Effects of dietary supplementation of formaldehyde and crystalline amino acids on gut microbial composition of nursery pigs.

Formaldehyde-based feed additives are approved in the US for Salmonella control and reducing bacterial contamination in animal feed. However, we hypothesize formaldehyde inclusion in swine diets may influence gut microbial composition due to its antimicrobial properties which might negatively influence microbial populations and pig growth performance. Also, formaldehyde inclusion in diets is known to reduce the dietary availability of amino acids. Therefore, our study was conducted to characterize if the effects of feed formaldehyde-treatment are due to influences on microbial population or diet amino acid (AA) sources. Dietary treatments were arranged in a (2 × 2) + 1 factorial with formaldehyde treatment (none vs. 1000 ppm formaldehyde) and crystalline AA inclusion (low vs. high) with deficient AA content plus a positive control diet to contain adequate AA content without dietary formaldehyde. Treating diets with formaldehyde reduced growth rate (P = 0.001) while the AA inclusion had no evidence of impact. Formaldehyde reduced feed bacterial content and altered fecal microbial communities (P < 0.05). Therefore, we conclude that the negative influence on growth was due to the impact on the fecal microbial community. Implications are that strategies for feed pathogen control need to take into account potential negative impacts on the gut microbial community.

The effects of copper source and concentration on growth performance, carcass characteristics, and pen cleanliness in finishing pigs.

A total of 1,143 pigs (PIC 337 × 1050, initially 25.1 ± 0.03 kg BW) were used in a 111-d study to determine the effects of copper sulfate (CuSO; Prince Agri-Products, Quincy, IL) or tribasic copper chloride (TBCC; IntelliBond C; Micronutrients, Indianapolis, IN) on growth performance, carcass characteristics, and pen cleanliness. Pens of pigs were allotted to 1 of 6 dietary treatments, balanced on average pen weight in a randomized complete block design with 25 to 28 pigs per pen and 7 replications per treatment. Treatments included a corn-soybean meal-based diet (corn-soy), a high-by-product diet with 30% distillers dried grains with solubles and 15% bakery meal (by-product diet), and the by-product diet with 75 or 150 mg/kg added Cu from CuSO or TBCC. All diets contained 20 mg/kg Cu from CuSO in the trace mineral premix. At the conclusion of the trial, a digital photo of each pen was taken to allow 3 independent observers to score manure texture and buildup and to assess pen cleanliness prior to power washing. Furthermore, the time required to power wash each pen was also measured. Overall, pigs fed the by-product diet tended to have increased ADFI ( = 0.083) and had decreased G:F ( = 0.005) compared to those fed the corn-soy diet. No Cu source × level interactions or Cu source differences were observed ( > 0.05). From d 0 to 71, pigs fed increasing Cu had increased (quadratic, < 0.05) ADG, d 71 BW, and ADFI. From d 71 to 111, pigs fed increasing Cu tended to have increased ADFI (linear, = 0.068) and decreased G:F (quadratic, = 0.056). Overall (d 0 to 111), increasing Cu increased (linear, < 0.01) ADG, final BW, and ADFI (quadratic, = 0.026). Hot carcass weight increased (linear, = 0.023) by 2.4 kg with increasing Cu. Increasing Cu also increased loin depth (linear, = 0.019) and percentage lean (quadratic, = 0.024). Manure buildup and wash time (s/pen) increased ( < 0.05) for by-product diet pens compared to corn-soy pens; however, neither wash time nor pen cleanliness were influenced by added Cu. In summary, increasing dietary Cu in high-by-product diets improved growth and feed intake, resulting in increased final BW and HCW for pigs fed both Cu sources, without influencing pen wash time.

Effects of distillers dried grains with solubles and added fat fed immediately before slaughter on growth performance and carcass characteristics of finishing pigs.

The addition of dietary fat has been shown to increase HCW and carcass yield in pigs fed low-fiber corn-soy diets; however, data on added fat in high-fiber, low-energy diets is less available. Therefore, the potential for dietary fat to ameliorate the negative effect high-fiber diets have on carcass yield during the last 3 wk before slaughter is of high importance. This experiment was conducted to determine the interactive effects of 30% distillers dried grains with solubles (DDGS) and 5% added fat fed before slaughter on growth performance and carcass characteristics. A total of 1,258 pigs in 2 groups (initially 105.8 ± 0.1 kg BW; group 1 PIC 337 × 1,050; group 2 PIC 327 × 1,050) were used in a 20-d experiment. All pigs were fed a common diet with 30% DDGS until 20 d before slaughter. Then, all pens were weighed and allotted to treatments with 20 replicate pens per treatment. Dietary treatments were arranged in a 2 × 2 factorial with 2 diet types (corn-soybean meal-based with or without 30% DDGS) and added fat (0 or 5%; group 1 = tallow; group 2 = choice white grease). Diets were formulated to a constant standardized ileal digestible Lys:NE ratio. There were no treatment × group interactions for any response criteria. Thus, data for the 2 groups were combined for analysis. Overall, there was a tendency for a diet type × added fat interaction for ADG ( = 0.054), whereas this was significant for G:F ( = 0.008). This was a result of 5% added fat increasing ADG and G:F to a greater magnitude for pigs fed the diet containing 30% DDGS (8.6 and 10.4%, respectively) than for pigs fed the corn-soy diet (2.0 and 2.9%, respectively). Although diet type did not affect final live BW, pigs fed the diet containing DDGS had decreased HCW and carcass yield ( < 0.05). Adding 5% fat did not affect carcass yield. In conclusion, adding 5% fat to finishing pig diets containing 30% DDGS approximately 20 d before slaughter improved ADG and G:F but did not overcome the reduction in carcass yield from feeding DDGS.

Evaluating the impact of maternal vitamin D supplementation: I. Sow performance, serum vitamin metabolites, and neonatal muscle characteristics.

In Exp. 1, 56 gestating sows (PIC 1050; 35 d postinsemination) were used in a 30-d trial to determine serum 25(OH)D response to increasing concentrations of dietary vitamin D. Sows were randomly allotted to 1 of 7 dietary D treatments (200, 800, 1,600, 3,200, 6,400, 12,800, or 25,600 IU of added D per kilogram of complete diet) with 8 sows per treatment. Increasing D increased (quadratic; < 0.001) serum 25(OH)D with the response depicted by the prediction equation: serum 25(OH)D, ng/mL = 35.1746 + (0.002353 × dietary D, IU/d) - (0.0000000156 × dietary D, IU/d). In Exp. 2, 112 sows and their litters were used to determine the effects of dietary vitamin D regimen on sow performance, subsequent preweaning pig performance, neonatal bone and muscle characteristics, and serum vitamin metabolites. Sows were allotted to 1 of 4 dietary treatments 3 to 5 d following breeding: 800, 2,000, or 9,600 IU of D per kilogram of the diet or 50 µg of 25(OH)D (2,000 IU of D equivalent from Hy-D, DSM Nutritional Products, Parsippany, NJ) per kilogram of diet. There were 25 to 27 sows per treatment. Increasing dietary D increased (linear, = 0.001) serum 25(OH)D of sows on d 100 of gestation, at farrowing, and at weaning. Increasing D in sow diets increased piglet serum 25(OH)D at birth (linear, = 0.001) and weaning (quadratic, = 0.033). Sows fed 50 µg of 25(OH)D/kg had intermediate ( < 0.004) serum 25(OH)D concentrations on d 100 of gestation, at farrowing, and at weaning compared with sows fed 2,000 IU of D/kg and sows fed 9,600 IU of D/kg. Pigs from sows fed 50 µg of 25(OH)D/kg had greater serum 25(OH)D compared with pigs from sows fed 2,000 IU of D/kg, but at weaning, serum 25(OH)D concentrations were similar. Also, pigs from sows fed 9,600 IU of D/kg had greater ( = 0.011) serum 25(OH)D at birth and weaning compared with pigs from sows fed 50 µg of 25(OH)D/kg. Maternal performance, litter characteristics, neonatal bone ash content, and neonatal muscle fiber characteristics were largely unaffected by the dietary vitamin D treatments. Overall, D and 25(OH)D are both useful at increasing serum 25(OH)D concentrations, but more D (on an equivalent IU basis) is needed to achieve similar serum 25(OH)D responses compared with feeding 25(OH)D. Concentration of maternal vitamin D supplementation in lactation impacted milk transfer of the vitamin more so than the form of the vitamin, as evidence by the weaned pig serum 25(OH)D concentrations.

Evaluating the impact of maternal vitamin D supplementation on sow performance: II. Subsequent growth performance and carcass characteristics of growing pigs.

A of subsample of 448 growing pigs (PIC 327 × 1050) weaned from 52 sows fed varying dietary vitamin D regimens were used in a split-plot design to determine the effects of maternal and nursery dietary vitamin D on growth performance. Sows were previously administered diets containing vitamin D as vitamin D (800, 2,000, or 9,600 IU/kg) or as 25(OH)D (50 µg [or 2,000 IU vitamin D equivalent]/kg from HyD; DSM Nutritional Products, Parsippany, NJ). Once weaned, pigs were allotted to pens on the basis of previous maternal vitamin D treatment, and then pens were randomly assigned to 1 of 2 nursery vitamin D dietary regimens (2,000 IU of vitamin D/kg or 50 µg 25(OH)D/kg). Pigs remained on nursery vitamin D treatments for 35 d, and then they were provided common finishing diets until market (135 kg). Growing pig serum 25(OH)D suggested that maternal dietary vitamin D influenced ( < 0.001 at weaning) serum concentrations early after weaning, but nursery vitamin D regimen had a larger impact ( < 0.001) on d 17 and 35 postweaning. Overall growth performance was not influenced by nursery vitamin D dietary treatments. From d 0 to 35 in the nursery, pigs from sows fed increasing vitamin D had increased (quadratic, < 0.003) ADG and ADFI, but G:F was similar regardless of maternal vitamin D regimen. Also, pigs from sows fed 50 µg/kg of 25(OH)D had increased ( = 0.002) ADG compared with pigs weaned from sows fed 800 IU of vitamin D. Throughout finishing (d 35 postweaning until 135 kg), ADG was increased (quadratic, = 0.005) and G:F was improved (quadratic, = 0.049) with increasing maternal dietary vitamin D. Also, pigs from sows fed 50 µg/kg of 25(OH)D had increased ( = 0.002) ADG compared with pigs weaned from sows fed 800 IU of vitamin D. Carcass data were collected from a subsample population separate from that used for the growth performance portion of the study, and a total of 642 carcasses from progeny of sows fed the varying dietary vitamin D treatments were used. Live BW of pigs at marketing and HCW were heavier ( < 0.030) for pigs from sows previously fed 25(OH)D compared with pigs from sows fed 9,600 IU of vitamin D. Overall, pigs from sows fed 2,000 IU of vitamin D grew faster after weaning compared with pigs from sows fed 800 or 9,600 IU of vitamin D. Pigs from sows fed 25(OH)D hag greater ADG compared with pigs from sows fed 800 IU of vitamin D, and they had increased final BW and HCW compared with pigs from sows fed 9,600 IU of vitamin D.

Effects of dietary copper, zinc, and ractopamine hydrochloride on finishing pig growth performance, carcass characteristics, and antimicrobial susceptibility of enteric bacteria.

A total of 480 pigs (PIC 327 × 1050; initially 48.7 ± 2.3 kg) were used to determine the interactive effects of supplemental Cu, Zn, and ractopamine HCl (RAC) on finishing pig growth performance, carcass characteristics, and antimicrobial susceptibility of enteric bacteria. Treatments were arranged in a 2 × 2 × 2 factorial with the main effects of added Cu (CuSO; 0 vs. 125 mg/kg Cu), Zn (ZnO; 0 vs. 150 mg/kg Zn), and RAC (0 vs. 10 mg/kg during the last 28 d prior to marketing). All diets contained 11 mg/kg Cu and 73 mg/kg Zn from the trace mineral premix. Pens of pigs were balanced and blocked on initial BW and then randomly allotted to 1 of the 4 mineral treatment diets. At 28 d prior to marketing, pens within each block and mineral treatment were randomly assigned to receive either 0 or 10 mg/kg RAC in addition to the mineral treatment. Adding either Cu or Zn alone did not improve ADG or ADFI yet resulted in numerical improvements in overall G:F and caloric efficiencies, but improvements were not additive (Cu × Zn, = 0.057, = 0.068, and = 0.064 for G:F and caloric efficiency on a ME and NE basis, respectively). Ractopamine improved ( < 0.001) overall ADG, G:F, and caloric efficiency, thereby increasing final BW by 3% with no change in ADFI. Ractopamine also increased ( < 0.001) HCW, percentage carcass yield, G:F, loin depth, and percent fat-free lean and decreased ( = 0.014) backfat. Adding Zn or Cu alone to diets containing RAC numerically improved percent yield and HCW G:F, but this effect was absent when the Cu or Zn was added to the control diet or when Cu and Zn were fed in combination in RAC diets (Cu × Zn × RAC, = 0.011 and = 0.018 for yield and HCW G:F, respectively). Fecal samples were collected on d 0 and at the conclusion of the finishing period (d 90) for bacterial isolation and antimicrobial susceptibility determinations according to Clinical and Laboratory Standards Institute minimal inhibitory concentrations breakpoints. spp. and isolates displayed varying levels of resistance to certain antibiotics prior to initiation of treatments on d 0. Resistance to most antibiotics decreased ( < 0.05) over time or was stable for those that had a low baseline percentage of resistance. Neither Zn nor RAC adversely affected antimicrobial resistance. However, extended feeding of 125 mg/kg Cu throughout the finishing period seems to decrease enterococcal susceptability to tetracycline, tylosin, and quinupristin/dalfopristin.

Influence of dietary fat source and feeding duration on finishing pig growth performance, carcass composition, and fat quality.

A total of 160 finishing pigs (PIC 327 × 1050; initially 45.6 kg) were used in an 84-d experiment to evaluate the effects of dietary fat source and feeding duration on growth performance, carcass characteristics, and carcass fat quality. There were 2 pigs per pen with 8 pens per treatment. The 10 dietary treatments were a corn-soybean meal control diet with no added fat and a 3 × 3 factorial with main effects of fat source (4% tallow, 4% soybean oil, or a blend of 2% tallow and 2% soybean oil) and feeding duration (d 0 to 42, 42 to 84, or 0 to 84). The control corn-soybean meal diet was fed in place of added fat diets when needed for duration treatment purposes. On d 0, 1 pig was identified in each pen and fat biopsy samples of the back, belly, and jowl were collected on d 0, 41, and 81 for fatty acid analysis. At the conclusion of the study, all pigs were harvested, carcass characteristics were determined, and back, belly, and jowl fat samples were collected for analysis. Overall (d 0 to 84), there were no differences among pigs fed the different fat sources for growth and carcass characteristics; however, pigs fed diets with added fat for the entire study had improved ( = 0.036) G:F compared with pigs fed the control diet without added fat. Pigs fed supplemental fat throughout the entire study also had improved ( < 0.05) ADG and G:F as well as heavier d-84 BW ( = 0.006) compared with pigs fed additional fat during only 1 period. Adding fat for the entire study increased ( = 0.032) backfat and tended to reduce ( = 0.079) the fat free lean index compared with pigs fed the control diet without added fat. Added fat also increased ( < 0.05) the iodine value (IV) when compared with pigs fed the control diet. Increasing the feeding duration of soybean oil lowered MUFA and increased PUFA concentrations for all fat depots, whereas these values remained relatively unchanged by the addition of tallow (duration × fat source interactions, < 0.05). Our study failed to show any feeding period × fat source interactions ( < 0.05) in fatty acid composition or IV for jowl fat, whereas this interaction occurred for belly fat and backfat, which would indicate a longer turnover rate for jowl fat. In conclusion, feeding additional fat improved ADG and G:F; however, feeding soybean oil for an increased duration, either alone or in combination with tallow, negatively affected the fatty acid composition and IV of different fat depots.

Effects of diet form and type on growth performance, carcass yield, and iodine value of finishing pigs.

Two experiments were conducted to determine the effects of pelleting, diet type (fat and fiber level), and withdrawal of dietary fiber and fat before marketing on growth performance, carcass yield, and carcass fat iodine value (IV) of finishing pigs. Each experiment used 288 pigs (initially 49.6 and 48.5 kg BW, respectively) with 6 dietary treatments arranged as 2 × 3 factorials. In Exp. 1, main effects were diet form (meal vs. pellet) and diet regimen. Diet regimens were 1) a low-fiber, low-fat (corn-soybean meal) diet from d 0 to 81, 2) a high-fiber, high-fat (30% dried distillers grains with solubles [DDGS] and 19% wheat middlings [midds]) diet from d 0 to 64 followed by the low-fiber, low-fat diet from d 64 to 81 (fiber and fat withdrawal), and 3) the high-fiber, high-fat diet fed from d 0 to 81. Pigs fed pelleted diets had increased ( < 0.05) ADG and G:F compared with those fed meal diets. Pigs fed pelleted diets had increased belly fat IV (2.9 mg/g) compared with those fed meal diets, with a greater increase when fed high-fiber, high-fat diets throughout the entire study (interaction, < 0.05). Pigs fed the low-fiber, low-fat diet throughout had increased ( < 0.001) G:F compared with pigs fed the other 2 treatments. Pigs fed low-fiber, low-fat diets throughout the study or pigs withdrawn from high-fiber, high-fat diets had increased ( < 0.001) carcass yield compared with pigs fed high-fiber, high-fat diets throughout. In Exp. 2, treatment main effects were diet form (meal vs. pellet) and diet type (corn-soybean meal-based control, the control with 30% DDGS and 19% midds, or the control diet with 3% corn oil). The diet containing corn oil was calculated to produce carcass fat IV similar to diets containing DDGS and midds. Overall, pigs fed pelleted diets had increased ( < 0.05) ADG, G:F, and belly fat IV (1.3 mg/g) compared with those fed meal diets. Pigs fed the diets containing DDGS and midds had decreased ( < 0.05) ADG, carcass yield, and HCW compared with pigs fed the control or corn oil diets and decreased ( < 0.001) G:F compared with pigs fed added corn oil. Belly IV was greatest ( < 0.001) for pigs fed diets with DDGS and midds and lowest for pigs fed the control diet, with pigs fed the corn oil diets intermediate. In conclusion, pelleting diets improves pig ADG (approximately 3%) and G:F (approximately 6%); however, a novel finding of this study is that pelleting diets fed to finishing pigs also increases belly fat IV.

Effect of dietary zinc and ractopamine hydrochloride on pork chop muscle fiber type distribution, tenderness, and color characteristics.

A total of 320 finishing pigs (PIC 327 × 1050; initially 98 kg) were used to determine the effects of adding Zn to diets containing ractopamine HCl (RAC) on muscle fiber type distribution, fresh chop color, and cooked meat characteristics. Dietary treatments were fed for approximately 35 d and consisted of a corn-soybean meal-based negative control (CON), a positive control diet with 10 mg/kg of RAC (RAC+), and the RAC+ diet plus 75, 150, or 225 mg/kg added Zn from either ZnO or Availa-Zn. Loins randomly selected from each treatment (n = 20) were evaluated using contrasts: CON vs. RAC+, interaction of Zn level × source, Zn level linear and quadratic polynomials, and Zn source. There were no Zn source effects or Zn source × level interactions throughout the study (P > 0.10). Pigs fed RAC+ had increased (P < 0.02) percentage type IIX and a tendency for increased (P = 0.10) percent type IIB muscle fibers. Increasing added Zn decreased (linear, P = 0.01) percentage type IIA and tended to increase (P = 0.09) IIX muscle fibers. On d 1, 2, 3, 4, and 5 of display, pork chops from pigs fed the RAC+ treatment had greater (P < 0.03) L* values compared to the CON. On d 0 and 3 of display, increasing added Zn tended to decrease (quadratic, P = 0.10) L* values and decreased (quadratic, P < 0.03) L* values on d 1, 2, 4, and 5. Pigs fed RAC+ had decreased (P < 0.05) a* values on d 1 and 4 of display and tended to have decreased (P < 0.10) a* values on d 0 and 2 compared to CON pork chops. Pork chops from the RAC+ treatment had a tendency for increased (P < 0.08) oxymyoglobin percentage compared to CON pork chops on d 1, 2, 4, and 5. On d 0, as dietary Zn increased in RAC+ diets, there was a decrease (linear, P < 0.01) in the formation of pork chop surface oxymyoglobin percentage. Metmyoglobin reducing ability (MRA) of pork chops on d 5 was decreased in the RAC+ group. Chops from pigs fed added Zn had increased (quadratic, P < 0.03) MRA on d 3 and 5 of the display period. There was a trend for increased (linear, P = 0.07) cooking loss with increasing Zn in RAC diets and treatments did not affect tenderness as measured by Warner-Bratzler shear force (P > 0.07). In conclusion, RAC+ diets produced chops that were lighter and less red but maintained a greater percentage of surface oxymyoglobin throughout a 5-d simulated retail display. Ractopamine reduced MRA at the end of the display period, but supplementing Zn to RAC diets restored MRA to near CON treatment levels at the end of the display period.

Effects of dietary L-carnitine and ractopamine HCl on the metabolic response to handling in finishing pigs.

Two experiments (384 pigs; C22 × L326; PIC) were conducted to determine the interactive effect of dietary L-carnitine and ractopamine HCl (RAC) on the metabolic response of pigs to handling. Experiments were arranged as split-split plots with handling as the main plot and diets as subplots (4 pens per treatment). Dietary L-carnitine (0 or 50 mg/kg) was fed from 36.0 kg to the end of the experiments (118 kg), and RAC (0 or 20 mg/kg) was fed the last 4 wk of each experiment. At the end of each experiment, 4 pigs per pen were assigned to 1 of 2 handling treatments. Gently handled pigs were moved at a moderate walking pace 3 times through a 50-m course and up and down a 15° loading ramp. Aggressively handled pigs were moved as fast as possible 3 times through the same course, but up and down a 30° ramp, and shocked 3 times with an electrical prod. Blood was collected immediately before and after handling in Exp. 1 and immediately after and 1 h after handling in Exp. 2. Feeding RAC increased (P < 0.01) ADG and G:F, but there was no effect (P > 0.10) of L-carnitine on growth performance. In Exp. 1 and 2, aggressive handling increased (P < 0.01) blood lactate dehydrogenase (LDH), lactate, cortisol, and rectal temperature and decreased blood pH. In Exp. 1, there was a RAC × handling interaction (P < 0.06) for the difference in pre- and posthandling blood pH and rectal temperature. Aggressively handled pigs fed RAC had decreased blood pH and increased rectal temperature compared with gently handled pigs, demonstrating the validity of the handling model. Pigs fed RAC had increased (P < 0.01) LDH compared with pigs not fed RAC. Pigs fed L-carnitine had increased (P < 0.03) lactate compared with pigs not fed L-carnitine. In Exp. 2, pigs fed RAC had lower (P < 0.02) blood pH immediately after handling, but pH returned to control levels by 1 h posthandling. Lactate, LDH, cortisol, and rectal temperature changes from immediately posthandling to 1 h posthandling were not different (P > 0.10) between pigs fed L-carnitine and those fed RAC, indicating that L-carnitine did not decrease recovery time of pigs subjected to aggressive handling. These results suggest that pigs fed 20 mg/kg of RAC are more susceptible to stress when handled aggressively compared with pigs not fed RAC. Dietary L-carnitine fed in combination with RAC did not alleviate the effects of stress. This research emphasizes the importance of using proper animal handling techniques when marketing finishing pigs fed RAC.

Interactive effects of dietary ractopamine HCl and L-carnitine on finishing pigs: I. Growth performance.

A total of 2,152 pigs (C22 × 336 PIC) were used in 4 experiments to determine the interactive effects of dietary l-carnitine and ractopamine HCl (RAC) on finishing pig growth performance. All trials were arranged as factorial arrangements with main effects of l-carnitine (0, 25, or 50 mg/kg in Exp. 1 and 2 and 0 or 50 mg/kg in Exp. 3 and 4) and RAC (0, 5, or 10 mg/kg in Exp. 1 and 0 or 10 mg/kg in Exp. 2, 3, and 4). Dietary carnitine was fed from 38 to 109 kg (Exp. 1 and 3) or for the last 4 or 3 wk before slaughter (118 kg; Exp. 2 and 4, respectively). Ractopamine HCl was fed for 4 wk (Exp. 1, 2, and 3) or 3 wk (Exp. 4) before slaughter. Experiments 1 and 2 were conducted in university research facilities, and Exp. 3 and 4 were conducted in a commercial research facility. All diets were formulated to contain 1.00% total Lys during the last phase of each experiment. In all experiments, pigs fed RAC had increased (P < 0.05) ADG and G:F compared with pigs fed no RAC. Feeding l-carnitine before the RAC feeding period did not affect pig growth performance. In Exp. 1 and 2, l-carnitine did not affect ADG during the last 4 wk; however, in Exp. 2, G:F tended (quadratic; P = 0.07) to improve with increasing l-carnitine. In Exp. 3, l-carnitine × RAC interactions were observed (P < 0.04) for ADG and G:F. Both added l-carnitine and RAC improved performance, but the response was not additive. In Exp. 4, pigs fed l-carnitine had increased (P < 0.04) ADG (0.88 vs. 0.84 kg) and G:F (0.36 vs. 0.35) compared with pigs fed no l-carnitine, and the response was additive to that of RAC. Analysis of treatments common to all experiments showed that pigs fed RAC had increased (P < 0.01) ADG (1.03 vs. 0.93 kg) and G:F (0.40 vs. 0.35) compared with pigs fed no RAC. Pigs fed l-carnitine tended to have increased (P = 0.07) ADG (1.00 vs. 0.96 kg) and improved (P < 0.01) G:F (0.38 vs. 0.37) compared with pigs not fed l-carnitine. These results confirm that RAC improves growth performance of finishing pigs. Added l-carnitine improved growth performance of finishing pigs, and the greatest response was observed in Exp. 3 and 4, which were conducted in commercial research environments. These experiments imply that adding l-carnitine to a finishing diet does not enhance the growth effects of RAC and that effects of RAC and l-carnitine on ADG and G:F are independent.

Interactive effects of dietary ractopamine HCl and L-carnitine on finishing pigs: II. Carcass characteristics and meat quality.

Three experiments using 1,356 pigs (C22 × 336 PIC) were conducted to determine the interactive effects of dietary L-carnitine and ractopamine hydrochloride (RAC) on carcass characteristics and meat quality of finishing pigs. Experiments were arranged as factorials with main effects of L-carnitine and RAC; L-carnitine levels were 0, 25, or 50 mg/kg in Exp. 1 and 2 and 0 or 50 mg/kg in Exp. 3, and RAC levels of 0, 5, or 10 mg/kg in Exp. 1 and 0 or 10 mg/kg in Exp. 2 and 3. Dietary L-carnitine was fed from 38 kg to slaughter (109 and 118 kg in Exp. 1 and 3, respectively) or for 4 wk before slaughter (109 kg in Exp. 2). Ractopamine HCl was fed for 4 wk in all experiments. Exp. 1 and 2 were conducted at university research facilities (2 pigs per pen), and Exp. 3 was conducted in a commercial research barn (23 pigs per pen). In Exp. 1, an L-carnitine × RAC interaction (P < 0.02) was observed for LM visual color, L*, and a*/b*. In pigs fed RAC, increasing L-carnitine decreased L* and increased visual color scores and a*/b* compared with pigs not fed RAC. Ultimate pH tended to increase (linear, P < 0.07) with increasing L-carnitine. Drip loss decreased (linear, P < 0.04) in pigs fed increasing L-carnitine. In Exp. 2, firmness scores decreased in pigs fed increasing L-carnitine when not fed RAC, but firmness scores increased and drip losses decreased with increasing L-carnitine when RAC was added to the diet (L-carnitine × RAC interaction, P < 0.04). Percentage lean was greater (P < 0.01) for pigs fed RAC in Exp. 2. In Exp. 3, fat thickness decreased and lean percentage increased in pigs fed L-carnitine or RAC, but the responses were not additive (L-carnitine × RAC interaction, P < 0.03). Furthermore, pigs fed L-carnitine tended (P < 0.06) to have decreased LM drip loss percentage whereas pigs fed RAC had decreased (P < 0.05) 10th rib and average backfat and decreased drip loss than pigs fed diets without RAC. These results suggest that dietary RAC increased carcass leanness and supplemental L-carnitine reduced LM drip loss when fed in combination with RAC.

Effects of L-carnitine supplementation on quality characteristics of fresh pork bellies from pigs fed 3 levels of corn oil.

Crossbred pigs (n = 216) were used to test the effect of supplemental L-carnitine (CARN) on the fatty acid composition and quality characteristics of fresh pork bellies from pigs fed diets formulated with different inclusion levels of corn oil. Pigs were blocked by BW (43.6 ± 1.0 kg) and allotted randomly to pens of 6 pigs within blocks. Then, within blocks, pens were assigned randomly to 1 of 6 dietary treatments in a 2 × 3 factorial arrangement, with either 0 or 100 mg/kg of supplemental CARN and 3 dietary inclusion levels (0, 2, or 4%) of corn oil (CO). When the lightest block weighed 125.0 kg, all pigs were slaughtered, and left-side bellies were captured during carcass fabrication for quality data collection. Fresh pork bellies were evaluated for length, width, thickness, and firmness (bar-suspension and Instron-compression methods) before a 2.5-cm-wide strip of belly was removed and subsequently dissected into subcutaneous fat, primary lean (latissimus dorsi), secondary lean (cutaneous trunci), and intermuscular fat for fatty acid composition determination. Although belly length, width, and thickness of fresh pork bellies were not affected by CARN (P ≥ 0.128) or CO (P ≥ 0.073), belly firmness decreased linearly (P < 0.001) with increasing dietary CO, but there was no (P ≥ 0.137) effect of CARN on any belly firmness measure. Dietary CARN increased (P < 0.05) the proportion of total SFA in the intermuscular fat layer, increased (P < 0.05) the proportion of total MUFA in the primary and secondary lean layers, and decreased (P < 0.05) the proportion of total PUFA in the intermuscular fat and secondary lean layers of pork bellies. Moreover, the SFA and MUFA compositions decreased linearly (P < 0.001) with increasing dietary CO, and the rate of the decrease in SFA composition was greater (P < 0.001) in the fat layers than the lean layers. Conversely, the PUFA content increased linearly (P < 0.001) with increasing dietary CO, and the rate of the increase in PUFA was greater (P < 0.001) in the fat than the lean layers, and greater (P = 0.022) in the primary than secondary lean layer. Results from this study would indicate that differences in the amount and rate of fatty acid deposition associated with feeding increased amounts of CO, along with moisture differences among the belly layers, combine to negatively affect fresh pork belly firmness.

Effects of feeding L-carnitine to gilts through day 70 of gestation on litter traits and the expression of insulin-like growth factor system components and L-carnitine concentration in foetal tissues.

We investigated the influence of supplemental L-carnitine on foetal blood metabolites, litter characteristics, L-carnitine concentration in skeletal muscle and insulin-like growth factor (IGF) axis components in foetal hepatic and skeletal muscle tissues at day 40, 55 and 70 of gestating gilts. A total of 59 gilts (body weight = 137.7 kg) received a constant feed allowance of 1.75 kg/day and a top-dress containing either 0 or 50 ppm of L-carnitine starting on the first day of breeding through the allotted gestation length. Foetuses from the gilts fed diets with L-carnitine tended to be heavier (p = 0.06) and the circulating IGF-II tended to be lower (p = 0.09) at day 70, compared with the foetuses from the control gilts. Insulin-like growth factor-I messenger RNA (mRNA) was lower (p = 0.05) in hepatic tissue in the foetuses collected from gilts fed L-carnitine. Free and total carnitine concentration increased (p < 0.05) in the skeletal muscle from the foetuses collected from gilts fed supplemental L-carnitine. This study showed that L-carnitine had beneficial effects on the average foetal weight at day 70 of gestation, associated with changes in the foetal IGF system.

Dietary L-carnitine affects periparturient nutrient metabolism and lactation in multiparous cows.

The objectives of this study were to determine the effects of dietary L-carnitine supplementation on liver lipid accumulation, hepatic nutrient metabolism, and lactation in multiparous cows during the periparturient period. Cows were assigned to treatments at d -25 relative to expected calving date and remained on the experiment until 56 d in milk. Treatments were 4 amounts of supplemental dietary carnitine: control (0 g/d of L-carnitine; n = 14); low carnitine (LC, 6 g/d; n = 11); medium carnitine (MC, 50 g/d; n = 12); and high carnitine (HC, 100 g/d; n = 12). Carnitine was supplied by mixing a feed-grade carnitine supplement with 113.5 g of ground corn and 113.5 g of dried molasses, which was then fed twice daily as a topdress to achieve desired daily carnitine intakes. Carnitine supplementation began on d -14 relative to expected calving and continued until 21 d in milk. Liver and muscle carnitine concentrations were markedly increased by MC and HC treatments. Milk carnitine concentrations were elevated by all amounts of carnitine supplementation, but were greater for MC and HC than for LC during wk 2 of lactation. Dry matter intake and milk yield were decreased by the HC treatment. The MC and HC treatments increased milk fat concentration, although milk fat yield was unaffected. All carnitine treatments decreased liver total lipid and triacylglycerol accumulation on d 10 after calving. In addition, carnitine-supplemented cows had higher liver glycogen during early lactation. In general, carnitine supplementation increased in vitro palmitate beta-oxidation by liver slices, with MC and HC treatments affecting in vitro palmitate metabolism more potently than did LC. In vitro conversion of Ala to glucose by liver slices was increased by carnitine supplementation independent of dose. The concentration of nonesterified fatty acids in serum was not affected by carnitine. As a result of greater hepatic fatty acid beta-oxidation, plasma beta-hydroxybutyric acid was higher for the MC and HC treatments. Serum insulin was greater for all carnitine treatments, although plasma glucose was unaffected. Plasma urea N was lower and plasma total protein was higher for the MC and HC treatments. By decreasing liver lipid accumulation and stimulating hepatic glucose output, carnitine supplementation might improve glucose status and diminish the risk of developing metabolic disorders during early lactation.

Effects of breeder hen age and dietary L-carnitine on progeny embryogenesis.

1. Ross 308 broiler breeder hens were given diets containing 0 or 25 mg L-carnitine/kg (8 replications per treatment) from 21 weeks of age. 2. Hens were inseminated with semen from Ross broiler breeder males. In a common facility, subsequent progeny hatchability and embryonic mortality at 25, 30, 32, and 38 weeks of breeder age were evaluated. 3. Subsequent egg component weights, incubational egg water loss, progeny embryo growth, and embryo, yolk sac and liver composition through 18 d of incubation at 27, 32, and 38 weeks of breeder age were evaluated. 4. Calculated additions of L-carnitine were in agreement with analysed contents of 3.5 and 31.1 mg free L-carnitine/kg of diet, respectively, and total L-carnitine concentrations increased by 48.6, 21.7, and 10.0% in 0-d yolk, 18-d yolk sac, and 18-d liver samples, respectively, due to the addition of dietary L-carnitine. 5. Supplemental L-carnitine resulted in increased (0.6%) relative 0-d egg yolk weight across weeks 27, 32, and 38, and reduced (0.38%) 18-d yolk sac palmitoleic acid concentration at week 27 without altering embryogenesis. 6. In conclusion, dietary L-carnitine (25 mg/kg of the diet) was deposited in the yolks of broiler breeder hens and was subsequently transferred to the embryonic liver via yolk sac absorption through 18 d of incubation. Furthermore, dietary L-carnitine supplementation increased ovarian follicle yolk deposition in 27-, 32-, and 38-week-old breeder hens, and influenced yolk sac fatty acid beta-oxidation in embryos from 27-week-old breeder hens causing yolk sac palmitoleic acid concentrations to be reduced by 18 d of incubation.

Effect of L-carnitine infusion and feed restriction on carnitine status in lactating Holstein cows.

Previously we determined that abomasal infusion of L-carnitine increased in vitro hepatic fatty acid oxidation, decreased liver lipid accumulation, and supported higher fat-corrected milk yield in feed-restricted lactating cows. The objectives of this study were to examine the effects of supplemental L-carnitine and amount of feed intake on free carnitine and carnitine ester concentrations in liver, muscle, milk, and plasma of lactating dairy cows. Eight lactating Holstein cows (132 +/- 36 d in milk) were used in a replicated 4 x 4 Latin square design with 14-d periods to test factorial combinations of water or L-carnitine infusion (20 g/d; d 5 to 14) and ad libitum or restricted (50% of previous 5-d intake; d 10 to 14) dry matter intake. Plasma was obtained 3 times daily on d 4, 8, and 12; milk samples were collected on d 8, 9, 13, and 14. Liver and muscle were biopsied on d 14 of each period. Free carnitine, short-chain acylcarnitine, and long-chain acylcarnitine concentrations were determined using a radioenzymatic assay coupled with ion exchange chromatography. Abomasal L-carnitine infusion increased total carnitine in plasma on d 8 and d 12. All liver carnitine fractions were increased by carnitine infusion. Feed restriction elevated concentrations of free carnitine, long-chain acylcarnitine, and total carnitine in liver tissue from carnitine-infused cows but not in those infused with water. In muscle, acid-soluble carnitine, long-chain acylcarnitine, and total carnitine concentrations were increased by carnitine infusion and feed restriction without significant interaction. Feed restriction increased free carnitine concentrations in muscle from water-infused cows but not in carnitine-infused cows. Carnitine infusion increased the concentration of each milk carnitine fraction as well as milk carnitine output on d 8 to 9. On d 13 to 14, all carnitine fractions except short-chain acylcarnitine were increased in milk from water-infused, feed-restricted cows, whereas all fractions were increased in carnitine-infused, feed-restricted cows. Carnitine infusion increased total carnitine in plasma, liver, muscle, and milk during feed restriction, whereas feed restriction alone increased carnitine concentrations in muscle and milk but not in liver. Liver carnitine concentrations might limit hepatic fatty acid oxidation capacity in dairy cows during the periparturient period; therefore, supplemental L-carnitine might decrease liver lipid accumulation in periparturient cows.

Growth characteristics, blood metabolites, and insulin-like growth factor system components in maternal tissues of gilts fed L-carnitine through day seventy of gestation.

A total of 59 gilts (BW = 137.7 kg) from 3 breeding groups were used to assess the effects of feeding l-carnitine during gestation on gilt growth characteristics, blood metabolites, and uterine and chorioallantoic expression of IGF axis components at d 40, 55, and 70 of gestation. Experimental treatments were arranged in a 2 x 3 factorial, with main effects of added l-carnitine (0 or 50 ppm) and day after initial breeding (d 40, 55, or 70 of gestation). All gilts received a constant feed allowance of 1.75 kg/d and a top-dress containing 0 or 50 ppm of l-carnitine beginning on the first day of breeding through the assigned day of gestation. No dietary treatment differences were observed for gilt BW, backfat, or estimated protein or fat mass at any day of gestation. No differences were observed in circulating total and free carnitine at breeding, but concentrations increased (P < 0.01) as day of gestation increased for gilts fed diets containing l-carnitine compared with those fed the control diet. Maternal IGF-I concentration decreased (P < 0.01) from d 0 to 70 for all gilts, with no differences between treatments. Insulin-like growth factor binding protein-3 mRNA (P = 0.05) and IGFBP-5 mRNA (P = 0.01) increased in the endometrium of gilts supplemented with l-carnitine. These data demonstrate that l-carnitine supplementation and day of gestation alter the expression of the IGF axis by changing the expression of IGFBP at the fetal-maternal interface in swine. These changes in the IGF axis at the fetal maternal interface may aid in determining the reasons for the effects of l-carnitine on reproductive traits.

Metabolic effects of abomasal L-carnitine infusion and feed restriction in lactating Holstein cows.

L-Carnitine is required for mitochondrial fatty acid oxidation, but the effects of carnitine supplementation on nutrient metabolism during dry matter intake depression have not been determined in dairy cows. Studies in other species have revealed responses to L-carnitine that may be of specific benefit to dairy cows during the periparturient period. Eight lactating Holstein cows (132 +/- 36 d in milk) were used in a replicated 4 x 4 Latin square experiment with 14-d periods. Treatments were factorial combinations of abomasal infusion of either water or L-carnitine (20 g/d; d 5 to 14) and either ad libitum or restricted intake (50% of previous 5-d dry matter intake; d 10 to 14) of a balanced lactation diet. Liver and muscle biopsies were obtained on d 14 of each period. Feed restriction induced negative balances of energy and metabolizable protein. In feed-restricted cows, carnitine infusion increased 3.5% fat-corrected milk yield compared with those infused with water. Total carnitine concentration in liver was increased in feed-restricted cows infused with carnitine but not in feed-restricted cows infused with water. Carnitine infusion stimulated in vitro oxidation of [1-(14)C] palmitate to acid-soluble products and decreased the proportion of [1-(14)C] palmitate that was converted to esterified products by liver slices. Feed-restricted cows infused with carnitine had lower liver total lipid concentration and tended to have decreased triglyceride accumulation compared with feed-restricted cows infused with water. Plasma nonesterified fatty acid concentration was not altered by carnitine infusion but was increased by feed restriction; serum beta-hydroxybutyric acid was increased by carnitine infusion in feed-restricted cows. In cows fed for ad libitum intake, carnitine infusion affected beta-hydroxybutyric acid, insulin, and urea N in serum, liver glycogen concentration, and in vitro alanine oxidation by liver slices, suggesting that hepatic and peripheral nutrient metabolism was influenced. L-Carnitine infusion effectively decreased liver lipid accumulation during feed restriction as a result of greater capacity for hepatic fatty acid oxidation. Further research examining dietary supplementation of L-carnitine during the periparturient period is warranted.

Effects of L-carnitine on fetal growth and the IGF system in pigs.

The effects of L-carnitine on porcine fetal growth traits and the IGF system were determined. Fourth-parity sows were fed a gestation diet with either a 50-g top dress containing 0 (control, n = 6) or 100 mg of L-carnitine (n = 6). At midgestation, fetuses were removed for growth measurements, and porcine embryonic myoblasts (PEM) were isolated from semitendinosus. Real-time quantitative PCR was used to measure growth factor messenger RNA (mRNA) levels in the uterus, placenta, muscle, hepatic tissue, and cultured PEM. A treatment x day interaction (P = 0.02) was observed for maternal circulating total carnitine. Sows fed L-carnitine had a greater (P = 0.01) concentration of total carnitine at d 57 than control sows. Circulating IGF-I was not affected (P = 0.55) by treatment. Supplementing sows with L-carnitine resulted in larger (P = 0.02) litters (15.5 vs. 10.8 fetuses) without affecting litter weight (P = 0.07; 1,449.6 vs. 989.4 g) or individual fetal weight (P = 0.88) compared with controls. No treatment effect was found for muscle IGF-I (P = 0.36), IGF-II (P = 0.51), IGFBP-3 (P = 0.70), or IGFBP-5 (P = 0.51) mRNA abundance. The abundance of IGF-I (P = 0.72), IGF-II (P = 0.34), and IGFBP-3 (P = 0.99) in hepatic tissue was not influenced by treatment. Uterine IGF-I (P = 0.46), IGF-II (P = 0.40), IGFBP-3 (P = 0.29), and IGFBP-5 (P = 0.35) mRNA abundance did not differ between treatments. Placental IGF-I (P = 0.30), IGF-II (P = 0.18), IGFBP-3 (P = 0.94), and IGFBP-5 (P = 0.42) mRNA abundance did not differ between treatments. There was an effect of side of the uterus for IGF-I (P = 0.04) and IGF-II (P = 0.007) mRNA abundance; IGF-I mRNA abundance was greater in the left uterine horn than in the right uterine horn (0.14 and 0.07 relative units, respectively). Placental IGF-II mRNA abundance was greater (P = 0.007) in the left than in the right uterine horn (483.5 and 219.59, respectively). The abundance of IGFBP-3 was not affected by uterine horns in either uterine (P = 0.66) or placental (P = 0.13) tissue. There was no treatment difference for IGF-I (P = 0.31) or IGFBP-5 (P = 0.13) in PEM. The PEM isolated from sows fed L-carnitine had decreased IGF-II (P = 0.02), IGFBP-3 (P = 0.03), and myogenin (P = 0.04; 61, 59, and 67%, respectively) mRNA abundance compared with controls. These data suggest that L-carnitine supplemented to gestating sows altered the IGF system and may affect fetal growth and development.