RESUMEN
To understand the effects of vitamin A on lipid deposition in rice field eels, integrated liver transcriptome and metabolome were conducted and the changes in the genes and metabolites were assessed. Three groups of rice field eel were fed with 0, 200, and 16,000 IU/kg vitamin A supplementations in their diets for 70 days. The total lipid content in the whole body of the rice field eels was significantly increased with the vitamin A supplementations (p < 0.05). Comparative transcriptome analysis revealed 14 pathways and 46 differentially expressed genes involved in lipid metabolism. Sphingolipid metabolism, glycerolipid metabolism, primary bile acid biosynthesis and steroid hormone biosynthesis were significantly enriched pathways. In these pathways, three differential genes phospholipid phosphatase 1a (PLPP1a), phospholipid phosphatase 2b (PLPP2b), cytochrome P450 21a2 (CYP21a2) were consistent with the change trend of lipid content, and the other three differential genes aldo-keto reductase family 1 member D1 (AKR1D1), uridine diphosphate glucuronic acid transferase 1a1 (UGT1a1), cytochrome P450 1a (CYP1a) were opposite. Metabolomic analysis revealed that primary bile acid biosynthesis, sphingolipid metabolism, steroid hormone biosynthesis and biosynthesis of unsaturated fatty acids were all critical for rice field eel metabolic changes in response to vitamin A. Six important differential metabolites (eicosapentaenoic acid, sphinganine, 11-beta-hydroxyprogesterone, hydroxyeicosatetraenoic acid, cholic acid, and glycochenodeoxycholate) were identified and have provided new insights into how vitamin A regulates lipid deposition. Integrated transcriptome and metabolome analyses revealed that primary bile acid biosynthesis was the only remarkably enriched pathway in both the transcriptome and metabolome while that sphingosine was the main metabolite. Based on the above results, we have concluded that vitamin A promotes lipid deposition in the rice field eel through the primary bile acid synthesis pathway, and lipid deposits are widely stored in cell membranes, mainly in the form of sphingosine. These results will provide reference data to help improve our understanding of how vitamin A regulates lipid metabolism.
RESUMEN
A high-carbohydrate diet lowers the rearing cost and decreases the ammonia emission into the environment, whereas it can induce liver injury, which can reduce harvest yields and generate economic losses in reared fish species. Macroalgae Saccharina japonica (SJ) has been reported to improve anti-diabetic, but the protective mechanism of dietary SJ against liver injury in fish fed a high-carbohydrate diet has not been studied. Therefore, a 56-day nutritional trial was designed for swamp eel Monopterus albus, which was fed with the normal diet [20% carbohydrate, normal carbohydrate (NC)], a high carbohydrate diet (32% carbohydrate, HC), and a HC diet supplemented with 2.5% SJ (HC-S). The HC diet promoted growth and lowered feed coefficient (FC), whereas it increased hepatosomatic index (HSI) when compared with the NC diet in this study. However, SJ supplementation increased iodine contents in muscle, reduced HSI, and improved liver injury, such as the decrease of glucose (GLU), total bile acid (TBA), and alanine aminotransferase (ALT) in serum, and glycogen and TBA in the liver. Consistently, histological analysis showed that SJ reduced the area of lipid droplet, glycogen, and collagen fiber in the liver (p < 0.05). Thoroughly, the underlying protective mechanisms of SJ supplementation against HC-induced liver injury were studied by liver transcriptome sequencing coupled with pathway analysis. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis of the differentially expressed genes (DEGs), such as the acetyl-coenzyme A synthetase (acss1), alcohol dehydrogenase (adh), interferon-induced protein with tetratricopeptide repeats 1 (ifit1), aldo-keto reductase family 1 member D1 (akr1d1), cholesterol 7-alpha-monooxygenase (cyp7a1), and UDP-glucuronosyltransferase (ugt), indicated that the pathway of glycolysis/gluconeogenesis was the main metabolic pathway altered in the HC group compared with the NC group. Meanwhile, hepatitis C, primary BA biosynthesis, and drug metabolism-cytochrome P450 were the three main metabolic pathways altered by SJ supplementation when compared with the HC group. Moreover, the BA-targeted metabolomic analysis of the serum BA found that SJ supplementation decreased the contents of taurohyocholic acid (THCA), taurochenodeoxycholic acid (TCDCA), taurolithocholic acid (TLCA), nordeoxycholic acid (NorDCA), and increased the contents of ursocholic acid (UCA), allocholic acid (ACA), and chenodeoxycholic acid (CDCA). In particular, the higher contents of UCA, ACA, and CDCA regulated by SJ were associated with lower liver injury. Overall, these results indicate that the 2.5% supplementation of SJ can be recommended as a functional feed additive for the alleviation of liver injury in swamp eel-fed high-carbohydrate diets.