Study Of The Effect Of Diets Type On Fatty Liver Syndrome In Chicken And The Underlying Epigenetic Mechanisms In Chicken

Fatty liver syndrome(FLS) is a metabolic disease affected by nutrition, genetic and so on. The caged hens show a high incidence and overconditioned hens are prone to occurring in the periods of peak egg production. FLS may decrease egg production and shorten egg peak. It might bring great economic losses to the poultry industry. DNA methylation regulates gene expression at the transcriptional level and is involved in many animal diseases. However, the role of DNA methylation in the formation of FLS is unclear.The 3 × 3 two-factor experiment was conducted to establish an appropriate FLS model in chicken. We selected Jingxinghuang(JXH), Beijingyou and White Leghorn chicken with the same genetic background and weight. The 18-week-old 120 hen and cock in each variety were randomly divided into three groups and fed the basal diet, high fat diet(HFD) and methyl-deficient diet(MDD). For different diets, average daily gross energy intake(ADGEI), average daily gain(ADG), alanine aminotransferase(ALT) was significantly higher in chickens fed HFD(P<0.05). But average feed intake(AFI) decreased significantly(P<0.05). This implies that HFD may cause liver damage, which may be related to the disorder of lipid export. MDD diet also led to ALT increased significantly(P<0.05). For different varieties, ADGEI, ADG, serum triglyceride(TG) and total cholesterol(TCHO) of JXH chickens were significantly higher than other varieties(P<0.05). On account of above results, we conclude JXH chickens may be susceptible to FLS. Meanwhile, MDD and HFD may induce the formation of fatty liver. The 36-week-old JXH chickens fed HFD for 18 weeks results show that the HFD-mediated FLS showed a significant increase in liver relative weight and TG(P<0.05). Besides, serum TG and TCHO of the offspring of FLS cock increased significantly(P<0.05), suggesting that FLS may be inherited by the parent and has effects on offspring lipid metabolism.18-week-old LH and JXH hens were fed MDD that causes fatty liver syndrome for 10 weeks, and the physiological and biochemical parameters, gene expression, and DNA methylation in livers was determined. The development of FLS in hens was accompanied by abnormal lipid accumulation. In JXH chickens, relative expression of acetyl-CoA carboxylase(ACC), fatty acid synthase(FAS) and microsomal triglyceride transfer protein(MTTP) were significantly up-regulated in the FLS group in comparison with the NFLS group(P<0.05). The transcript abundance of sterol regulatory element binding protein 1(SREBP-1c), stearoyl-CoA desaturase(SCD), liver X receptor alpha(LXRα), peroxisome proliferator-activated receptor alpha(PPARα) and peroxisome proliferator-activated receptor gamma(PPARγ) did not differ between the two groups. Interestingly, MTTP and ACC mRNA abundance were negatively correlated with the level of promoter methylation. The extent of DNA methylation of the cytosine-guanine(CpG) sites in the SREBP-1c, FAS, PPARα and LXRα promoter regions was also analyzed by direct sequencing but none differed between FLS and NFLS birds. In LH chickens, relative expression of FAS、ACC、MTTP、SREBP-1c、SCD and PPARγ were significantly up-regulated in the FLS group in comparison with the NFLS group. The transcript abundance of sterol LXRα and PPARα did not differ between the two groups. The extent of DNA methylation in the gene promoter regions did not differ between FLS and NFLS birds.In summary, the model of FLS is successfully established by the feeding experiment. Compared to other varieties, JXH chickens are susceptible to FLS by the above results. Besides, HFD and MDD are likely to induce the formation of FLS. The relationships between FLS and DNA methylation are researched, and the results suggest that DNA methylation may be play a part role in the formation of FLS.