared with sows fed 44 mg/kg of DL-α-TAc. Sows fed 66 mg/kg DL-α-TAc also had greater (P = 0.022) plasma α-tocopherol at weaning than sows fed 44 mg/kg DL-α-TAc. Bioavailability coefficients for D-α-TAc relative to DL-α-TAc ranged from 1.9 to 4.2 for sow and pig plasma α-tocopherol, 2.9 to 3.6 for colostrum α-tocopherol, 1.6 for milk α-tocopherol, and 1.7 to 2.0 for pig heart and liver α-tocopherol. Overall, this study indicates the bioavailability for D-α-TAc relative to DL-α-TAc varies depending on the response criteria but is greater than the standard potency value of 1.36.

Relative vitamin E status of pigs fed natural or synthetic vitamin E was evaluated based on serum and tissue alpha-tocopherol concentrations. Individually fed finishing gilts at a BW of 70.5 kg (n = 24) were allotted to dietary treatments based on initial BW. The 5 dietary treatments consisted of a positive control diet using synthetic vitamin E acetate (Syn E Ac) supplemented at 22 mg/kg, and 4 dietary levels of natural vitamin E acetate (Nat E Ac) supplemented at 6.71, 8.33, 11.00, and 16.18 mg/kg of diet. Before initiation of the 32-d experiment, pigs were fed a non-vitamin E-fortified diet for 30 d. Diets were formulated to contain true ileal digestible lysine of 0.9 and 0.8% for the pretest and test diets. Serum samples were collected on d 15 and 32, whereas tissue samples were collected on d 32 for alpha-tocopherol analysis. Serum alpha-tocopherol concentrations on d 15 and 32 were greater (P < 0.05) in pigs fed 8.33, 11.00, or 16.18 mg/kg of Nat E Ac than in pigs fed 22 mg/kg of Syn E Ac. When compared with pigs fed 22 mg/kg of Syn E Ac, alpha-tocopherol concentrations were greater (P < 0.05) in 6 tissues (heart, kidney, spleen, liver, lung, and adipose) in pigs fed 16.18 mg/kg of Nat E Ac; greater (P < 0.05) in heart, kidney, spleen, liver, and adipose tissue in pigs fed 11.00 mg/kg of Nat E Ac; and greater (P < 0.05) in spleen, loin, and adipose tissue in pigs fed 8.33 mg/kg of Nat E Ac. As dietary Nat E Ac increased from 6.71 to 16.18 mg/kg, serum alpha-tocopherol increased linearly (P < 0.01) on d 15 and 32 of the experiment. Increasing dietary Nat E Ac linearly increased (P < 0.05) alpha-tocopherol concentrations for lung, heart, kidney, spleen, and liver. These results indicate that Nat E Ac was an effective vitamin E source and its relative bioavailability was substantially greater than 1.36 for finishing swine when compared with Syn E Ac.

Three experiments conducted with weanling pigs evaluated the effects of vitamin E added to the drinking water or diet on plasma and tissue alpha-tocopherol concentrations. When natural or synthetic vitamin E was used, it was added at an IU-equivalent basis, but natural vitamin E was 73.5% (mg basis) of the synthetic vitamin E. Experiment 1 used 18-d-old weanling pigs (n = 120) in a 3 x 2 factorial arrangement of treatments in a randomized complete block design with 4 replicates. The first factor evaluated the dietary levels of natural vitamin E (RRR-alpha-tocopheryl acetate) added at 0, 50, or 300 IU/kg, whereas the second factor was the natural vitamin E added to the drinking water at 0 or 100 IU/L. Pigs were bled at periodic intervals, and 1 pig per pen was killed at the end of the 21-d trial and tissues (liver, heart, lung, and loin) were collected for alpha-tocopherol analysis. When vitamin E was not added to the diet or water, plasma alpha-tocopherol declined over the 21-d period. Although there were some interactions (P < 0.01), tissue and plasma alpha-tocopherol concentrations increased linearly when vitamin E was added to the diet or water. Experiment 2 was a 3 x 2 factorial in a randomized complete block design with 4 replicates. A total of 96 pigs weaned at 18 d of age, with an initial BW of 6.2 kg, were fed a nonvitamin E fortified diet, but natural or synthetic (all-rac-alpha-tocopheryl acetate) vitamin E was added to their drinking water at 50, 100, or 150 IU/L. Pigs were bled at 0, 3, 7, 10, 14, and 21 d postweaning, with tissues (liver, lung, heart, and loin) collected for alpha-tocopherol analysis at d 21. The results indicated that plasma alpha-tocopherol concentrations increased (P < 0.01) as vitamin E increased, with greater tissue alpha-tocopherol concentrations (P < 0.01) when natural vitamin E was provided. Experiment 3 was conducted in 2 replicates, but pigs (n = 60) were not provided vitamin E in the diet or water for 7 d postweaning, and then natural or synthetic vitamin E was added to the drinking water as in Exp. 2 (50, 100, or 150 IU/L). Pigs were bled at 0, 2, 4, 6, 8, 10, and 24 h after being provided vitamin E to evaluate the absorption from each vitamin E source and level. Plasma alpha-tocopherol increased quadratically (P < 0.01) and plateaued at 8 to 10 h for each treatment group. These results indicate that adding vitamin E to the pig's water supply at weaning was more effective in increasing plasma alpha-tocopherol than when it was added to the diet during the initial 14 d postweaning, and that natural vitamin E was a superior source compared with synthetic vitamin E.

Thirty-two beef heifers were used to examine the effect of dietary copper depletion and repletion on neutrophil and lymphocyte functions. Heifers allotted to the control group (C+; n = 8) were fed a basal roughage/concentrate diet with Cu-sulfate supplementation (Cu > or = 8 ppm). To induce a Cu deficiency (depletion phase d 0 to 60), treated (T; n = 24) heifers received a diet supplemented with sulfur (.3% of diet) and sodium molybdate to achieve a Cu:Mo ratio of 1:1.5. Liver biopsies were collected on d 0, 27, and 60. Despite random allocation, T heifers had lower initial liver Cu concentrations (P < .01) than C+ heifers. At the start of the repletion phase (d 0, equal to d 60 of depletion), treated heifers were allotted by liver Cu concentration to three treatments (n = 8/treatment): Cu sulfate (S; Cu = 10 ppm), Cu proteinate (P; Cu = 10 ppm), or a negative control (C-) that remained on Mo and S supplementation. During the repletion phase, livers were biopsied on d 0, 14, and 45. By d 45, both S and P heifers had greater (P < .05) liver Cu concentrations than C- heifers. For both depletion and repletion phases, no treatment differences were detected in liver Mo or S concentrations. Jugular blood was collected on d 0, 27, and 55 of the depletion phase and d 0, 13, and 42 of the repletion phase. Neutrophils were isolated and incubated with Staphylococcus aureus to determine neutrophil bactericidal capacity (NBC).(ABSTRACT TRUNCATED AT 250 WORDS)

Chronic cannulas were placed in the hepatic portal vein, ileal vein, and carotid artery in seven crossbred growing gilts trained to consume once daily 1.2 kg of a 16% CP corn-soybean meal diet. Eleven days after surgery, each pig (37.4 kg BW) was placed in an open-circuit calorimeter and its cannulas were connected to a system for determining portal absorption of nutrients. The whole-animal heat production and net portal absorption of gut VFA were measured simultaneously for 12 h after the pig was fed 1.2 kg of feed. Plasma concentrations of VFA, including acetic, propionic, isobutyric, butyric, isovaleric, and valeric acids, in portal and arterial samples were determined by gas chromatography after a cleanup by ion-exchange chromatography. The net portal absorption of VFA was calculated by multiplying the porto-arterial plasma concentration difference of the VFA by portal vein plasma flow. Plasma flow was estimated by the indicator-dilution technique using p-aminohippuric acid as the indicator. The energy value of absorbed VFA was the sum of products of each individual VFA multiplied by its corresponding value of the heat of combustion. The mean hourly energy value of absorbed VFA during the 12-h postprandial period was .65 +/- .03 kcal.h-1.kg BW-1. The mean hourly whole-animal heat production was 2.70 +/- .04 kcal.h-1.kg BW-1. Thus, in our 37.4-kg pigs, which were trained to consume 1.2 kg of a 16% CP corn-soybean meal diet once daily, the gut VFA absorbed into the portal vein could contribute 23.8 +/- 1.1% to whole-animal heat production if all of the absorbed VFA were combusted to CO2.

Twenty-eight genetically obese and 24 lean barrows (65.0 and 68.7 kg average BW, respectively) were allotted within genotype to a 16% CP corn-soybean meal basal diet or this basal diet + 20 ppm ractopamine (a phenethanolamine beta-adrenergic agonist) and allowed ad libitum access to feed for 48 d. Compared to lean pigs, obese pigs had lower ADG, gain to feed ratio, longissimus muscle area, predicted amount of muscle, and weights of trimmed loin and ham, ham lean, heart, spleen, kidney and gastrointestinal tract (P less than .05). Obese pigs also had shorter carcass but higher dressing percentage, backfat thickness, fat depth, fat area, untrimmed loin weight and fasting plasma urea N concentration (P less than .05). Dietary supplementation with 20 ppm ractopamine reduced daily feed intake and improved gain to feed ratio in both lean and obese pigs (P less than .05). Pigs fed ractopamine had shorter carcasses, less fat depth and fat area, smaller weights of stomach and colon plus rectum, but higher dressing percentages, longissimus muscle areas, weights of trimmed Boston butts, picnics and loins, ham lean and predicted amounts of muscle than pigs not fed ractopamine (P less than .05). Supplemental ractopamine had no effect on fasting plasma concentrations of urea N, nonesterified fatty acids, triglyceride or glucose (P greater than .05). No genotype x ractopamine interactions for the criteria described above were detected (P greater than .05). These results suggest that ractopamine will improve the efficiency of feed utilization and carcass leanness in swine with different propensities for body fat deposition.

Twenty-four genetically obese and 24 lean barrows were allotted within genotype to either a 16% CP corn-soybean meal basal diet, the basal + .69 ppm cimaterol or the basal + 1.38 ppm cimaterol. Pigs had ad libitum access to their diets from 59.3 kg to 104.5 kg body weight. No genotype x cimaterol interactions were detected (P greater than .05). Neither genotype nor cimaterol supplementation had any effect (P greater than .05) on average daily weight gain or gain-to-feed ratio. Compared with lean pigs, obese pigs had higher fasting plasma urea nitrogen (BUN), a smaller gastrointestinal tract and a greater dressing percentage with a shorter and fatter carcass (P less than .05). Cimaterol produced a higher fasting plasma BUN, a greater dressing percentage with a leaner carcass and a higher shear force value for loin chops (P less than .05). Cimaterol also tended (P less than .10) to increase heart weight. However, no difference was observed in these measurements between pigs fed .69 or 1.38 ppm cimaterol. In lean pigs fed the basal or .69 ppm cimaterol diet, there was no difference (P greater than .05) in the 8 to 24 h postprandial whole-animal heat production. Cimaterol effectively decreased fat deposition and increased lean accretion both in genetically obese and in lean pigs; there were no differential responses to cimaterol in pigs with different propensities to deposit body fat.

Three hundred fifty rats were used in three experiments to: 1) validate the everted gut procedure as an in vitro technique for estimating Zn absorption, 2) determine the effect of increasing ratios of picolinic acid (PA) to Zn on Zn absorption and 3) determine the effect of PA on absorption of Zn and amino acid complexes at pH 6, 7 and 8. In the first experiment the time delay between tissue collection with subsequent storage in ice-cold saline and start of tissue incubation was 0, 10, 20 or 30 min. A linear decrease was observed for 65Zn uptake with increasing delay time. Lysine absorption was not affected by delay time. In the second experiment, molar ratios of PA:Zn of 0, .5, 1.0, 1.5, 2.0 and 2.5 with Zn held constant were evaluated. A linear decrease in 65Zn absorption from 65ZnCl2 occurred as the molar ratio of PA to Zn increased. In the third experiment, 0 and 5 molar ratios of PA to a constant Zn level were evaluated using 65ZnCl2, 65Zn-14C-methionine (ZnMet) and 65Zn-3H-lysine (ZnLys) at pH 6, 7 and 8. The addition of PA decreased Zn absorption regardless of Zn source. The data suggest that the Zn sources used were of similar biological value. The data do not support the theory that PA facilitates Zn absorption.

Two experiments were conducted to determine the effect of sources of dietary zinc on gain, feed conversion and blood and bone traits of swine. In the first experiment 96 pigs were used in a 28-d study. The pigs were fed diets with no supplemental Zn or with either 9 or 12 ppm supplemental Zn from zinc sulfate (ZnSO4), zinc methionine (ZnMet) or zinc methionine with picolinic acid (ZnMet w/PA), each with or without 5% added corn oil. There were differences (P less than .05) in average daily gain (ADG) and average daily feed intake (ADFI) between the pigs fed the two organic Zn sources, with those fed ZnMet w/PA showing the better gains and feed conversion. However, neither organic Zn source resulted in pig performance that was different from either the diet with no supplemental Zn or the diets supplemented with Zn from ZnSO4. In the second experiment the same dietary Zn sources and treatments were fed as in Exp. 1 except that corn oil was deleted as a variable. No differences in ADG, ADFI, feed/gain (F/G) or in changes in serum Zn or Cu were observed among treatments during either the 21-d nursery or the 56-d growing periods. During the subsequent 56-d finishing period ADG and ADFI were greater (P less than .01) for pigs fed the Zn-supplemented diets than for those fed the diets without supplemental Zn. There were no differences among treatments in F/G during the finishing period. Zn content of bone ash was lower (P less than .01) in the non-Zn-supplemented pigs. These data suggest that the Zn sources used are of similar biological value and do not support the theory that picolinic acid aids Zn absorption.

Cement kiln dust (CKD) samples of which have been reported to stimulate growth in cattle and sheep, was fed to weanling pigs in a 42-d experiment. CKD at levels of 1.5 and 3.0% was added to a corn-soybean meal-oats-whey-type diet containing inadequate amounts of Ca (.4% of the diet) to provide final dietary Ca levels of .85 and 1.3%. A diet containing 3% limestone (1.3% dietary Ca) served as a positive control. Body weight gain was depressed by 3.0% CKD, and histopathological lesions of the humerus, not typical of nutritional secondary hyperparathyroidism or rickets, were observed. The lesions detected were osteonecrosis, thinning of the cortex and reduction in the width of the epiphyseal cartilage. Width of the proximal epiphyseal plate and cortical index of the humerus (width of cortex divided by total diameter at narrowest point of diaphysis) were smaller in pigs fed 3% CKD than in pigs fed 3% limestone. CKD contained 2.3% A1, 15 ppm Cd and 110 ppm Pb, providing 690, .45 and 3.3 ppm of A1, Cd and Pb, respectively, in the diet containing 3% CKD. Kidney, liver and bone ash concentrations of these three minerals were not increased by CKD, and typical toxicity signs were absent. It is concluded that CKD may contain one or more factors that interfere with normal bone metabolism in growing pigs when the diet contains 3.0% CKD.