Effect of chronic cyclic heat stress and supplemented inorganic and organic zinc source levels on grow-finish pig growth performance and estimated body composition.

Zinc (Zn) supplementation has proved to mitigate the effects of heat stress with varying effects evident with Zn source during acute heat events. However, the effects of Zn supplementation during long-term summer weather patterns have yet to be explored. Therefore, the objective of this study was to identify the effects of supplementation source and level of Zn to mitigate the negative effects of long-term, cyclic heat stress in finishing swine. Six hundred cross-bred pigs were housed under thermoneutral (TN) or cyclic heat (HS) conditions simulating summer heat with acute 3-d heat waves for a 70-d study. Thermoneutral conditions were 16.7 to 18.9 °C throughout the study. HS pigs were housed at the same temperature as TN from days 0 to 18, then 28 °C/24 °C for 12 h/12 h on days 18 to 21, followed by 30 °C/26.7 °C for 12 h/12 h on days 24 to 70, except during acute heat (32 to 33 °C/29 to 30 °C, 12 h/12 h) on days 21 to 24, 42 to 45, and 63 to 66. Treatments were arranged in a 2 × 6 factorial with main effects of environment (HS vs. TN) and dietary available Zn supplementation: (1) 50 mg/kg zinc oxide (ZnO), (2) 130 mg/kg ZnO, (3) 50 mg/kg of organic Zn (Availa Zn), (4) 50 mg/kg ZnO + 40 mg/kg organic Zn, (5) 50 mg/kg ZnO + 60 mg/kg organic Zn, and (6) 50 mg/kg ZnO + 80 mg/kg organic Zn. Pigs (5 pigs/pen) were blocked by initial body weight (72.2 kg) and randomly allotted to 1 of 12 temperature and diet treatment combinations across 10 replicates. Body weight and feed intake were determined at the beginning and end of each acute heat event. All pigs were ultrasonically scanned at the 10th rib (TR) to predict loin muscle area (LMA), backfat (BF), and percent lean. Data were analyzed by the MIXED procedure in SAS with pen as the experimental unit. At day 63, HS pigs were lighter (P < 0.05), had lower overall average daily gain (ADG; P < 0.05) and average daily feed intake (P < 0.05). A diet-by-environment interaction was observed for overall ADG (P < 0.05) with diet 5 HS pigs having a 3.9% reduction in ADG whereas diet 6 had 14.4% reduction in ADG, while under TN temperatures diet 6 had the greatest overall ADG of all treatments. Other diets were intermediate in their ADG under both HS and TN conditions. Pigs under HS had less BF at the TR (P < 0.05) and a smaller LMA (P < 0.05), and a greater calculated percent lean (P < 0.05). Our results indicate that a blend of supplemental Zn sources at 50/60 mg/kg may mitigate the reduction in growth performance due to HS. While not directly contrasted, the NRC requirement of 50 mg/kg Zn may be too low to optimize finishing pig growth performance under both TN and HS conditions.

Interactions between corticotropin releasing factor signaling and prophylactic antibiotics on measures of intestinal function in weaned and transported pigs.

The study objective was to evaluate the interaction between corticotrophin releasing factor (CRF) receptor signaling and prophylactic antibiotic administration on intestinal physiology in newly weaned and transported pigs. Pigs (n = 56; 5.70 ± 1.05 kg) were weaned (20.49 ± 0.64 d), a blood sample was taken, and then pigs were given an intraperitoneal injection of saline (SAL; n = 28 pigs) or a CRF receptor antagonist (CRFA; n = 28 pigs; 30 µg/kg body weight; Astressin B), and then were transported in a livestock trailer for 12 h and 49 min. A second and third intraperitoneal injection was given at 4 h 42 min and 11 h 36 min into the transport process, respectively. Following transport, 4 SAL and 4 CRFA pigs were blood sampled and euthanized. The remaining 48 pigs were individually housed and given dietary antibiotics [AB; n = 12 SAL and 12 CRFA pigs; chlortetracycline (441 ppm) + tiamulin (38.6 ppm)] or no dietary antibiotics (NAB; n = 12 SAL and 12 CRFA pigs) for 14 d post-transport. Blood was collected at 12 h and on d 3, 7, and 14, and then pigs were euthanized on d 7 (n = 24) and d 14 (n = 24) post-weaning and transport. Circulating cortisol was reduced (p = 0.05) in CRFA pigs when compared to SAL pigs post-weaning and transport. On d 7, jejunal villus height and crypt depth was greater overall (p < 0.05) in AB-fed pigs versus NAB-fed pigs. On d 14, ileal crypt depth was reduced (p = 0.02) in CRFA pigs when compared to SAL pigs. Jejunal CRF mRNA abundance tended to be reduced (p = 0.09) on d 7 in CRFA pigs versus SAL pigs. On d 14, jejunal tumor necrosis factor-alpha was reduced (p = 0.01) in AB-fed pigs versus NAB-fed pigs. On d 7, change in glucose short-circuit current tended to be increased (p = 0.07) in CRFA pigs fed the AB diet when compared to CRFA pigs fed the NAB diet. In conclusion, CRFA pigs and pigs fed AB had some similar biological intestinal function measures post-weaning and transport.

The effect of dietary vitamin D supplementation on sodium-dependent phosphate uptake and expression of NaPi-IIb in the small intestine of weanling pigs.

Two experiments were conducted to investigate the effects of 1,25(OH)2D3 to stimulate Na+-dependent phosphate uptake in Caco-2 cells, and the effects of dietary vitamin D supplementation to vitamin D-deficient nursery pigs on Na+-dependent nutrient uptake and mRNA expression of NaPi-IIb cotransporter and calbindin D9k in the jejunum. In Exp. 1, 250,000 Caco-2 cells were seeded on Costar 12 mm Snapwell inserts with a 0.40 µm polycarbonate filter and a seeding density of 0.25 × 106 and studied at 15 d postconfluence. Cells were treated with 10 nM of either 1,25(OH)2D3 or vehicle for 48 h and then mounted in modified Ussing chambers for transepithelial measurements. In Exp. 2, pigs (n = 32) were removed from sows at 3 d of age, placed on a vitamin D-deficient milk replacer diet and housed in a room devoid of sunlight and UV light in the range of 280 to 300 nm. On day 28, serum 25(OH)D3 concentrations were measured to verify low vitamin D status. Pigs (BW 10.10 ± 0.38 kg) were then individually housed day 28 postweaning and allotted to 1 of 2 dietary treatments. Dietary treatments consisted of corn-soybean-based diets with vitamin D supplementations of 0 or 1,500 IU/kg diet for 12 d. Blood samples were taken from the brachiocephalic vein on the initial (day 0) and final day (day 10, 11, or 12) of the study for analysis of serum 25(OH)D3, P, and Ca. Pigs were euthanized and jejunal segments were harvested and used in modified Ussing chambers and for RNA isolation and subsequent quantitative RT-PCR analysis. In Exp. 1, treating Caco-2 cells with 10 nM 1,25(OH)2D3 resulted in a 52% increase (P < 0.005) in Na+-dependent phosphate uptake compared with cells treated with a vehicle. In Exp. 2, Na+-dependent phosphate and glucose transport did not differ (P > 0.10) among treatment groups. Additionally, NaPi-IIb and calbindin D9k mRNA expression were not different (P > 0.10) between treatment groups. No differences (P > 0.10) were detected in final serum P or 25(OH)D3 concentrations between treatments. However, serum Ca linearly increased (P < 0.05) as the concentration of supplemental vitamin D increased in the diet. Overall, while 1,25(OH)2D3 stimulated Na+-dependent phosphate uptake in Caco-2 cells, supplementing diets with 1,500 IU/kg vitamin D3 from cholecalciferol did not increase jejunal Na+-dependent phosphate uptake or NaPi-IIb mRNA expression over that of pigs fed diets with no supplemental cholecalciferol.

Time course determination of the effects of rapid and gradual cooling after acute hyperthermia on body temperature and intestinal integrity in pigs.

Rapid cooling after acute hyperthermia may cause a sustained increase in body temperature and exacerbate intestinal damage in pigs. Therefore, the study objective was to evaluate the temporal effects of rapid and gradual cooling on body temperature response and intestinal integrity after acute hyperthermia in pigs. In three repetitions, 54 pigs [83.3 ± 6.7 kg initial body weight (BW)], balanced by sex were exposed to thermoneutral conditions for 6 h (TN; n = 6 pigs/repetition; 21.1 ± 2.0°C), or heat stress conditions (HS; 39.3 ± 1.6°C) for 3 h, followed by a 3 h recovery period of gradual cooling [HSGC; n = 6 pigs/repetition; gradual decrease from HS to TN conditions] or rapid cooling [HSRC; n = 6 pigs/repetition; rapid TN exposure and cold water (4.0°C) dousing every 30 min for 1.5 h]. Feed was withheld throughout the entire 6 h period, but water was provided ad libitum. Gastrointestinal (TGI) and rectal (TR) temperatures were recorded every 15 min during the HS and recovery periods. Six pigs per repetition (n = 2/treatment) were euthanized and jejunal and ileal samples were collected for histology immediately after (d 0), 2 d after, and 4 d after the recovery period. Data were analyzed using PROC MIXED in SAS 9.4. Overall, rapid cooling reduced TR and TGI (P < 0.01; 0.95°C and 0.74°C, respectively) compared to gradual cooling. Jejunal villus height was reduced overall (P = 0.02; 14.01%) in HSGC compared to HSRC and TN pigs. Jejunal villus height-to-crypt depth ratio was reduced overall (P = 0.05; 16.76%) in HSGC compared to TN pigs. Ileal villus height was reduced overall (P < 0.01; 16.95%) in HSGC compared to HSRC and TN pigs. No other intestinal morphology differences were detected. In summary, HSRC did not cause a sustained increase in body temperature and did not negatively impact biomarkers of intestinal integrity in pigs.

Effects of antibiotic-free pig rearing on ammonia emissions from five pairs of swine rooms in a wean-to-finish experiment.

Antibiotic use and ammonia (NH3) emissions during animal production are two environmental issues of worldwide concern. However, the role of antibiotics on NH3 emissions is still unknown. This study evaluated the effects of rearing pigs without antibiotics on NH3 emissions from a swine experimental building starting with 657 piglets during a wean-to-finish production cycle of 154 days. Pigs were reared in two groups of 10 rooms that were divided into five 2-room pairs (P1-P5) and fed in nine dietary phases. Each pair consisted of one room without antibiotics (no antibiotics in the diet, water, or injectable) and another room as a positive control. Control animals were fed diets containing carbadox-10 (phases 1-4), chlortetracycline (CTC, phase 5), lincomix (phases 6-7), and tylan 40 (phases 8-9). Temperatures in the pig living space and the under-floor manure pit headspace were continuously measured. Ventilation rates at all wall fans and pit fans were obtained by continuous monitoring. Ammonia concentrations in the wall and pit fan exhaust air, and in room inlet air were measured with two multi-gas monitors. Only days that contained at least 18 h of data each day were validated and used. The study generated 1337 room-days of valid data of NH3 emission rates, with a data completeness of 88.6%. Daily mean NH3 emission patterns demonstrated large variations between the paired rooms and among different pairs. Within the individual 2-room pairs, no NH3 emission differences were found in P1 (rooms 1 and 2, p = 0.34) and P2 (rooms 3 and 4, p = 0.44). Significant differences were found in P3-P5 (p < 0.01). The antibiotic-free rooms emitted more NH3 from P3 and P4, but less NH3 from P5. However, the combined cycle mean NH3 emissions from the group of five antibiotic-free rooms and the group of five control rooms were 41.6 ±â€¯10.5 and 39.4 ±â€¯10.6 g d-1 AU-1 (mean ±â€¯standard deviation. AU = 500 kg live body weight), respectively. Therefore, there was no statistical difference in combined cycle mean NH3 emissions from rearing pigs with or without antibiotics (p = 0.78). This study also revealed that experiments with multiple replicates and long NH3 monitoring durations were necessary to avoid potential misinterpretation of experimental results.

Hydrogen sulfide emissions from a swine building affected by dietary crude protein.

Hydrogen sulfide (H2S) is a toxic air pollutant at animal facilities; but the understanding of its generation and emission processes has been limited. This paper studied H2S emissions during a complete cycle of wean-finish pigs from a research building, where 12 pig rooms were divided into three groups that were fed with standard feed (control), and 2.1-3.8% (T1) and 4.4-7.8% (T2) reduced dietary crude protein (CP) feed. The group cycle mean H2S emission rates were 4.0 ± 2.9, 4.3 ± 3.2, and 5.4 ± 4.0 g d-1 AU-1 (Animal Unit = 500 kg live mass), respectively, for the control, T1, and T2 groups. Emissions of H2S were promoted by 10.0 and 36.7%, respectively, for the T1 and T2 groups (p < 0.001), although large variabilities existed in the emissions from different rooms within the same groups. The enhanced H2S emissions from the T1 and T2 groups were related to the reduced manure pH and were possibly affected through a number of pathways, which could involve volatile fatty acids and nitrogen concentrations, and microbial activities in manure.

Preventing, treating, and predicting barbering: A fundamental role for biomarkers of oxidative stress in a mouse model of Trichotillomania.

Barbering, where a "barber" mouse plucks hair from its cagemates or itself, is both a spontaneously occurring abnormal behavior in mice and a well validated model of Trichotillomania (TTM). N-Acetylcysteine, (NAC) a cysteine derived food additive, is remarkably effective in treating TTM patients, but its mechanism of action is unknown. Reactive Oxygen Species (ROS), also known as free radicals, form as a natural byproduct of the normal metabolism of oxygen. Under normal circumstances, cells are able to defend themselves against ROS damage with antioxidant pathways. NAC is the precursor to the main antioxidant produced to defend the brain. Therefore, we hypothesized that barbering is a disease of oxidative stress, whereby ROS and/or a failure of antioxidant defenses leads to neuronal damage that induces barbering in susceptible animals. We tested this hypothesis in 32 female C57BL/6J mice by treating half with 1g/kg BW/day of NAC in their diet, and testing for protection against developing barbering behavior and curing of barbering behavior, and simultaneously testing for a panel of biomarkers of oxidative stress. NAC reduced the chance that mice would be barbers, and this effect did not differ between healthy (i.e. prevention) and affected animals (i.e. cure). Barbering animals had elevated urinary antioxidant capacity, indicative of oxidative stress, at all timepoints. Additionally, after treatment the risk of barbering increased with decreasing hydroxy-2'-deoxyguanosine (8-OHdG) levels, and with increasing glutathione (GSH) and oxidized glutathione (GSSG) levels, further indicating that barbering mice were under oxidative stress regardless of treatment with NAC. We did not find compelling evidence that urinary total antioxidant capacity, or urinary 8-OHdG, could predict response to NAC treatment. We conclude that NAC is effective in preventing and/or curing barbering at least in part by promoting GSH synthesis, thereby preventing oxidative damage.

Mitigation of ammonia emissions from pig production using reduced dietary crude protein with amino acid supplementation.

To mitigate ammonia (NH3) emissions from pig production and understand dynamic emission profiles, reduced dietary crude protein (CP) with amino acid supplementation was studied with 720 pigs in a 12-room research building for 155days that covered from weaned to finishing stages. The pigs were divided into three 4-room groups and fed with 2.1-3.8% reduced CP (T1), 4.4-7.8% reduced CP (T2), and standard (control) diets, respectively. Compared with the control group, T1 and T2 decreased manure volumes and manure NH4+-N concentrations. Group-mean NH3 emission from the control group was 68.9gd-1AU-1 (AU=500kg live mass). Emissions from T1 (46.7gd-1AU-1) and T2 (29.8gd-1AU-1) were reduced by 33.0% and 57.2% (p<0.05), respectively. Dynamic peak NH3 emissions appeared during the third nursery phase for T1 and T2, but delayed to the first grower phase for the control group.

Effect of High-Calcium Diet on Coronary Artery Disease in Ossabaw Miniature Swine With Metabolic Syndrome.

BACKGROUND: Calcium is a shortfall essential nutrient that has been a mainstay of osteoporosis management. Recent and limited findings have prompted concern about the contribution of calcium supplementation to cardiovascular risk. A proposed mechanism is through the acceleration of coronary artery calcification. Determining causality between calcium intake and coronary artery calcification has been hindered by a lack of sensitive methodology to monitor early vascular calcium accumulation. The primary study aim was to assess the impact of high calcium intake on coronary artery calcification using innovative calcium tracer kinetic modeling in Ossabaw swine with diet-induced metabolic syndrome. Secondary end points (in vitro wire myography, histopathology, intravascular ultrasound) assessed coronary disease. METHODS AND RESULTS: Pigs (n=24; aged ≈15 months) were fed an atherogenic diet with adequate calcium (0.33% by weight) or high calcium (1.90% from calcium carbonate or dairy) for 6 months. Following 5 months of feeding, all pigs were dosed intravenously with (41)Ca, a rare isotope that can be measured in serum and tissues at a sensitivity of 10(-18) mol/L by accelerator mass spectrometry. Kinetic modeling evaluated early coronary artery calcification using (41)Ca values measured in serial blood samples (collected over 27 days) and coronary artery samples obtained at sacrifice. Serum disappearance of (41)Ca and total coronary artery (41)Ca accumulation did not differ among groups. Secondary end points demonstrated no treatment differences in coronary artery disease or function. CONCLUSION: There was no detectable effect of high calcium diets (from dairy or calcium carbonate) on coronary artery calcium deposition in metabolic syndrome swine.

Sodium-dependent phosphate uptake in the jejunum is post-transcriptionally regulated in pigs fed a low-phosphorus diet and is independent of dietary calcium concentration.

In rodents, severe dietary P restriction increases active phosphate absorption by the intestine. However, it remains unknown if moderate dietary P restriction has a similar effect. Weanling pigs (n = 32; body weight 7.4 +/- 0.55 kg) were used in a 2 x 2 factorial design and fed dietary available P (aP) concentrations of 0.23 or 0.40% and Ca concentrations of 0.58 or 1.00% for 14 d. Diets were formulated on an aP basis instead of a total P basis, because pigs are unable to absorb phytate-P present in corn and soybean meal. Jejunal segments were mounted in modified Ussing chambers for determination of Na(+)-dependent nutrient transport. Intestinal mucosal scrapings were taken for RNA isolation and brush border membrane (BBM) vesicle isolation. Na(+)-dependent phosphate uptake and gene expression of Na-phosphate cotransporter IIb (NaPi-IIb), SGLT-1 (sodium/glucose cotransporter-1), and calbindin D(9k) and protein expression of NaPi-IIb were evaluated. Na(+)-dependent phosphate transport increased (P < 0.05) 46% as dietary aP concentration was decreased. However, increased Na(+)-dependent phosphate uptake was not accompanied by increased NaPi-IIb mRNA expression. Expression of NaPi-IIb protein in the BBM increased (P < 0.01) 84% in pigs fed low-P diets compared with pigs fed adequate-P diets. No dietary Ca effects or aP x Ca interactions were detected for Na-dependent P uptake, mRNA or protein expression of NaPi-IIb, or mRNA expression of calbindin D(9k). These data suggest that restricting dietary aP concentration by only 43% stimulates Na(+)-dependent phosphate uptake and expression of the NaPi-IIb protein in the BBM of the small intestine and through a post-transcriptional mechanism.