Two hundred and sixteen weanling gilts (6.65+/-0.08 kg) were used to determine the effects of decreasing supplemental concentrations of Zn, Cu, Fe, and Mn, and trace mineral source (inorganic vs. chelated) on growth performance, mineral status, and fecal mineral concentrations from weaning through development. The study was conducted over three trials with 72 pigs in each trial. Gilts were blocked by weight and randomly assigned to either 1) control, 2) reduced inorganic, or 3) reduced chelated trace minerals. The control diet was supplemented with 25, 150, 180, and 60 mg/kg of Cu, Zn, Fe, and Mn (in sulfate forms), respectively, during the nursery phase and 15, 100, 100, and 40 mg/kg of supplemental Cu, Zn, Fe, and Mn, respectively, during the growing and gilt-developer phases. Reduced inorganic and reduced chelated treatments were supplemented during all phases with 5, 25, 25, and 10 mg/kg of Cu, Zn, Fe, and Mn, respectively. The reduced chelated treatment supplied 50% of the supplemental Cu, Zn, Fe, and Mn in the form of metal proteinates, with the remainder from sulfate forms. Performance by control pigs did not differ from pigs fed the reduced trace mineral treatments during the nursery and grower-development periods. Gain:feed was lower (P < 0.05) for pigs fed the reduced inorganic compared with those fed the reduced chelated treatment during the nursery period. Trace mineral source did not affect performance during the growing or gilt-developer phase. Plasma Zn concentration and alkaline phosphatase activity were higher (P < 0.01) in control pigs than in those receiving reduced trace minerals during the nursery and growing phases. Plasma Cu concentration and ceruloplasmin activity were generally not affected by treatment. Hemoglobin concentrations were lower (P < 0.05) for the reduced inorganic compared with the reduced chelated treatment in the nursery phase. Fecal concentrations of Cu, Zn, and Mn were lower (P < 0.05) in pigs fed reduced trace minerals than in controls during all production phases. Fecal Zn concentration during the nursery and fecal Cu concentrations during the growing and gilt-developer phases were lower (P < 0.05) in pigs fed the reduced chelated compared with the reduced inorganic treatment. Results indicate that reducing the concentrations of Zn, Cu, Mn, and Fe typically supplemented to pig diets will greatly decrease fecal mineral excretion without negatively affecting pig performance from weaning through development.

Thirty weanling, crossbred barrows (SUS SCROFA) were used to determine the effects of amount and source of dietary Cu on small intestinal morphology and lipid peroxidation, Cu metabolism, and mRNA expression of proteins involved in hepatic Cu homeostasis. At 21 d of age, pigs were stratified by BW (6.33 ± 0.23 kg) and allocated to 1 of the following dietary treatments: i) control (no supplemental Cu; 6.7 mg Cu/kg), ii) 225 mg supplemental Cu/kg diet from Cu sulfate (CuSO(4)), or iii) 225 mg supplemental Cu/kg diet from tribasic Cu chloride (TBCC). Pigs were housed 2 pigs per pen and were fed a 3-phase diet regimen until d 35 or 36 of the study. During harvest, bile and liver were obtained for mineral analysis, and liver samples were also obtained for analysis of liver glutathione (GSH) and mRNA expression of Cu regulatory proteins. Segments of duodenum, proximal jejunum, and ileum were obtained for mucosal morphology, and duodenal mucosal scrapings were collected from all pigs for analysis of malondialdehyde (MDA). Duodenal villus height was reduced in CuSO(4) pigs compared with control (P = 0.001) and TBCC (P = 0.03) pigs. Villus height in the proximal jejunum of CuSO(4) pigs was reduced (P = 0.03) compared with control pigs, but ileal villus height was not affected (P = 0.82) by treatment. Duodenal MDA concentrations were greater (P = 0.03) in CuSO(4) pigs and tended to be greater (P = 0.10) in pigs supplemented with TBCC compared with control pigs. Liver Cu was greater (P = 0.01) in CuSO(4) vs. control pigs, and tended (P = 0.07) to be greater in TBCC pigs than control pigs. Bile Cu concentrations were greater (P < 0.001) in CuSO(4) and TBCC pigs vs. controls and were also greater (P = 0.04) in TBCC vs. CuSO(4) pigs. Total liver GSH concentrations were less (P = 0.02) in pigs fed diets supplemented with CuSO(4) vs. pigs fed control diets but total liver GSH did not differ (P = 0.11) between control and TBCC pigs. Hepatic mRNA of cytochrome c oxidase assembly protein 17 was less (P = 0.01) in CuSO(4) and tended to be less (P = 0.08) in TBCC pigs vs. control pigs. Expression of antioxidant 1 mRNA was greater (P = 0.04) in TBCC pigs and tended to be greater (P = 0.06) in CuSO(4) pigs compared with control pigs. Results of this study indicated that, when fed at 225 mg Cu/kg diet, TBCC may cause less oxidative stress in the duodenum than CuSO(4). Feeding weanling pigs increased Cu resulted in modulation of certain Cu transporters and chaperones at the transcription level.

Thirty-six Angus and Angus×Simmental heifers, averaging 291 kg, were used to determine the effects of dietary Cr, in the form of Cr propionate (Cr Prop), on glucose metabolism and serum insulin concentrations following glucose administration. Heifers were stratified by body weight (BW) within a breed and randomly assigned to treatments. Treatments consisted of 0, 3, 6, or 9 mg of supplemental Cr/d from Cr Prop. Based on dry matter (DM) intakes, the daily doses of Cr were equivalent to 0.47, 0.94, and 1.42 mg of supplemental Cr/kg of DM. Heifers were individually fed a corn silage-based diet at a level of 2% of BW. Each heifer was also fed 0.45 kg of a ground corn supplement daily that served as a carrier for supplemental Cr. Glucose tolerance tests were performed on d 44 of the study. Glucose was infused via jugular catheters at a level of 0.45 g/kg of BW(0.75) over a course of 1 to 2 min. Blood samples were collected at -10, 0, 5, 10, 15, 30, 45, 60, 90, 120, 150, and 180 min relative to glucose dosing for glucose and insulin determination. Area under the glucose response curve was lower (1,603 vs. 1,964 mg/dL per minute) in heifers supplemented with Cr from 0 to 45 min following glucose challenge. Serum insulin concentrations were lower in Cr-supplemented heifers than in controls following glucose infusion. The molar ratio of insulin to glucose was also lower in Cr-supplemented heifers relative to controls. Serum insulin and serum insulin to glucose ratios did not differ among heifers supplemented with 3, 6, or 9 mg of Cr/d. Results indicate that Cr Prop supplementation increased tissue sensitivity to insulin in growing heifers. Based on insulin sensitivity, Cr requirements (as Cr Prop) of growing heifers can be met by supplementing with 3 mg of Cr/d or 0.47 mg of Cr/kg of DM.

An experiment was conducted to determine the long-term effects of dietary boron (B) on growth performance, immune function, and plasma and serum characteristics in gilts. Fifty weanling gilts were allotted to 10 pens based on weaning weight and litter origin. Pens were randomly assigned to receive one of two dietary treatments. Treatments consisted of a basal diet low in B (control) and the basal diet supplemented with 5 mg B/kg diet as sodium borate. Gilts remained on their respective experimental diets and with their penmates throughout the nursery, growing, and finishing phases. The B concentration of the basal diet was 0.98, 2.1, and 2.2 mg/kg diet during the nursery, growing, and finishing phases, respectively. At the end of each production phase, animals were weighed and feed consumption was determined to assess growth performance variables. In addition, blood samples were obtained from three randomly selected gilts per pen at the completion of each phase. Boron had no affect (P > 0.58) on growth performance during the nursery phase, but gilts receiving supplemental B had increased (P < 0.05) ADG at the end of the finishing phase and over the entire growing-finishing period. Serum concentrations of triiodothyronine (T3) tended (P < 0.07) to be reduced by dietary B at the end of the nursery phase, but serum thyroxine (T4) was not affected (P = 0.46) by B. At the completion of the growing phase, supplemental B decreased (P < 0.05) the concentrations of T3 and T4 in the serum. In addition, serum concentrations of total cholesterol and the activity of alkaline phosphatase were increased (P < 0.05) by dietary B at the end of the growing phase. Serum concentrations of urea N tended (P < 0.09) to be increased by B at the end of the growing phase. Beginning at d 95 of the experimental period, measures of immune function were assessed in randomly selected gilts. Boron decreased (P < 0.05) the inflammatory response to an intradermal injection of phytohemagglutinin. Boron did not affect (P > 0.30) the blastogenic response of isolated lymphocytes to mitogen stimulation or the humoral immune response against a sheep red blood cell suspension. Results indicate that B may affect serum thyroid hormone concentrations, the inflammatory response, and growth in pigs.

No abstract

Sixty Angus (n = 29) and Angus-Sim-mental cross (n = 31) steers, averaging 9 mo of age and 277 kg of initial BW, were used in a 148-d study to determine the bioavailability of copper glycinate (CuGly) relative to feed-grade copper sulfate (CuSO(4)) when supplemented to diets high in S and Mo. Steers were blocked by weight within breed and randomly assigned to 1 of 5 treatments: 1) control (no supplemental Cu), 2) 5 mg of Cu/kg of DM from CuSO(4), 3) 10 mg of Cu/kg of DM from CuSO(4), 4) 5 mg of Cu/kg of DM from CuGly, and 5) 10 mg of Cu/kg of DM from CuGly. Steers were individually fed a corn silage-based diet (analyzed 8.2 mg of Cu/kg of DM), and supplemented with 2 mg of Mo/kg of diet DM and 0.15% S for 120 d (phase 1). Steers were then supplemented with 6 mg of Mo/kg of diet DM and 0.15% S for an additional 28 d (phase 2). Average daily gain and G:F were improved by Cu supplementation regardless of source (P = 0.01). Final ceruloplasmin, plasma Cu, and liver Cu values were greater (P < 0.05) in steers fed supplemental Cu compared with controls. Plasma Cu, liver Cu, and ceruloplasmin values were greater (P < 0.05) in steers supplemented with 10 mg of Cu/kg of DM vs. those supplemented with 5 mg of Cu/kg of DM. Based on multiple linear regression of final plasma Cu, liver Cu, and ceruloplasmin values on dietary Cu intake in phase 1 (2 mg of Mo/kg of DM), bioavailability of Cu from CuGly relative to CuSO(4) (100%) was 140 (P = 0.10), 131 (P = 0.12), and 140% (P = 0.01), respectively. Relative bio-availability of Cu from CuGly was greater than from CuSO(4) (P = 0.01; 144, 150, and 157%, based on plasma Cu, liver Cu, and ceruloplasmin, respectively) after supplementation of 6 mg of Mo/kg of DM for 28 d. Results of this study suggest that Cu from CuGly may be more available than CuSO(4) when supplemented to diets high in S and Mo.

An experiment was conducted to examine the effects of dietary Mn on growth, reproductive performance, and Mn status of beef heifers. Eighty Angus (n = 40) and Simmental (n = 40) heifers, averaging 249 kg, were stratified by BW within a breed and randomly assigned to 1 of 4 treatments providing 0 (control), 10, 30, or 50 mg of supplemental Mn/kg of DM from MnSO(4). Heifers were individually fed a diet containing cottonseed hulls, corn gluten feed, citrus pulp, and ground corn, and the control diet contained 15.8 mg of Mn/kg of DM by analysis. Average daily gain, DMI, and G:F for the 196-d period were not affected by Mn supplementation. Control heifers had reduced (P = 0.04) liver Mn when contrasted with the 3 levels of supplemental Mn. Serum cholesterol was greater (P = 0.001) in Angus compared with Simmental heifers over the course of the 196-d experiment but was not affected by treatment. Dietary Mn did not significantly affect measures of reproductive performance. Results of this study indicate that 15.8 mg of Mn/kg of diet DM should be adequate for growth, onset of estrus, and conception of beef heifers.

Forty-eight weanling barrows were used to determine the effects of amount and source of dietary Cu on Cu metabolism, oxidative stress in the duodenum, and VFA ratios in the cecum of weanling pigs in short-term feeding. At 21 d of age, newly weaned pigs were stratified by BW (7.03 ± 1.20 kg) and equally assigned to 1 of the following dietary treatments: 1) control (5 mg supplemental Cu/kg diet from CuSO4), 2) 225 mg supplemental Cu/kg diet from CuSO4, or 3) 225 mg supplemental Cu/kg diet from tribasic Cu chloride (TBCC). Pigs were housed 2 pigs per pen and were fed a complex diet until harvest on d 11 and 12. During harvest, bile and liver were obtained for mineral analysis, and liver samples were obtained for analysis of mRNA expression of Cu regulatory proteins. Digesta of duodenum, proximal jejunum, and ileum were collected for soluble Cu analysis. Mucosal scrapings of duodenum, proximal jejunum, and ileum were obtained for analysis of mucosal Cu concentration and mRNA expression of Cu regulatory proteins. Duodenal mucosal scrapings were also collected for analysis of malondialdehyde (MDA). Pigs fed high Cu had markedly greater (P < 0.0001) Cu concentrations in the duodenal, proximal jejunal, and ileal mucosa than controls. Copper in the duodenal mucosa was greater (P = 0.003) in CuSO4 than TBCC pigs. Duodenal MDA concentrations were greater (P = 0.003) in CuSO4 vs. control pigs and tended (P = 0.06) to be greater than in TBCC pigs. Duodenal antioxidant 1 (Atox1) mRNA was downregulated (P < 0.01) in pigs fed high Cu compared to controls and was not affected by Cu source. Compared with control pigs, those fed CuSO4 and TBCC had greater (P < 0.001) liver and bile Cu concentrations. Liver Cu was also greater (P = 0.0007) in TBCC than CuSO4-fed pigs. Hepatic Cu transporting β-polypeptide ATPase (Atp7b) was upregulated (P = 0.02) in the Cu-supplemented pigs compared with controls and did not differ among Cu sources. The acetate:propionate ratio in cecal contents was much greater in pigs supplemented with 225 mg Cu/kg diet than in controls. When fed at 225 mg Cu/kg diet, TBCC may cause less oxidative stress in the duodenum than CuSO4. Feeding weanling pigs increased Cu resulted in modulation of duodenal and liver at the transcription level.