Abstract
Largemouth bass is sensitive to the dietary starch level and excess starch can induce metabolic liver diseases (MLD). Hepatic fibrosis is a typical pathological phenotype of MLD in largemouth bass, but the molecular basis underlying is largely unclear. This study fed fish with a low or high starch diet for 4 weeks. Liver tissues with or without fibrotic symptoms were recognized through histopathological and molecular markers analysis of hepatic fibrosis, following TMT Quantitative proteomics and conducted Parallel Reaction Monitoring (PRM) analyses. 2455 differentially expressed proteins with 1618 up-regulated and 837 down-regulated were identified in this study. In GO terms, up-regulated proteins were correlated with cytoskeleton organization, supramolecular fiber, cytoskeleton protein binding, and actin-binding, while down-regulated proteins were involved in mainly metabolism-related processes, and molecular binding activity. Down-regulated proteins were enriched in 63 KEGG pathways and concentrated in metabolism-related pathways, especially glucose, lipid, and amino acid metabolism. 70 KEGG pathways of up-regulated proteins mainly included immunity and inflammation-related pathways. The expression trends of 11 differentially expressed proteins were consistent with proteome results by PRM analysis. In conclusion, the development of hepatic fibrosis induced by high starch may be related to multi-signaling pathways, metabolism processes, and targets, which provides important data for further study on revealing the molecular mechanism of hepatic fibrosis.
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More From: Comparative Biochemistry and Physiology Part D: Genomics and Proteomics
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