Effects of long-term hypoxia acclimation on liver glycolipid metabolism in zebrafish (Danio rerio)
WANG Yanxin,XIANG Meng,CHEN Lei,XIAN Chenwei,HU Ruiqin,ZHOU Yan,XU Qianghua*
1.College of Marine Sciences,Shanghai Ocean University,Shanghai 201306,China;2.Key Laboratory of Sustainable Exploitation of Ocean Fisheries Resources,Ministry of Education,Shanghai 201306,China;3.International Research Center for Marine Biosciences,Ministry of Science and Technology,Shanghai 201306,China;4.Key Laboratory of Exploration and Utilization of Aquatic Genetic Resources,Ministry of Education,Shanghai 201306,China
Abstract: To better understanding the effects of long-term hypoxia on hepatic glycolipid metabolism of zebrafish (Daniorerio), changes in the microscopic and ultramicroscopic structure changes and transcriptome were compared between the zebrafish exposed to normoxia (6.5 mg/L±0.2 mg/L) and long-term hypoxia(1.5 mg/L±0.2 mg/L). It was found that non-alcoholic fatty liver disease (NAFLD) pathological phenomena were observed in the fish exposed to long-term hypoxia, including distinct vacuolization, lipid accumulations, mitochondrial swelling, and internal structural disorders in hepatocytes under light and electron microscopic sections. Comparative transcriptomes of normoxic and hypoxic livers revealed that 362 differentially expressed genes (DEGs) were identified. GO (gene ontology) and KEGG (kyoto encyclopedia of genes and genomes) enrichment analysis showed that carbon metabolism, lipid metabolism and PML (promyelocytic leukemia protein) body were significantly enriched among the significant differentially expressed genes. Further correlation analysis revealed that genes enriched in PML body GO term were generally positively correlated with the genes involved in carbon metabolism and fatty acid metabolism pathways, indicating that PML body may act as a protective mechanism to reduce the liver damage caused by long-term hypoxia stress. The findings showed that long-term hypoxia caused abnormal liver glycolipid metabolism and induced the pathology of NAFLD in hepatocytes in zebrafish.