ABSTRACT
Objective: Environmental factors can influence obesity by epigenetic mechanisms. The aim of this study was to investigate obesity-related epigenetic changes and the potential for reversal of these changes in the liver of Göttingen minipigs subjected to diet interventions. Methods: High-throughput liquid hybridization capture-based bisulfite sequencing (LHC-BS) was used to quantify the methylation status of gene promotor regions in liver tissue in three groups of male castrated Göttingen minipigs: a standard chow group (SD, N = 7); a group fed high fat/fructose/cholesterol diet (FFC, N = 10) and a group fed high fat/fructose/cholesterol diet during 7 months and reversed to standard diet for 6 months (FFC/SD, N = 12). Expression profiling by qPCR of selected metabolically relevant genes was performed in liver tissue from all pigs. Results: The pigs in the FFC diet group became morbidly obese. The FFC/SD diet did not result in a complete reversal of the body weight to the same weight as in the SD group, but it resulted in reversal of all lipid related metabolic parameters. Here we identified widespread differences in the patterning of cytosine methylation of promoters between the different feeding groups. By combining detection of differentially methylated genes with a rank-based hypergeometric overlap algorithm, we identified 160 genes showing differential methylation in corresponding promoter regions in the FFC diet group when comparing with both the SD and FFC/SD groups. As expected, this differential methylation under FFC diet intervention induced de-regulation of several metabolically-related genes involved in lipid/cholesterol metabolism, inflammatory response and fibrosis generation. Moreover, five genes, of which one is a fibrosis-related gene (MMP9), were still perturbed after diet reversion. Conclusion: Our findings highlight the potential of exploring diet-epigenome interactions for treatment of obesity.
ABSTRACT
Given the increase in sow mortality in Danish pig herds over the last 10 years, we have investigated the causes of spontaneous death and killing of sows, especially those due to locomotive disorders. A total of 265 culled sows (93 spontaneously dead sows and 172 killed sows) from 10 different herds were sent for complete necropsy, and grouped according to primary diagnoses. From 35 of these sows, tissue for histological evaluation and samples for bacteriological cultivation were also collected, and secondary diagnoses and body condition were recorded. The main causes for killing were related to the locomotive system (72%), arthritis (24%) and fractures (16%) being the most frequent lesions. The main causes of spontaneous death were related to the gastrointestinal system and spleen (45%) and the reproductive system (24%). Arthrosis was a secondary diagnosis in 88% of the killed sows and in 92.5% of the spontaneously dead sows. Arcanobacterium pyogenes was the main cause of arthritis. The killed sows had significantly lower body condition compared with spontaneously dead sows. The first two parities and the time around farrowing were associated with the highest mortality in both groups. Hopefully, these observations can guide breeding units attempting to monitor, control and reduce sow mortality.
