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ABSTRACT: To explore the differences in foie gras performance between geese raised in cages and on the ground, we conducted an integrative analysis of liver transcriptome and gut microbial metagenomes. The results showed extremely significant differences in the liver weight (P < 0.01) and liver lipid accumulation of FRS and CRS groups. The levels of triglyceride (TG), high-density lipoprotein cholesterol (HDL-C) and low-density lipoprotein cholesterol (LDL-C) of CRS were significantly higher than those of FRS (P < 0.05). Transcriptome analysis showed that 3,917 upregulated and 1,395 downregulated genes were identified, and lipid metabolism pathway and fatty acid metabolism were significantly enriched. Analysis of cecum microbiota revealed that several inflammation-related bacteria (including Gallibacterium, Escherichia-Shigella, Desulfovibrio, Alistipes, and Fournierella) were enriched in CRS, while beneficial bacteria (including Lactobacillus, Limosilactobacillus, and Ligilactobacillus) were significantly enriched in FRS. In conclusion, CRS was better than FRS in foie gras production, which was more conducive to lipid deposition in the goose liver.

ABSTRACT: 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 significantly 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 (4-PBA). 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 4-PBA. 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.

To comprehensively provide insight into goose fatty liver formation, we performed an integrative analysis of the liver transcriptome, lipidome, and amino acid metabolome, as well as peripheral adipose tissue transcriptome analysis using samples collected from the overfed geese and normally fed geese. Transcriptome analysis showed that liver metabolism pathways were mainly enriched in glucolipid metabolism, amino acid metabolism, inflammation response, and cell cycle; peripheral adipose tissue and the liver cooperatively regulated liver lipid accumulation during overfeeding. Liver lipidome patterns obviously changed after overfeeding, and 157 different lipids were yielded. In the liver amino acid metabolome, the level of Lys increased after overfeeding. In summary, this is the first study describing goose fatty liver formation from an integrative analysis of transcriptome, lipidome, and amino acid metabolome, which will provide a whole new dimension to understanding the mechanism of goose fatty liver formation.

ABSTRACT: Our previous study described the mechanism of goose fatty liver formation from cell culture and transcriptome. However, how lipidome of goose liver response to overfeeding is unclear. In this study, we used the same batch of geese (control group and corn flour overfeeding group) to explore the lipidome changes and underlying metabolic mechanisms of goose fatty liver formation. Liquid chromatography-mass spectrometry (LC-MS) was provided to lipidome detection. Liver lipidomics profiles analysis was performed by principal component analysis (PCA), partial least squares-discriminant analysis (PLS-DA) and orthogonal partial least squares-discriminant analysis (OPLS-DA), different lipids were identified and annotated, and the enriched metabolic pathways were showed. The results of PCA, PLS-DA, and OPLS-DA displayed a clear separation and discrimination between control group and corn flour overfeeding group. Two hundred and fifty-one different lipids were yielded, which were involved in triglyceride (TG), diglyceride (DG), phosphatidic acids (PA), phosphatidylinositols (PI), phosphatidylethanolamines (PE), phosphatidylcholines (PC), lyso-phosphatidylcholines (LPC), monogalactosylmonoacylglycerol (MGMG), sphingolipids (SM), ceramides (Cer), and hexaglycosylceramides (Hex1Cer). Different lipids were enriched in glycerophospholipid metabolism, glycerolipid metabolism, phosphatidylinositol signaling system, inositol phosphate metabolism, glycosylphosphatidylinositol (GPI)-anchor biosynthesis and sphingolipid metabolism. In conclusion, this is the first report describing the goose fatty liver formation from lipidomics, this study might provide some insights into the underlying glucolipid metabolism disorders in the process of fatty liver formation.

To further explore the fructose pro-steatosis mechanism, we performed an integrative analysis of liver transcriptome and lipidome as well as peripheral adipose tissues transcriptome analysis using samples collected from geese overfed with maize flour (control group) and geese overfed with maize flour supplemented with 10% fructose (treatment group). Overfeeding period of the treatment group was significantly shorter than that of the control group (p < 0.05). Dietary supplementation with 10% fructose induced more severe steatosis in goose liver. Compared with the control group, the treatment group had lower in ceramide levels (p < 0.05). The key differentially expressed genes (DEGs) (control group vs. treatment group) involved in liver fatty acid biosynthesis and steroid biosynthesis were downregulated. The conjoint analysis between DEGs and different lipids showed that fatty acid biosynthesis and steroid biosynthesis were the highest impact score pathways. In conclusion, fructose expedites goose liver lipid accumulation maximization during overfeeding.

ABSTRACT: Previous research in our lab showed that 10% glucose, 10% fructose, and 10% sucrose can induce lipid deposition in goose fatty liver formation process more efficiently. However, whether the overfeeding diet supplement with sugar can affect the meat quality is unclear. The aim of this research was to estimate the meat quality of geese overfed with overfeeding diet adding with different types of sugar. The results indicated there were no significant differences in the diameter of muscle fiber, the muscle fiber density, pH0, pH24, the meat color, the cooking loss, the drip loss, the shear force and the dry matter in breast muscle and thigh muscle between corn flour groups and three sugars groups (P > 0.05). The crude fat content of breast muscle in fructose group was significantly higher than that in sucrose group (P < 0.05); the inosinic acid content of leg muscle in fructose group was significantly higher than that in the sucrose group (P < 0.05); the ratios of essential amino acids to total amino acids (EAA/TAA) in the breast muscle of maize flour group, fructose group, sucrose group and glucose group were 42%, 35%, 32% or 34%;57%, 64%, 64%, and 62%, respectively; the ratios of essential amino acids to total amino acids in leg muscle of maize flour group, fructose group, sucrose group and glucose group were 31%, 33%, 35%, and 34%, respectively. The contents of C16:1 and C18:1 n-9c in breast muscle in fructose group were significantly higher than that in sucrose group (P < 0.05). Compared with maize flour group, the contents of C18:0 and C20:0 were lower in leg muscle of sugar group (P < 0.05). Compared with the maize flour group, the activities of hydrogen peroxide (H2O2) and glutathione peroxidase (GSH-PX) in breast muscle were higher than those of sucrose group (P < 0.05), the total antioxidant capacity (T-AOC) levels in breast muscle was higher than that of fructose group and sucrose group (P < 0.05). Cluster analysis and principal component analysis (PCA) showed that there was no difference in meat quality between maize flour and sugar group. In conclusion, the overfeeding with maize flour supplement with 10% sugar had no evident influence on the meat quality.

ABSTRACT: Early research in our lab indicated that the effect of glucose, fructose and sucrose on the levels of triacylglycerol, and inflammatory factor was significantly different, and it is speculated that the regulatory mechanism of lipid deposition by different type of sugar in the liver is different. In order to explore lipid deposition difference mediated by different types of sugar (glucose, fructose, and sucrose) in goose fatty liver formation, this experiment was performed from cell culture, overfeeding experiment, and transcriptome analysis at 3 levels. Cell culture experiment results indicated that the levels of intracellular triglyceride, total cholesterol, and lipid content of fructose and sucrose treatment were significantly higher than those of glucose treatment (P < 0.05). In slaughter performance, the liver weight, the ratio of liver weight to body weight, feed conversion ratio (liver weight/feed consumption) were better in sucrose overfeeding group (P < 0.05). In addition, the liver of the sucrose overfeeding group contained a lot of unsaturated fatty acids, especially (n-3) polyunsaturated fatty acids (P < 0.05). Transcriptome analysis shown that the peroxisome proliferators-activated receptor (PPAR) signaling pathway is highly enriched in the fructose and sucrose overfeeding groups; cell cycle, and DNA replication pathways were highly enriched in the glucose overfeeding group. In conclusion, due to the decrease of lipids outward transportation and the anti-inflammation of unsaturated fatty acids, fructose, and sucrose have better ability to induce steatosis in goose fatty liver formation.

Summary: To explore the role of insulin and forkhead box protein O1 (FoxO1) on cell proliferation regulated by sirtuin 1 (Sirt1) in goose primary hepatocyte, goose primary hepatocytes were isolated and incubated with Sirt1 inhibitor and nicotinamide, and then, some hepatocytes were transfected with FoxO1 interference plasmid or treated with insulin. The indexes related with cell proliferation were measured. The results first showed Sirt1 inhibition induced by nicotinamide increased cell proliferation in goose primary hepatocytes (P 0.05), protein content of p21 (P > 0.05), and cell proliferative index (PI) (67.40 vs. 69.00%). Finally, the PI of cotreatment with nicotinamide and insulin (56.65%) was lower than the single nicotinamide treatment (67.40%); the DNA synthesis rate in cotreatment of nicotinamide and insulin was lower than the single nicotinamide treatment (P