Deciphering the metabolic perturbation in hepatic alveolar echinococcosis: a 1 H NMR-based metabolomics study

Background: Hepatic alveolar echinococcosis (HAE) is caused by the growth of Echinococcus multilocularis larvae in the liver. It is a chronic and potentially lethal parasitic disease. Early stage diagnosis for this disease is currently not available due to its long asymptomatic incubation period. In...

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Main Authors: Lin, Caigui, Chen, Zhong, Zhan, Lingqiang, Wei, Zhiliang, Cheng, Kian-Kai, Liu, Yueyue, Shen, Guiping, Fan, Haining, Dong, Jiyang
Format: Article
Language:English
Published: BioMed Central Ltd. 2019
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Online Access:http://eprints.utm.my/id/eprint/96958/1/ChengKianKai2019_DecipheringTheMetabolicPerturbationInHepaticAlveolarEchinococcosis.pdf
http://eprints.utm.my/id/eprint/96958/
http://dx.doi.org/10.1186/s13071-019-3554-0
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Institution: Universiti Teknologi Malaysia
Language: English
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Summary:Background: Hepatic alveolar echinococcosis (HAE) is caused by the growth of Echinococcus multilocularis larvae in the liver. It is a chronic and potentially lethal parasitic disease. Early stage diagnosis for this disease is currently not available due to its long asymptomatic incubation period. In this study, a proton nuclear magnetic resonance (1H NMR)-based metabolomics approach was applied in conjunction with multivariate statistical analysis to investigate the altered metabolic profiles in blood serum and urine samples obtained from HAE patients. The aim of the study was to identify the metabolic signatures associated with HAE. Results: A total of 21 distinct metabolic differences between HAE patients and healthy individuals were identified, and they are associated with perturbations in amino acid metabolism, energy metabolism, glyoxylate and dicarboxylate metabolism. Furthermore, the present results showed that the Fischer ratio, which is the molar ratio of branched-chain amino acids to aromatic amino acids, was significantly lower (P < 0.001) in the blood serum obtained from the HAE patients than it was in the healthy patient group. Conclusions: The altered Fischer ratio, together with perturbations in metabolic pathways identified in the present study, may provide new insights into the mechanistic understanding of HAE pathogenesis and potential therapeutic interventions.