Genome-wide methylation profile following prenatal and postnatal dietary omega-3 fatty acid supplementation in pigs.

The objective of this study was to determine how prenatal and postnatal dietary omega-3 fatty acids alter white blood cell (leukocyte) DNA methylation of offspring. Fifteen gilts (n = 5 per treatment) were selected from one of three treatments: (i) control diet throughout gestation, lactation and nursery phase (CON); (ii) algal omega-3 fatty acid supplementation enriched in EPA and DHA (Gromega™ ) fed throughout gestation, lactation and nursery phase (Cn3); or (iii) Gromega™ supplementation maternally, during gestation and lactation only, and control diet during the nursery phase (Mn3). At 11 weeks of age and after 8 weeks of post-weaning nursery feeding, buffy coat genomic DNA was subjected to methyl CpG binding protein sequencing. The methylation enriched profile mapped to 26% of the porcine genome. On chromosome 4, a 27.7-kb differentially methylated region downstream of RUNX1T1 was hypomethylated in the Mn3 and Cn3 groups by 91.6% and 85.0% respectively compared to CON pigs. Conversely, hypermethylation was detected in intergenic regions of chromosomes 4 and 12. Regulatory impact factor and differential hubbing methods were used to identify pathways that were coordinately regulated by methylation due to feeding EPA and DHA during pregnancy. Despite limited ability to detect differential methylation, we describe methods that allow the identification of coordinated epigenetic regulation that could not otherwise be detected from subtle single locus changes in methylation. These data provide evidence of novel epigenetic regulation by maternal and early life supplementation of omega-3 fatty acids that may have implications to growth and inflammatory processes.

Carcass composition of market weight pigs subjected to heat stress in utero and during finishing.

Objectives were to investigate the effects of prolonged gestational and/or postnatal heat stress on performance and carcass composition of market weight pigs. Pregnant gilts were exposed to gestational heat stress (GHS, 28°C to 34°C, diurnal) or thermal neutral (18°C to 22°C, diurnal) conditions during the entire gestation or during the first or second half of gestation. At 14 wk of age (58 ± 5 kg), barrows were housed in heat stress (32°C, HS) or thermal neutral (21°C, TN) conditions. Feed intake and BW were recorded weekly, and body temperature parameters were monitored twice weekly until slaughter (109 ± 5 kg). Organs were removed and weighed, and loin eye area (LEA) and back fat thickness (BF) were measured after carcass chilling. Carcass sides were separated into lean, separable fat, bone, and skin components and were weighed. Moisture, lipid, and protein content were determined in the LM at the 10th rib. Data were analyzed using a split plot with random effect of dam nested within gestational treatment. Carcass measurements included HCW as a covariate to control for weight. Planned orthogonal contrast statements were used to evaluate the overall effect of GHS in the first half, second half, or any part of gestation. Gestational heat stress did not alter postnatal performance or most body temperature parameters (P > 0.10). However, ADFI in the finishing period was increased (P < 0.05) in response to GHS, particularly in pigs receiving GHS in the first half of gestation. Gestational heat stress during the first half of gestation decreased head weight as a percent of BW (P = 0.02), whereas GHS in the second half of gestation decreased bone weight as a percent of BW (P = 0.02). Heat stress reduced ADG, BW, and HCW (P < 0.0001). Lean tissue was increased in HS pigs on both a weight and percentage basis (P < 0.0001), but LEA was similar to TN carcasses (P = 0.38). Carcasses from HS barrows also had less carcass separable fat (P < 0.01) and tended to have less BF (P = 0.06) compared with those from TN barrows, even after controlling for HCW. However, percent intramuscular fat did not differ between treatments (P = 0.48). The LM from HS carcasses had a greater moisture to protein ratio (P = 0.04). HS barrows also had decreased heart (P < 0.001) and kidney (P < 0.0001) as a percent of BW compared with TN pigs. In summary, GHS may affect head and bone development, subsequently affecting carcass composition. Chronic HS during finishing results in longer times to reach market weight and a leaner carcass once market weight is achieved.

Heat stress reduces barrier function and alters intestinal metabolism in growing pigs.

High ambient temperature exposure can cause major reductions in intestinal function, pig performance, and, if severe enough, mortality. Therefore, our objective was to examine how acute heat stress (HS) alters growing pig intestinal integrity and metabolism. Individually penned crossbred gilts and barrows (46 ± 6 kg BW) were exposed to either thermal neutral (TN; 21°C; 35 to 50% humidity; n = 8) or HS conditions (35°C; 24 to 43% humidity; n = 8) for 24 h. All pigs had ad libitum access to feed and water. Rectal temperature (Tr), respiration rates (RR), BW, and feed intake (FI) were measured. Pigs were killed after 24 h of environmental exposure and freshly isolated ileum and colon samples were mounted into modified Ussing chambers. Segments were analyzed for glucose and glutamine nutrient transport and barrier integrity [transepithelial electrical resistance (TER) and fluorescein isothiocyanate-labeled dextran transport]. As expected, pigs exposed to HS had an increase in Tr (39.3 vs. 40.9°C; P < 0.01) and RR (52 vs. 119 breaths per minute; P < 0.05). Heat stress decreased FI (53%; P < 0.05) and BW (-2.2 kg; P < 0.05) compared to TN pigs. Compared to TN pigs, mucosal heat shock protein 70 increased (101%; P < 0.05) whereas intestinal integrity was compromised in the HS pigs (ileum and colon TER decreased 52 and 24%, respectively; P < 0.05). Furthermore, serum endotoxin concentrations increased 200% due to HS (P = 0.05). Intestinal glucose transport and blood glucose were elevated due to HS (P < 0.05). However, ileal sucrase and maltase activities decreased in HS pigs (30 and 24%, respectively; P < 0.05). Altogether, these data indicate that high ambient heat loads reduce intestinal integrity and increase circulating endotoxin and stress in pigs. Furthermore, glucose transport and digestive capacity are altered during acute HS.