SRP159511 PRJNA489234 GSE119421 Transcriptomic Analysis between Normal and High-intake Feeding Geese Provides Insight into Adipose Deposition and Susceptibility to Fatty Liver in Migratory Birds Geese have a high tolerance of massive energy intake and exhibit little pathological development. We assessed phenotypes and transcriptomes of Tianfu geese to investigate the dynamic expression network behind goose adipogenesis. Goose liver exhibited higher fat accumulation than adipose tissues during fattening. We identified differentially expressed genes that function in several important lipid metabolism pathways, immune response, regulation of cancer, and differentially expressed long noncoding RNAs that might be involved in regulation of these pathways. We found that genes like BGE1 and SCD, which have key roles in glycolysis and synthesis of fatty acids, had higher fold change in liver than in adipose tissue. we suppose that the evolutionary split from mammals in adipogenesis is a result of adaptive evolution to long-distance migration. Overall design: Twenty 126-day-old Tianfu meat geese were randomly assigned to two group (N=10). One group was designed to simulate the high-intake feeding, while the other group was normally fed. The feeding trial was 19 days in total. The high-intake feeding group was given increased amount of dietary across the feeding process. The weight for each goose was recorded every 3 days during the feeding process, and all geese were sacrificed at the end of 19 days. Tissues including liver, abdominal adipose, subcutaneous adipose, heart, breast muscle, leg muscle, duodenum, gizzard, gadular stomach, spleen and bursa of fabricius. Weight for each tissue was recorded and liver, abdonimal adipose as well as subcutaneous adipose were performed red oil staining. Lipid content in liver was quantified by Soxhlet extraction. We chose 3 replicates from each tissue and treatment (in total of 18) and sent them to perform total RNA-seq and subjected the data to further analysis. GSE119421 pubmed 31088359