Insights into the influence of three types of sugar on goose fatty liver formation from endoplasmic reticulum stress (ERS)

This study analyzed the formation of goose fatty liver due to endoplasmic reticulum stress (ERS) caused by 3 types of sugar. Transcriptome analysis was performed for liver tissues from geese fed a traditional diet (maize flour), geese overfed with traditional diet, and geese overfed with diet supplemented with glucose, fructose, or sucrose. Correlation analysis of the liver tissue transcriptomes showed that differentially expressed genes (DEGs) involved in ERS were signifi- cantly negatively correlated with DEGs involved in inflammation response in the sucrose overfeeding group, and significantly positively correlated with the DEGs involved in lipid metabolism in fructose overfeeding group. Goose primary hepatocytes were isolated in vitro and then treated with glucose or fructose. Some were also treated with ERS inhibitor 4-phenylbutyric acid (4PBA). In the hepatocytes, mRNA expression of X -Box Binding Protein 1 (XBP1), activating transcription factor 6 (AFT6) and glucose -regulated protein 78 (GRP78) genes increased in the two sugar groups (glucose and fructose), but were suppressed by adding 4PBA. The mRNA expression data, protein kinase contents, and triglyceride (TG) and very low -density lipoprotein (VLDL) concentrations all suggest that ERS regulates lipid deposition induced by glucose and fructose via elevating lipid synthesis, inhibiting fatty acid oxidation, and decreasing lipid transportation. In conclusion, glucose, or fructose cause ERS and then ERS causes lipid deposition in goose primary hepatocytes. Three types of sugar cause lipid accumulation and then lipid accumulation prevents ERS during goose fatty liver formation, which suggests a potential mechanism protects goose livers from ERS. The different sugars may induce lipid deposition in different ways.