This study was conducted to examine whether Cu could exert its growth-promoting effect when injected, rather than being fed, and thus bypass the gastrointestinal tract. In two 18-d experiments, pigs were injected every 2 d with a Cu histidinate or histidine solution. Amounts of Cu injected were calculated to simulate varying absorption rates in pigs fed 250 ppm of dietary Cu. In Exp. 1, 44 pigs were randomly assigned to four groups of 11 pigs each. Pigs were injected with four levels of Cu histidinate (0, 5, 10, and 15% estimated apparent absorption coefficients based on calculated feed intake). Average daily gain responded quadratically (P < .05) to levels of Cu histidinate; maximum growth was seen in the 5% group. At d 6, serum mitogenic activity also exhibited a similar quadratic response (P < .05). In Exp. 2, estimated Cu absorptions of 0, 2, 4, 6, and 8% were tested. Forty-five pigs were randomly assigned to five groups of nine pigs each and injected as in Exp. 1. Both ADG and serum mitogenic activity displayed a quadratic response (P < .05); the maximum response was seen in the 4% group. Liver Cu content, superoxide dismutase activity, and serum Cu concentrations were linearly increased (P < .05) with increasing dosage of Cu in both Exp. 1 and 2. Also, brain Cu content linearly increased (P < .05) with increasing dosage of Cu in both Exp. 1 and 2. Also, brain Cu hormone mRNA concentrations in Exp. 2 were not significantly influenced by treatments.(ABSTRACT TRUNCATED AT 250 WORDS)
Two experiments were conducted to study the role of feed intake and feed efficiency in Cu-stimulated growth of weanling pigs. In Exp. 1, 42 pigs were randomly assigned into three treatments: 1) control: ad libitum access to a corn-soybean meal-dried whey basal diet; 2) ad libitum/Cu: ad libitum access to the basal diet supplemented with 215 ppm of Cu; or 3) pair-fed/Cu: pair-fed the Cu-supplemented diet to the level of the control. Over the 14-d experiment, the ad libitum/Cu pigs had greater (P < .05) ADG and ADFI than the control pigs. The pair-fed/Cu group had an intermediate ADG. Gain:feed (GF) was not significantly affected by treatments but tended to be improved in the pair-fed/Cu pigs. Feeding copper increased (P < .05) the concentration of Cu in the serum, liver, and brain. Also, feeding Cu increased (P < .05) serum mitogenic activity and growth hormone mRNA concentrations for both feeding methods. In Exp. 2, a 2 x 2 x 2 factorial arrangement of treatments with two levels of Cu (15 vs 200 ppm), two levels of feeding (ad libitum vs restricted [85% of the ad libitum]), and two sources of Cu (Cu sulfate vs Cu lysine) was used in a 24-d experiment involving 96 pigs. Feeding copper increased (P < .05) ADG and GF. The magnitude of the Cu-stimulated growth was reduced by restricted feeding (Cu level x feeding level interaction; P < .05). The ADFI was greater (P < .05) for the pigs fed high dietary Cu only during d 1 to 6. Pigs fed Cu lysine had greater ADG and ADFI than those fed Cu sulfate (P < .05); the benefit in ADG from Cu lysine was reduced by restricted feeding (Cu source x feeding level interaction, P < .05). High dietary Cu stimulated (P < .05) serum mitogenic activity; the stimulation was greater for Cu lysine than for Cu sulfate. Feeding Cu numerically increased GH mRNA concentration. Restricted feeding reduced overall serum mitogenic activity (P < .05), but the response to high dietary Cu and Cu lysine was still evident. In summary, Cu-stimulated growth was largely dependent on a simultaneous increase in feed intake, but there were some improvements in GF. The influence of Cu on serum mitogenic activity was independent of feed intake or growth in both experiments, which indicates a direct action of Cu on the growth regulatory system.
Bone 113 Brain 70 Heart 96 Kidney 141 Liver 151 Red muscle 137 Mixed muscle 89 White muscle 67 Pancreas 161 Spleen 107 Hair 20 1 Skin 28 Erythrocytes (pg/g packed cells) 7.7 Tissuesb Integumentsb a Data compiled from Hoekstra et al. (1956, 1967), Cassens et al. (1967), Miller et al. (l968), Crofton et al. (1983) and Zhou et al. (1994). Data of leucocytes, tissues and integuments are expressed as p.p.m. on a DM basis.
In a 36-d experiment, 32 pigs were depleted of Zn (24 d) using a soy-isolate (basal) diet (17 mg/kg of Zn) and then fed the basal diet (12 d) supplemented with 45 mg/kg of Zn from ZnSO4 (purified zinc sulfate dry powder, ZnSO4.nH2O) or from a Zn amino acid chelate (ZnAAC) to study the effectiveness of these dietary Zn sources in restoring serum and soft tissue Zn concentrations. Concurrently, nondepleted pigs were pair-fed both Zn-supplemented diets (eight pigs per diet) throughout the experiment. Serum Zn concentrations and serum alkaline phosphatase (ALP) activity of pigs fed the diets with no supplemental Zn were lower (P < .05) than those of nondepleted pigs after 7 and 14 d, respectively. After 24 d, concentrations of Zn in liver, pancreas, kidney, brain, and small intestine of Zn-depleted pigs were lower (P < .01) than those of nondepleted pigs. Except for decreased (P < .001) kidney Cu, soft tissue Cu and Fe concentrations were not affected by Zn status or Zn source. From d 24 to 36 (Zn repletion), serum and tissue Zn concentrations and serum ALP activities increased (P < .05), but the response was similar for both Zn sources in Zn-depleted and nondepleted pigs. At d 30 and 36, kidney Cu was increased (P < .01) in Zn-depleted pigs fed 45 mg/kg of Zn as either ZnSO4 or ZnAAC. Furthermore, Fe concentration was higher (P < .05) in intestinal segments of Zn-depleted and nondepleted pigs fed ZnAAC than in pigs fed ZnSO4. Accumulations of Cu in the kidney and Fe in the small intestine were affected by depletion and repletion of Zn and by dietary Zn source, respectively. In conclusion, serum and soft tissue Zn concentrations were clearly affected by Zn status: however, an effect of Zn source was not observed.
The effects of hemoglobin (Hb) status and coping style of pigs on performance and humoral immune response were studied. Twenty-four, 4-wk-old crossbred barrows were assigned to groups of three pigs based on weight and litter origin. Groups were allotted according to a 2 x 2 factorial treatment arrangement: two blood Hb concentration classes (low vs high) and two immunization procedures (control vs immunized). Immunized pigs received an antigen cocktail containing keyhole limpet hemocyanin (KLH), ovalbumin (OA), and tetanus toxoid (TT) at weaning. Additionally, pigs were stratified according to behavioral coping style in response to exposure to a stressor. During 41 d after weaning (approximate time of immunization), blood Hb concentration, ADG, and ADFI were measured weekly and serum antibody titers to KLH, OA, and TT twice weekly. Average Hb concentration differed between low and high Hb pigs (P < .001; 10.0 vs 12.0 g/dL), but this difference declined with time after weaning. Neither immunization procedure nor coping style affected Hb concentrations. In addition, ADG and ADFI were unaffected by any of the treatments. However, ADG was slightly greater in high Hb status pigs (586 vs 633 g/d) and was paralleled by a slightly greater ADFI in high Hb status pigs (812 vs 899 g/d). Antibody responses were negatively or not related to Hb status at weaning. Antibody responses (depending on isotype and antigen) were or tended to be lower in pigs with high blood Hb concentrations. Behavioral coping style strongly affected humoral immune responsiveness; enhanced or accelerated antibody responses were found in pigs that had a passive coping style.
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