Abstract
Although geese possess an adaptive physiological capacity for lipid storage, few candidate genes contributing to this ability are characterised. By comparing the genomes of individuals with extremely high and low fatty liver weights (FLW), candidate genes were identified, including ARAP2, GABRE, and IL6. Single-nucleotide polymorphisms in or near these genes were significantly (p < 0.05) associated with carcass traits (FLW) and biochemical indexes (very-low-density lipoprotein and N-terminal procollagen III), suggesting contribution to trait variation. A common variant at the 5′-end of LCORL explained ~ 18% and ~ 26% of the phenotypic variance in body weight with/without overfeeding and had significant effects on FLW (p < 0.01). ZFF36L1, ARHGEF1 and IQCJ, involved in bile acid metabolism, blood pressure, and lipid concentration modulation, were also identified. The presence of highly divergent haplotypes within these genes suggested involvement in protection against negative effects from excessive lipids in the liver or circulatory system. Based on this and transcriptomic data, we concluded that geese hepatosteatosis results from severe imbalance between lipid accumulation and secretion, comparable to human non-alcohol fatty liver disease but involving other genes. Our results provided valuable insights into the genesis of geese fatty liver and detected potential target genes for treatment of lipid-related diseases.
Highlights
Geese possess an adaptive physiological capacity for lipid storage, few candidate genes contributing to this ability are characterised
For the indices reflecting blood lipid levels, no correlations were found with fatty liver weights (FLW), five major indices were tested: very-low-density lipoprotein (VLDL), high-density lipoprotein (HDL), low-density lipoprotein (LDL), total cholesterol (TC), and TG (Fig. 1b)
Some genes were not discussed intensively due to ambiguous functions, our results provided us with more insights into the genetic architecture shaping the ability of geese to accumulate lipids in such a short time
Summary
Geese possess an adaptive physiological capacity for lipid storage, few candidate genes contributing to this ability are characterised. The presence of highly divergent haplotypes within these genes suggested involvement in protection against negative effects from excessive lipids in the liver or circulatory system Based on this and transcriptomic data, we concluded that geese hepatosteatosis results from severe imbalance between lipid accumulation and secretion, comparable to human non-alcohol fatty liver disease but involving other genes. The downregulations are likely to suppress inflammation in hepatocytes when geese are subjected to severe hepatic steatosis[18] These findings, at the transcriptional level, increased our understanding for the underpinnings of lipid metabolism in overfed geese, the specific genes responsible for fatty liver formation or lipid metabolism remain ambiguous.
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