Fatty liver is a widespread disease in chickens that causes a decrease in egg production and even death. The characteristics of the inherited phenotype of acquired fatty liver and the molecular mechanisms underlying it, however, are largely unknown. In the current study, fatty liver was induced in 3 breeds by a high-fat (HF) diet and a methionine choline-deficient (MCD) diet. The results showed that the dwarf Jingxing-Huang (JXH) chicken was more susceptible to fatty liver compared with the layer White Leghorns (WL) and local Beijing-You (BJY) breeds. In addition, it was found that the paternal fatty livers induced by HF diet in JXH chickens were inherited. Compared to birds without fatty liver in the control group, both offsprings and their sires with fatty livers in the paternal group exhibited altered hepatic gene expression profiles, including upregulation of several key genes involved in fatty acid metabolism, lipid metabolism and glucose metabolism (ACACA, FASN, SCD, ACSL5, FADS2, FABP1, APOA4 and ME1). This study uniquely revealed that acquired fatty liver in cocks can be inherited. The hepatic gene expression profiles were altered in chickens with the inherited phenotype of acquired paternal fatty liver and several genes could be candidate biomarkers.

This study investigated the effects of CCHMA on growth performance, slaughter performance, serum biochemical indicators, intestinal morphology and microbiota of Zi goose. Initially, it was determined the optimal addition concentration of CCHMA to be 3 g/kg by the first feeding experiment. Then, 78 Zi geese were divided into control and CCHMA supplemented groups. The results showed that the body weight (BW) and average daily gain (ADG) of the CCHMA supplemented group was significantly increased (p < 0.05), and the feed/gain (F/G) of the CCHMA supplemented group was significantly decreased (p < 0.05) compared with the control group. The dressed yield percentage in the CCHMA supplemented group significantly increased by 0.78% (p < 0.05). Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were significantly lower in the CCHMA fed birds than in the control group (p < 0.05). Further, 16S rDNA gene sequencing conducted for cecal flora composition found that 3 g/kg CCHMA significantly increased the abundance of beneficial bacteria (CHKCI001, Colidextribacter and Subdoligranulum) (p < 0.05; p < 0.01) and suppressing harmful bacteria (Bacteroidetes and Methanobrevibacter) (p < 0.05) in the cecum of Zi goose. In conclusion, adding 3 g/kg of CCHMA in the diet can improve the growth performance, slaughter performance of Zi goose, and optimize the cecum microflora.

Goose meat is consumed by consumers because it contains a relatively high proportion of polyunsaturated fatty acids (PUFAs). This study was conducted to explore the main differences in production performance, breast meat quality traits, and cecal microbiota compositions between the Zi goose (ZG) and Xianghai flying goose (FG). The production performance and breast meat quality trait analyses showed that compared with the ZG, the FG had a higher right breast muscle index, ileum villi height/crypt depth ratio (VH/CD), and cecum fermentation rate (higher short-chain fatty acid (SFCA) concentration); a lower abdominal fat index; a higher proportion of PUFAs; and a lower shear force. Spearman’s correlation coefficients between the cecal microbiota composition and production performance indexes suggested that the genus Faecalibacterium was positively associated with production performance; in contrast, the genus Candidatus Saccharimonas was negatively correlated with production performance; moreover, the Ruminococcus torques group, Parasutterella, and Methanobrevibacter were negatively related to the VH/CD. Taken together, in this particular trial, FG had better production performance, healthier meat quality traits, and better intestinal digestion and absorption capacities than ZG. These results not only provide a useful data reference for the production of healthy geese for human consumption but can also help guide the utilization of goose breed resources.

Chickens are one of the most important sources of meat worldwide, and the occurrence of fatty liver syndrome (FLS) is closely related to production efficiency. However, the potential mechanism of FLS remains poorly understood. An integrated analysis of data from whole-genome bisulfite sequencing and long noncoding RNA (lncRNA) sequencing was conducted. A total of 1177 differentially expressed genes (DEGs) and 1442 differentially methylated genes (DMGs) were found. There were 72% of 83 lipid- and glucose-related genes upregulated; 81% of 150 immune-related genes were downregulated in fatty livers. Part of those genes was within differentially methylated regions (DMRs). Besides, sixty-seven lncRNAs were identified differentially expressed and divided into 13 clusters based on their expression pattern. Some lipid- and glucose-related lncRNAs (e.g., LNC_006756, LNC_012355, and LNC_005024) and immune-related lncRNAs (e.g., LNC_010111, LNC_010862, and LNC_001272) were found through a co-expression network and functional annotation. From the expression and epigenetic profiles, 23 target genes (e.g., HAO1, ABCD3, and BLMH) were found to be hub genes that were regulated by both methylation and lncRNAs. We have provided comprehensive epigenetic and transcriptomic profiles on FLS in chicken, and the identification of key genes and epigenetic markers will expand our understanding of the molecular mechanism of chicken FLS.

Low-density lipoprotein receptor-related protein 1 (LRP1) is an important signal protein that is widely involved in physiological processes, such as

The liver of poultry is the primary site of lipid synthesis. The excessive production of lipids accumulates in liver tissues causing lipid metabolism disorders, which result in fatty liver disease and have a transgenerational effect of acquired phenotypes. However, its specific mechanisms have not yet been fully understood. In this study, the differentially expressed miR-375 as well as its target gene MAP3K1 (mitogen-activated protein kinase kinase kinase 1) were screened out by interaction network analysis of microRNA sequencing results and transcriptome profiling in the fatty liver group of the F0–F3 generation (p < 0.05 or p < 0.01). Furthermore, the results showed that the number of lipid droplets and triglyceride content were significantly decreased after upregulation of miR-375 in primary hepatocyte culture in vitro (p < 0.05 or p < 0.01). The MAP3K1 knockdown group exhibited the opposite trends (p < 0.05 or p < 0.01). P53, Bcl-x, PMP22, and CDKN2C related to cell proliferation were significantly upregulated or downregulated after knocking down MAP3K1 (p < 0.05). This research uniquely revealed that silencing miR-375 inhibits lipid biosynthesis and promotes cell proliferation, which may be due to the partial regulation of the expression level of MAP3K1, thereby further participating in the transgenerational inheritance process of regulating liver lipid metabolism. These results reveal the pathogenesis of fatty liver in noncoding RNA and provide good candidate genes for breeding progress of disease resistance in chickens.