ArticleNutrition & metabolism2020
Proteome characteristics of liver tissue from patients with parenteral nutrition-associated liver disease.
Article in Nutrition & metabolism, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 8 citations in OpenAlex.
- Integrated transcriptomics-metabolomics analysis reveals biomarkers and metabolic dysregulation characteristics of parenteral nutrition-associated liver disease.Frontiers in nutrition · 2026Article
- Cyclic infusion mitigates liver dysfunction associated with continuous total parenteral nutrition in a novel murine model.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Molecular mechanisms and biomarkers of total parenteral nutrition-induced hepatotoxicity revealed by iTRAQ proteomics analysis.International journal of medical sciences · 2025Article
- Identifying and Analyzing Topic Clusters in a Nutri-, Food-, and Diet-Proteomic Corpus Using Machine Reading.Nutrients · 2023Review
- Changes in the intestinal expression of drug metabolism-related genes in a piglet model of parenteral nutrition.Nutrition & metabolism · 2022Article
- Deciphering the Protein, Modular Connections and Precision Medicine for Heart Failure With Preserved Ejection Fraction and Hypertension Based on TMT Quantitative Proteomics and Molecular Docking.Frontiers in physiology · 2021Article
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundParenteral 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.
methodsLiver tissue was derived and compared across selected patients with (
resultsA 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).
conclusionOverall, 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.
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