GC-TOF-MS-Based Metabolomics Analyses of Liver and Intestinal Contents in the Overfed vs. Normally-Fed Geese.

Abstract

Simple SummaryNon-alcoholic fatty liver disease has been considered as one of the most important causes of liver disease, and it is a threat to human and animal health worldwide. Interestingly, goose fatty liver can reach 8–10 times the weight of normal liver with no overt pathological symptoms, suggesting that there are some protective mechanisms. Scientists have indicated that gut microbiota participate in the formation of non-alcoholic fatty liver disease in human and mammalian animals. However, it is unclear whether gut microbiota and their metabolites contribute to goose fatty liver. The aim of the present study was to investigate the metabolomic analyses of liver and intestinal contents in overfed vs. normally fed geese. The results showed that the formation of goose fatty liver is accompanied by obvious changes in the metabolic profiles of liver and intestinal contents. The intestinal metabolites can affect the formation of goose fatty liver by affecting the metabolisms of glucose and fatty acid, oxidative stress, and inflammatory reactions. These findings provide a basis for future work addressing the relationship between intestinal metabolites and the development of non-alcoholic fatty liver disease.No overt pathological symptoms are observed in the goose liver with severe steatosis, suggesting that geese may host unique protective mechanisms. Gas chromatography time-of-flight mass spectrometry-based metabolomics analyses of liver and intestinal contents in overfed vs. normally fed geese (26 geese in each treatment) were investigated. We found that overfeeding significantly changed the metabolic profiles of liver and intestinal contents. The differential metabolites mainly belong to fatty acids, amino acids, organic acids, and amines. The differential metabolites were involved in glycolysis/gluconeogenesis, glycerolipid metabolism, the pentose phosphate pathway, fatty acid degradation, the sphingolipid signaling pathway, and the biosynthesis of unsaturated fatty acids. Moreover, we determined the biological effects of arachidonic acid (ARA) and tetrahydrocorticosterone (TD) in goose primary hepatocytes and intestinal cells. Data showed that the mRNA expression of arachidonate 5-lipoxygenase (ALOX5) in goose primary intestinal cells was significantly induced by 0.50 mM ARA treatment. Cytochrome P-450 27A1 (CYP27A1) mRNA expression was significantly inhibited in goose primary hepatocytes by 1 µM TD treatment. In conclusion, the formation of goose fatty liver is accompanied by significant changes in the metabolic profiles of liver and intestinal contents, and the changes are closely related to the metabolisms of glucose and fatty acids, oxidative stress, and inflammatory reactions.