Abstract
BackgroundDysregulation of adipogenesis causes metabolic diseases, like obesity and fatty liver. Migratory birds such as geese have a high tolerance of massive energy intake and exhibit little pathological development. Domesticated goose breeds, derivatives of the wild greyleg goose (Anser anser) or swan goose (Anser cygnoides), have high tolerance of energy intake resembling their ancestor species. Thus, goose is potentially a model species to study mechanisms associated with adipogenesis.ResultsPhenotypically, goose liver exhibited higher fat accumulation than adipose tissues during fattening (liver increased by 3.35 fold than 1.65 fold in adipose), showing a priority of fat accumulation in liver. We found the number of differentially expressed genes in liver (13.97%) was nearly twice the number of that in adipose (6.60%). These differentially expressed genes in liver function in several important lipid metabolism pathways, immune response, regulation of cancer, while in adipose, terms closely related to protein binding, gluconeogenesis were enriched. Typically, genes like MDH2 and SCD, which have key roles in glycolysis and fatty acids metabolism, had higher fold change in liver than in adipose tissues. Three hundred two differentially expressed long noncoding RNAs involved in regulation of metabolism in liver were also identified. For example, lncRNA XLOC_292762, which was 5.7 kb downstream of FERMT2, a gene involved phosphatidylinositol-3,4,5-trisphosphate binding, was significantly down-regulated after the high-intake feeding period. Further investigation of documented obesity-related orthologous genes in goose suggested that understanding the evolutionary split from mammals in adipogenesis will make goose fatty liver a better resource for future research.ConclusionsOur research reveals that goose uses liver as the major tissue to regulate a distinct lipid synthesis and degradation flux and the dynamic expression network analyses showed numerous layers of positive responses to both massive energy intake and possible pathological development. Our results offer insights into goose adipogenesis and provide a new perspective for research in human metabolic dysregulation.
Highlights
Dysregulation of adipogenesis causes metabolic diseases, like obesity and fatty liver
We identified an average of 77.44% protein-coding genes with FPKM ≥0.1 and 1702 putative long noncoding RNA (lncRNA) (Most lncRNAs were sense intergenic lncRNAs (44.6%), followed by divergent lncRNAs, and other 3 categories, Additional file 2)
The obesity in human was widely considered as a metabolic syndrome in adipose tissues [22], suggesting the important role of adipose tissues in mammals. These results indicated that lipid deposition in goose under high-intake feeding is different from mammals and this distinct difference in lipid deposition in liver and adipose tissues under high-intake feeding, compared to normal intake, implies there may be an intrinsic difference in transcriptional regulation
Summary
Dysregulation of adipogenesis causes metabolic diseases, like obesity and fatty liver Migratory birds such as geese have a high tolerance of massive energy intake and exhibit little pathological development. Excessive energy intake results in an increase in the volume and weight of adipocytes and causes dysregulation of lipid metabolism in the body [2] Such dysregulation is reflected by variable lipid deposition in different adipose tissues, and it is usually associated with abnormal liver lipid accumulation, which can lead to steatosis and obesity [3]. Research has demonstrated that the formation of goose fatty liver shares similar phenotypic changes with human non-alcoholic fatty liver, but differs in pathological development because goose fatty liver only shows a low level of inflammation and other immune responses [7, 9, 10] This distinct difference in the phenotype indicates that goose fatty liver might become a resource for better understanding lipid deposition in birds and for human fatty liver research. We envision that goose is a model for understanding lipid metabolism
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