Effects of potential detoxifying agents on growth performance and deoxynivalenol (DON) urinary balance characteristics of nursery pigs fed DON-contaminated wheat.

Two experiments were conducted to evaluate potential detoxifying agents on growth of nursery pigs fed deoxynivalenol (DON)-contaminated diets. Naturally DON-contaminated wheat (6 mg/kg) was used to achieve desired DON levels. In a 21-d study, 238 pigs (13.4 ± 1.8 kg BW) were used in a completely randomized design with a 2 × 2 + 1 factorial arrangement. Diets were: 1) Positive control (PC; < 0.5 mg/kg DON), 2) PC + 1.0% Product V (Nutriquest LLC, Mason City, IA), 3) Negative control (NC; 4.0 mg/kg DON), 4) NC + 1.0% Product V, and 5) NC + 1.0% sodium metabisulfite (SMB; Samirian Chemicals, Campbell, CA). There were 6 or 7 replicate pens/treatment and 7 pigs/pen. Analyzed DON was decreased by 92% when pelleted with SMB, but otherwise matched formulated levels. Overall, a DON × Product V interaction was observed for ADG ( 0.05) with a tendency for an interaction for ADFI ( 0.10). As anticipated, DON reduced ( 0.001) ADG and ADFI, but the interaction was driven by even poorer growth when Product V was added to NC diets. Pigs fed NC diets had 10% poorer G:F ( 0.001) than PC-fed pigs. Reductions in ADG due to DON were most distinct (50%) during the initial period. Adding SMB to NC diets improved ( 0.01) ADG, ADFI, and G:F, and improved ( 0.02) ADG and G:F compared to the PC diet. A urinary balance study was conducted using diets 3 to 5 from Exp. 1 to evaluate Product V and SMB on DON urinary metabolism. A 10 d adaptation was followed by a 7 d collection using 24 barrows in a randomized complete block design. Pigs fed NC + SMB diet had greater urinary DON output ( 0.05) than pigs fed NC + Product V, with NC pigs intermediate. Daily DON excretion was lowest ( 0.05) in the NC + SMB pigs. However, degradation of DON-sulfonate back to the parent DON molecule was observed as pigs fed NC + SMB excreted more DON than they consumed (164% of daily DON intake), greater ( 0.001) than pigs fed the NC (59%) or NC + Product V (48%). Overall, Product V did not alleviate DON effects on growth nor did it reduce DON absorption and excretion. However, hydrothermally processing DON-contaminated diets with 1.0% SMB restored ADFI and improved G:F. Even so, the urinary balance experiment revealed that some of the converted DON-sulfonate can degrade back to DON under physiological conditions. While further research is needed to discern the stability of the DON-sulfonate, SMB appears promising to restore performance in pelleted DON-contaminated diets.

The progression of deoxynivalenol-induced growth suppression in nursery pigs and the potential of an algae-modified montmorillonite clay to mitigate these effects.

Two experiments were conducted to characterize the progression of deoxynivalenol (DON)-induced growth suppression and to investigate algae-modified montmorillonite clay (AMMC) as a means to alleviate the effects of DON in nursery pigs. In both experiments, naturally DON-contaminated wheat was used to produce diets with desired DON levels. In Exp. 1, 280 barrows and gilts (10.0 ± 0.2 kg BW) were used in a 28-d experiment arranged in a 2 × 2 + 1 factorial design with 8 replicates per treatment. The 5 treatments consisted of 2 positive control (PC) diets with DON below detection limits and with or without 0 or 0.50% AMMC and 3 negative control (NC) diets with 5 mg/kg of DON and containing 0, 0.25, or 0.50% AMMC. No DON × AMMC interactions were observed. Overall, pigs fed DON had decreased ( < 0.001) ADG and final BW regardless of AMMC addition. Feeding DON-contaminated diets elicited the most severe depression ( < 0.001) in ADFI and G:F from d 0 to 3, remaining poorer overall ( < 0.01) but lessening in severity as exposure time increased. Pigs fed DON diets had greater ( < 0.05) within pen BW variation (CV) on d 28. Although the addition of 0.50% AMMC to diets restored ( < 0.05) ADFI from d 14 to 21 to levels similar to the PC, no other differences were observed for AMMC inclusion. In Exp. 2, 360 barrows (11.4 ± 0.2 kg BW) were used in a 21-d experiment with 9 dietary treatments arranged in a 3 × 3 factorial design with DON and AMMC inclusion as main effects. There were 8 replicate pens per treatment. Treatments consisted of 3 PC diets without DON, 3 low-DON (1.5 mg/kg DON) NC diets, and 3 high-DON (3 mg/kg DON) NC diets with 0, 0.17, or 0.50% AMMC incorporated at each DON level. No DON × AMMC interactions were observed. As DON level increased, ADG and final BW decreased (quadratic, < 0.05), driven by decreased (quadratic, < 0.01) ADFI and poorer (quadratic; < 0.05) G:F. At both 1.5 and 3 mg/kg DON, reductions in ADG were most marked from d 0 to 7 (15 to 22% lower) and were least distinct from d 14 to 21 (5 to 6% lower). Incorporating AMMC at increasing levels had no effect on ADG, ADFI, G:F, or final BW. Overall, these experiments reinforce DON effects on feed intake but also indicate that the effects of DON on G:F may be more severe than previously thought. Furthermore, some pigs appear to develop tolerance to DON, as effects on ADFI and G:F lessen over time. However, the addition of AMMC did not offset the deleterious effects of DON.

The effects of deoxynivalenol-contaminated corn dried distillers grains with solubles in nursery pig diets and potential for mitigation by commercially available feed additives.

Four experiments were conducted to investigate the effects of deoxynivalenol (DON) from naturally contaminated dried distillers grains with solubles (DDGS) and the efficacy of feed additives in nursery pig diets. In Exp. 1, 180 pigs (10.3 ± 0.2 kg BW) were fed 1 of 5 diets for 21 d. Diets were 1) Positive Control (PC; < 0.5 mg/kg DON), 2) Negative Control (NC; 4 mg/kg DON), 3) NC + 0.10% Biofix (Biomin Inc., Herzogenburg, Austria), 4) NC + 0.15% Cel-can (VAST Inc., Mason City, IA) and 0.50% bentonite clay, and 5) NC + 0.25% Defusion Plus (Cargill Animal Nutrition, Minneapolis, MN). Pigs fed the NC diet had poorer ( < 0.01) ADG than those fed the PC. Pigs fed Defusion Plus had improved ( < 0.03) ADG over those fed NC, whereas pigs fed Biofix or Cel-can with bentonite clay had reduced ADG ( < 0.01) compared with those fed PC. In Exp. 2, 340 pigs (11.7 ± 0.1 kg BW) were fed 1 of 8 diets for 21 d. Diets were 1) PC (< 0.5 mg/kg DON), 2) Low NC (1.5 mg/kg DON), 3) Low NC + 0.15% Biofix, 4) Low NC + 0.30% Biofix, 5) High NC (3.0 mg/kg DON), 6) High NC + 0.30% Biofix, 7) High NC + 0.45% Biofix, and 8) Diet 7 with 5% added water. Increasing the DON level reduced (linear; < 0.05) ADG, ADFI, and pig BW, and Biofix did not improve performance. In Exp. 3, 1,008 pigs (12.5 ± 0.3 kg BW) were fed 6 treatments for 24 d. Diets were 1) PC ( < 0.5 mg/kg DON), 2) NC (3 mg/kg DON), 3) NC + 0.25% Defusion, 4) NC + 0.50% Defusion, 5) Diet 3 with supplemental nutrients, and 6) Diet 5, pelleted. Pigs fed the NC had decreased ( < 0.01) ADG and ADFI, but adding Defusion improved (linear; < 0.04) ADG and ADFI over pigs fed NC. Pelleting improved ( < 0.01) both ADG and G:F, resulting in ADG above PC pigs. In Exp. 4, 980 pigs (12.0 ± 0.3 kg BW) were fed 1 of 7 diets in a 28-d trial in a 2 × 3 + 1 factorial arrangement. The 7 treatments were based on 3 diets fed in meal or pellet form: 1) PC (< 0.5 mg/kg DON), 2) NC (3 mg/kg DON), and 3) NC + 0.25% Defusion. Treatment 7 was Diet 3 with supplemental nutrients in pellet form. No interactions were observed between pelleting and Defusion. Pigs fed the NC had decreased ( < 0.01) ADG and ADFI, and pelleting improved ( < 0.01) ADG to PC levels, driven by improved ( < 0.01) G:F. Adding nutrients or Defusion had no effect. Overall, these studies show that Defusion and pelleting can help overcome some of the negative effects of DON, whereas other feed additives and additional nutrients do not.

Effects of preslaughter feed withdrawal time on finishing pig carcass, body weight gain, and food safety characteristics in a commercial environment.

The effects of feed withdrawal time before slaughter on finishing pig carcass composition were evaluated in 2 studies. In Exp. 1, 728 pigs (BW = 128.9 ± 1.2 kg) were allotted to 1 of 4 treatments in a randomized design with number of pigs per pen and location within barn balanced across treatment. The 4 treatments were feed withdrawal times of 8, 24, 36, or 48 h and there were 12 replicate pens per treatment. Before feed withdrawal, pigs were fed a standard corn-soybean meal diet containing dried distillers grains with solubles (DDGS), bakery coproducts, and 5.0 mg/kg ractopamine HCl. Feed withdrawal time decreased (linear; P < 0.02) live weight, HCW, and backfat while increasing percentage yield (quadratic; P < 0.01) and fat-free lean index (FFLI; linear; P < 0.001). In Exp. 2, 843 pigs (BW = 125.4 ± 1.6 kg) were used to determine the impact of feed withdrawal on growth, carcass, blood lactate, and meat quality. There were 4 treatments: withholding feed for 8, 12, 24, or 36 h, with 10 replicates per treatment. Pigs were fed a common corn-soybean meal-based diet containing 20% DDGS and 5.0 mg/kg ractopamine HCl. Withholding feed decreased (linear; P < 0.001) live weight, ultimately resulting in decreased (P < 0.01) HCW. There were no differences in FFLI or backfat, but percentage yield (linear; P < 0.001) increased with longer withdrawal times. Carcass contaminations by stomach contents escaping from the oral cavity after shackling (leaking ingesta) or visible fecal contamination of the exterior of the carcass (runny bung) were also measured. Although withholding feed did not affect runny bung, it increased (linear; P < 0.001) the incidence of leaking ingesta, whereas blood lactate, visual color score, and purge loss were unaffected. Withholding feed increased 45-min pH (quadratic; P > 0.02) and ultimate pH (linear; P < 0.01) and increased (quadratic; P < 0.03) visual marbling score. Withholding feed decreased (linear; P < 0.001) feed intake, resulting in feed savings of up to 3 kg/pig. Although several heavyweight pigs were removed before trial commencement and the variable number of remaining pigs per pen may have influenced the response to feed withdrawal, the present data indicates that finishing pigs can experience between 24 and 36 h of feed withdrawal without negatively affecting carcass composition. However, the increased incidence of leaking ingesta beyond 12 h of feed withdrawal is concerning.

Amino acid digestibility and energy concentration of high-protein corn dried distillers grains and high-protein sorghum dried distillers grains with solubles for swine.

A study was conducted to determine the AA digestibility and energy concentration of a specialized high-protein corn distillers dried grains (HPC-DDG) product and a high-protein sorghum dried distillers grains with solubles (HPS-DDGS) product. Six growing barrows (BW = 22.7 kg) were surgically fitted with T-cannulas at the terminal ileum and allotted randomly to 3 treatments in a crossover design with 3 periods. The treatment diets were 1) 67% HPC-DDG and 2) 50% HPS-DDGS as the sole protein sources, and 3) an N-free diet for determining basal endogenous AA loss. All diets contained 0.25% chromic oxide as an inert marker. Digesta and fecal samples were collected and analyzed for AA and energy concentrations. After chemical analysis, standardized and apparent ileal digestible (SID and AID, respectively) AA and GE were determined for each coproduct. The DE, ME, and NE values for HPC-DDG and HPS-DDGS also were calculated. The chemical composition of HPC-DDG and HPS-DDGS on a DM basis was 40.8% CP, 5.4% fat, 22.9% ADF, 36.6% NDF, 0.04% Ca, and 0.42% P and 48.2% CP, 3.1% fat, 17.5% ADF, 20.4% NDF, 0.13% Ca, and 0.82% P, respectively. The DM content of HPC-DDG and HPS-DDGS was 89.50 and 91.88%, respectively. Analyzed AA content of HPC-DDG was greater than that of traditional corn DDGS. The Lys content of HPC-DDG was 1.36% (DM basis), resulting in a Lys-to-CP ratio of 3.2%. In HPS-DDGS, most AA were present in greater proportions than in HPC-DDG or conventional sorghum DDGS. The HPS-DDGS Lys content was 1.7% (DM basis), equivalent to a Lys-to-CP ratio of 3.5%. In HPC-DDG, the AID for Lys, Met, Thr, and Trp were 65.9 ± 1.7, 87.0 ± 1.9, 72.8 ± 3.4, and 76.2% ± 3.5, respectively, and SID values were 67.8 ± 1.7, 87.5 ± 1.9, 75.0 ± 3.5, and 78.6 ± 3.7%, respectively. For HPS-DDGS, the AID for Lys, Met, Thr, and Trp were 51.9 ± 5.3, 73.0 ± 3.1, 60.6 ± 5.3, and 71.7 ± 3.4%, respectively, and SID values were 53.7 ± 4.9, 73.8 ± 3.0, 63.0 ± 4.9, and 73.8 ± 3.0%, respectively. The GE, DE, and calculated ME and NE values were 5,293, 3,703 ± 121, 3,426 ± 121, and 2,131 ± 88 kcal/kg of DM, respectively, for HPC-DDG and 5,108, 3,878, 3,549, and 2,256 kcal/kg of DM, respectively, for HPS-DDGS. Results indicate that both coproducts are well suited for use in swine diets and that actual AA digestibility values and calculated energy concentrations can now be used in swine diet formulation.

Suppressor of cytokine signalling-3 expression inhibits cytokine-mediated destruction of primary mouse and rat pancreatic islets and delays allograft rejection.

AIMS/HYPOTHESIS: The pro-inflammatory cytokines IL-1 and IFNgamma are critical molecules in immune-mediated beta cell destruction leading to type 1 diabetes mellitus. Suppressor of cytokine signalling (SOCS)-3 inhibits the cytokine-mediated destruction of insulinoma-1 cells. Here we investigate the effect of SOCS3 in primary rodent beta cells and diabetic animal models. METHODS: Using mice with beta cell-specific Socs3 expression and a Socs3-encoding adenovirus construct, we characterised the protective effect of SOCS3 in mouse and rat islets subjected to cytokine stimulation. In transplantation studies of NOD mice and alloxan-treated mice the survival of Socs3 transgenic islets was investigated. RESULTS: Socs3 transgenic islets showed significant resistance to cytokine-induced apoptosis and impaired insulin release. Neither glucose-stimulated insulin release, insulin content or glucose oxidation were affected by SOCS3. Rat islet cultures transduced with Socs3-adenovirus displayed reduced cytokine-induced nitric oxide and apoptosis associated with inhibition of the IL-1-induced nuclear factor-kappaB and mitogen-activated protein kinase (MAPK) pathways. Transplanted Socs3 transgenic islets were not protected in diabetic NOD mice, but showed a prolonged graft survival when transplanted into diabetic allogenic BALB/c mice. CONCLUSIONS/INTERPRETATION: SOCS3 inhibits IL-1-induced signalling through the nuclear factor-kappaB and MAPK pathways and apoptosis induced by cytokines in primary beta cells. Moreover, Socs3 transgenic islets are protected in an allogenic transplantation model. SOCS3 may represent a target for pharmacological or genetic engineering in islet transplantation for treatment of type 1 diabetes mellitus.

Suppressor of cytokine signalling (SOCS)-3 protects beta cells against IL-1beta-mediated toxicity through inhibition of multiple nuclear factor-kappaB-regulated proapoptotic pathways.

AIMS/HYPOTHESIS: The proinflammatory cytokine IL-1beta induces apoptosis in pancreatic beta cells via pathways dependent on nuclear factor-kappaB (NF-kappaB), mitogen-activated protein kinase, and protein kinase C. We recently showed suppressor of cytokine signalling (SOCS)-3 to be a natural negative feedback regulator of IL-1beta- and IFN-gamma-mediated signalling in rat islets and beta cell lines, preventing their deleterious effects. However, the mechanisms underlying SOCS-3 inhibition of IL-1beta signalling and prevention against apoptosis remain unknown. METHODS: The effect of SOCS-3 expression on the global gene-expression profile following IL-1beta exposure was microarray-analysed using a rat beta cell line (INS-1) with inducible SOCS-3 expression. Subsequently, functional analyses were performed. RESULTS: Eighty-two known genes and several expressed sequence tags (ESTs) changed expression level 2.5-fold or more in response to IL-1beta alone. Following 6 h of IL-1beta exposure, 23 transcripts were up-regulated. Of these, several, including all eight transcripts relating to immune/inflammatory response pathways, were suppressed by SOCS-3. Following 24 h of IL-1beta exposure, secondary response genes were detected, affecting metabolism, energy generation, protein synthesis and degradation, growth arrest, and apoptosis. The majority of these changes were prevented by SOCS-3 expression. Multiple IL-1beta-induced NF-kappaB-dependent proapoptotic early response genes were inhibited by SOCS-3 expression, suggesting that SOCS-3 inhibits NF-kappaB-mediated signalling. These observations were experimentally confirmed in functional analyses. CONCLUSIONS/INTERPRETATION: This study suggests that there is an unexpected cross-talk between the SOCS/IFN and the IL-1beta pathways of signalling in pancreatic beta cells, which could lead to a novel perspective of blocking two important proapoptotic pathways in pancreatic beta cells by influencing a single signalling molecule, namely SOCS-3.