The optimal ratio of omega-6 to omega-3 polyunsaturated fatty acids (PUFAs) is important for keeping the homeostasis of biological processes and metabolism, yet the underlying biological mechanism is poorly understood. The objective of this study was to identify changes in the pig liver transcriptome induced by a diet enriched with omega-6 and omega-3 fatty acids and to characterize the biological mechanisms related to PUFA metabolism.Polish Landrace pigs (n = 12) were fed diet enriched with linoleic acid (LA, omega-6) and α-linolenic acid (ALA, omega-3) or standard diet as a control. The fatty acid profiling was assayed in order to verify how feeding influenced the fatty acid content in the liver, and subsequently next-generation sequencing (NGS) was used to identify differentially expressed genes (DEG) between transcriptomes between dietary groups. The biological mechanisms and pathway interaction networks were identified using DAVID and Cytoscape tools. Fatty acid profile analysis indicated a higher contribution of PUFAs in the liver for LA- and ALA-enriched diet group, particularly for the omega-3 fatty acid family, but not omega-6. Next-generation sequencing identified 3565 DEG, 1484 of which were induced and 2081 were suppressed by PUFA supplementation. A low ratio of omega-6/omega-3 fatty acids resulted in the modulation of fatty acid metabolism pathways and over-representation of genes involved in energy metabolism, signal transduction, and immune response pathways.In conclusion, a diet enriched with omega-6 and omega-3 fatty acids altered the transcriptomic profile of the pig liver and would influence animal health status.Electronic supplementary materialThe online version of this article (doi:10.1186/s12263-016-0517-4) contains supplementary material, which is available to authorized users.
Pigs are faced with various perturbations throughout their lives, some of which are induced by management practices, others by natural causes. Resilience is described as the ability to recover from or cope with a perturbation. Using these data, activity patterns of an individual, as well as deviations from these patterns, can potentially be used to quantify resilience. Dynamic indicators of resilience (DIORs) may measure resilience on a different dimension by calculating variation, autocorrelation and skewness of activity from the absolute activity data. The aim of this study was to investigate the potential of using DIORs of activity, such as average, root mean square error (RMSE), autocorrelation or skewness as indicators of resilience to infection with the Porcine Reproductive and Respiratory Syndrome Virus (PRRSV). For this study, individual activity was obtained from 232 pigs equipped with ear tag accelerometers and inoculated with PRRSV between seven and 9 weeks of age. Clinical scores were assigned to each individual at 13 days post-challenge and used to distinguish between a resilient and non-resilient group. Mortality post-challenge was also recorded. Average, RMSE, autocorrelation and skewness of activity were calculated for the pre-and post-challenge phases, as well as the change in activity level pre-vs. post-challenge (i.e., delta). DIORs pre-challenge were expected to predict resilience to PRRSV in the absence of PRRSV infection, whereas DIORs post-challenge and delta were expected to reflect the effect of the PRRSV challenge. None of the pre-challenge DIORs predicted morbidity or mortality post-challenge. However, a higher RMSE in the 3 days post-challenge and larger change in level and RMSE of activity from pre-to post-challenge tended to increase the probability of clinical signs at day 13 post-infection (poor resilience). A higher skewness post-challenge (tendency) and a larger change in skewness from pre-to post-challenge increased the probability of mortality. A decrease in skewness post-challenge lowered the risk of mortality. The post-challenge DIOR autocorrelation was neither linked to morbidity nor to mortality. In conclusion, results from this study showed that post-challenge DIORs of activity can be used to quantify resilience to PRRSV challenge.
As a result of genetic selection for increased litter size, modern, highly prolific sows often produce large litters with an increased percentage of light birth weight (BiW) piglets compared with less prolific females. However, there is limited information elucidating what proportion of light BiW piglets that express compensatory growth and how these pigs might be identified at a young age. The objective of this study was to analyze the effect of birth weight and early phase growth on preweaning mortality, subsequent growth performance, and carcass characteristics of pigs. Individual records collected on 7,654 commercial crossbred pigs were used for analyses. A segmented regression model was used to analyze the effect of birth weight on preweaning survival and a series of mixed models were used to analyze the effect of birth weight (n = 7,654) group on weights recorded at: weaning (n = 6,777), nursery exit (n = 4,805), and finishing exit (n = 1,417); hot carcass weight (HCW), and lean percentage (n = 4,572). The effect of growth rate group was defined during suckling (< 225 or ≥ 225 g/d) or the nursery phase (< 424 or ≥ 424 g/d). Preweaning mortality, growth rate, BW, and carcass traits were adjusted to a standard age, and ADG and lean percentage were calculated. Results of segmented regression analysis showed that the slope of preweaning mortality on birth weights below 0.99 kg differed (P < 0.05) from the slope of preweaning mortality regressed on birth weights above 0.99 kg. The mixed model analyses showed a positive linear effect (P < 0.05) of BiW and quadratic effect (P < 0.05) of sow parity on age-adjusted finishing weight (FiW), HCW, and lean percentage. The positive influences of increasing BiW were greater (P < 0.05) in age-adjusted FiW and HCW for pigs with slow suckling growth rate compared with those with fast suckling growth rate. Pigs with fast nursery growth rate had greater (P < 0.05) age-adjusted FiW and HCW compared with the slow growing nursery contemporaries. In conclusion, piglets born weighing less than 1 kg were at a higher risk of preweaning mortality than piglets born weighing 1 kg or greater. Light BiW pigs, but not heavy BiW pigs, may lose compensatory growth capability if growth rate during the suckling phase is below the average level.
Background: The level of omega-6 and omega-3 polyunsaturated fatty acids can affect many cellular systems and function via nuclear receptors or the bioactive lipid regulation of gene expression. The objective of this study was to investigate changes in the muscle transcriptome and the biological functions regulated by increased consumption of omega-3 and omega-6 fatty acids in the pig gluteus medius muscle. Results: The transcriptome of the gluteus medius muscle was studied for pigs subjected to either a control diet or a diet supplemented with linseed and rapeseed oil to increase polyunsaturated fatty acid content. Next-generation sequencing (NGS) was used to generate the muscle tissue transcriptome database pointing differentially expressed genes (DEG). Comparative expression analyses identified 749 genes significantly differing at least in the twofold of change between two groups of animals fed with divergent level of omega-3 and omega-6 fatty acids. The expression of 219 genes was upregulated, and the expression of 530 genes was downregulated in the group of pigs supplemented with omega-3 and omega-6 fatty acids in relation to control group pigs. Results of RNA-seq indicated a role of fatty acid in the regulation of the expression of genes which are essential for muscle tissue development and functioning. Functional analysis revealed that the identified genes were important for a number of biological processes including inflammatory response, signaling, lipid metabolism, and homeostasis. Conclusions: Summarizing, obtained results provide strong evidence that omega-6 and omega-3 fatty acids regulate fundamental metabolic processes in muscle tissue development and functioning.
A major QTL for host response to porcine reproductive and respiratory syndrome (PRRS) virus (PRRSV) infection was identified in a previous study. Single nucleotide polymorphism WUR10000125 (WUR), which is in complete linkage disequilibrium with the putative causative mutation, can be used as a tag SNP for the QTL. However, the effect of WUR following PRRS vaccination and/or coinfection with other pathogens is not known. Therefore, objectives of this study were to estimate the effect of WUR on host response following PRRS vaccination and coinfection of PRRSV with porcine circovirus type 2b (PCV2b), to estimate genetic parameters for host response to vaccination and coinfection, and to estimate the effect of previously identified candidate SNP under PRRSV-only or PCV2b-only infection on host response to coinfection. Data from 2 trials, comprising a total of 396 commercial crossbred nursery pigs from a single genetic source, were used for all analyses. Pigs were preselected based on WUR genotype: approximately half AA and half AB, where B is the favorable and dominant allele. At weaning, pigs were shipped to Kansas State University, where half of the pigs were vaccinated with a PRRS modified live virus vaccine. Four weeks later, all pigs were coinfected with field strains of PRRSV and PCV2b and followed for 42 d. Body weight and serum viremia measurements were collected following vaccination and coinfection to calculate ADG and viral load (VL), respectively. Average heritability estimates for PRRS VL, PCV2b VL, and ADG were 0.29, 0.09, and 0.40, respectively. After vaccination, AB pigs had lower vaccination VL ( = 0.03) and faster gain ( = 0.004) than AA pigs, as expected. After coinfection, AB pigs had lower PRRSV VL ( < 0.001) but did not significantly differ from AA pigs in growth rate ( = 0.86). For PCV2b VL, suggestive evidence of an interaction between vaccination and WUR genotype ( = 0.11) was detected, where AB pigs had significantly lower PCV2b VL when vaccinated ( = 0.007) but not when they were not vaccinated ( = 0.87). In addition to WUR, several PRRS-associated SNP and a PCV2b-associated SNP had significant effects on host response to coinfection. In conclusion, marker-assisted selection based on WUR genotype alone, or along with other candidate SNP for PRRSV and PCV2b infection, is a promising strategy to select for improved host response to not just PRRS but also coinfection of PRRSV with PCV2b and perhaps other pathogens.
A major QTL for host response to porcine reproductive and respiratory syndrome (PRRS) virus (PRRSV) infection was identified in a previous study. Single nucleotide polymorphism WUR10000125 (WUR), which is in complete linkage disequilibrium with the putative causative mutation, can be used as a tag SNP for the QTL. However, the effect of WUR following PRRS vaccination and/or coinfection with other pathogens is not known. Therefore, objectives of this study were to estimate the effect of WUR on host response following PRRS vaccination and coinfection of PRRSV with porcine circovirus type 2b (PCV2b), to estimate genetic parameters for host response to vaccination and coinfection, and to estimate the effect of previously identified candidate SNP under PRRSV-only or PCV2b-only infection on host response to coinfection. Data from 2 trials, comprising a total of 396 commercial crossbred nursery pigs from a single genetic source, were used for all analyses. Pigs were preselected based on WUR genotype: approximately half AA and half AB, where B is the favorable and dominant allele. At weaning, pigs were shipped to Kansas State University, where half of the pigs were vaccinated with a PRRS modified live virus vaccine. Four weeks later, all pigs were coinfected with field strains of PRRSV and PCV2b and followed for 42 d. Body weight and serum viremia measurements were collected following vaccination and coinfection to calculate ADG and viral load (VL), respectively. Average heritability estimates for PRRS VL, PCV2b VL, and ADG were 0.29, 0.09, and 0.40, respectively. After vaccination, AB pigs had lower vaccination VL ( = 0.03) and faster gain ( = 0.004) than AA pigs, as expected. After coinfection, AB pigs had lower PRRSV VL ( < 0.001) but did not significantly differ from AA pigs in growth rate ( = 0.86). For PCV2b VL, suggestive evidence of an interaction between vaccination and WUR genotype ( = 0.11) was detected, where AB pigs had significantly lower PCV2b VL when vaccinated ( = 0.007) but not when they were not vaccinated ( = 0.87). In addition to WUR, several PRRS-associated SNP and a PCV2b-associated SNP had significant effects on host response to coinfection. In conclusion, marker-assisted selection based on WUR genotype alone, or along with other candidate SNP for PRRSV and PCV2b infection, is a promising strategy to select for improved host response to not just PRRS but also coinfection of PRRSV with PCV2b and perhaps other pathogens.
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