Proteome characteristics of liver tissue from patients with parenteral nutrition-associated liver disease

• Main Authors: Gulisudumu Maitiabola, Feng Tian, Haifeng Sun, Li Zhang, Xuejin Gao, Bin Xue, Xinying Wang
• Format: Article
• Language: English
• Published: BMC 2020-06-01
• Series: Nutrition & Metabolism
• Subjects: Parenteral nutrition associated liver disease; Mitochondria; Oxidative phosphorylation; Metabolic disorder; Oxidative stress
• Online Access: http://link.springer.com/article/10.1186/s12986-020-00453-z

Abstract Background Parenteral nutrition (PN)-associated liver disease (PNALD) is a common and life-threatening complication in patients receiving PN. However, its definitive etiology is not yet clear. Therefore, performed proteomic analyses of human liver tissue to explore the same. Methods Liver tissue was derived and compared across selected patients with (n = 3) /without (n = 4) PNALD via isobaric Tag for Relative and Absolute Quantitation (iTRAQ)-based quantitative proteomics. Bioinformatics analysis was performed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) databases to explore the mechanisms of PNALD based on differentially expressed proteins (DEPs). The essential proteins that were differentially expressed between the two groups were explored and verified by western blotting. Results A total of 112 proteins were found to be differentially expressed, of which 73 were downregulated, and 39 were upregulated in the PNALD group. Bioinformatics analysis showed DEPs to be associated with mitochondrial oxidative phosphorylation (mainly involved in mitochondrial respiratory chain complex I assembly), hepatic glycolipid metabolism (involved primarily in glycogen formation and gluconeogenesis), and oxidative stress (mainly involved in antioxidant change). Conclusion Overall, our results indicated that mitochondrial energy metabolism impairment, hepatic glycolipid metabolism disorder, and excessive oxidative stress injury might explain the comprehensive mechanism underlying PNALD. Moreover, we have provided multiple potential targets for further exploring the PNALD mechanism.