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The Potential Biomarkers to Identify the Development of Steatosis in Hyperuricemia
Hyperuricemia (HU) often progresses to combine with non-alcoholic fatty liver disease (NAFLD) in the clinical scenario, which further exacerbates metabolic disorders; early detection of biomarkers, if obtained during the HU progression, may be beneficial for preventing its combination with NAFLD. Th...
Autores principales: | , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Public Library of Science
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4758628/ https://www.ncbi.nlm.nih.gov/pubmed/26890003 http://dx.doi.org/10.1371/journal.pone.0149043 |
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author | Tan, Yong Liu, Xinru Zhou, Ke He, Xiaojuan Lu, Cheng He, Bing Niu, Xuyan Xiao, Cheng Xu, Gang Bian, Zhaoxiang Zu, Xianpeng Zhang, Ge Zhang, Weidong Lu, Aiping |
author_facet | Tan, Yong Liu, Xinru Zhou, Ke He, Xiaojuan Lu, Cheng He, Bing Niu, Xuyan Xiao, Cheng Xu, Gang Bian, Zhaoxiang Zu, Xianpeng Zhang, Ge Zhang, Weidong Lu, Aiping |
author_sort | Tan, Yong |
collection | PubMed |
description | Hyperuricemia (HU) often progresses to combine with non-alcoholic fatty liver disease (NAFLD) in the clinical scenario, which further exacerbates metabolic disorders; early detection of biomarkers, if obtained during the HU progression, may be beneficial for preventing its combination with NAFLD. This study aimed to decipher the biomarkers and mechanisms of the development of steatosis in HU. Four groups of subjects undergoing health screening, including healthy subjects, subjects with HU, subjects with HU combined with NAFLD (HU+NAFLD) and subjects with HU initially and then with HU+NAFLD one year later (HU→HU+NAFLD), were recruited in this study. The metabolic profiles of all subjects’ serum were analyzed by liquid chromatography quadruple time-of-flight mass spectrometry. The metabolomic data from subjects with HU and HU+NAFLD were compared, and the biomarkers for the progression from HU to HU+NAFLD were predicted. The metabolomic data from HU→HU+NAFLD subjects were collected for further verification. The results showed that the progression was associated with disturbances of phospholipase metabolism, purine nucleotide degradation and Liver X receptor/retinoic X receptor activation as characterized by up-regulated phosphatidic acid, cholesterol ester (18:0) and down-regulated inosine. These metabolic alterations may be at least partially responsible for the development of steatosis in HU. This study provides a new paradigm for better understanding and further prevention of disease progression. |
format | Online Article Text |
id | pubmed-4758628 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Public Library of Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-47586282016-02-26 The Potential Biomarkers to Identify the Development of Steatosis in Hyperuricemia Tan, Yong Liu, Xinru Zhou, Ke He, Xiaojuan Lu, Cheng He, Bing Niu, Xuyan Xiao, Cheng Xu, Gang Bian, Zhaoxiang Zu, Xianpeng Zhang, Ge Zhang, Weidong Lu, Aiping PLoS One Research Article Hyperuricemia (HU) often progresses to combine with non-alcoholic fatty liver disease (NAFLD) in the clinical scenario, which further exacerbates metabolic disorders; early detection of biomarkers, if obtained during the HU progression, may be beneficial for preventing its combination with NAFLD. This study aimed to decipher the biomarkers and mechanisms of the development of steatosis in HU. Four groups of subjects undergoing health screening, including healthy subjects, subjects with HU, subjects with HU combined with NAFLD (HU+NAFLD) and subjects with HU initially and then with HU+NAFLD one year later (HU→HU+NAFLD), were recruited in this study. The metabolic profiles of all subjects’ serum were analyzed by liquid chromatography quadruple time-of-flight mass spectrometry. The metabolomic data from subjects with HU and HU+NAFLD were compared, and the biomarkers for the progression from HU to HU+NAFLD were predicted. The metabolomic data from HU→HU+NAFLD subjects were collected for further verification. The results showed that the progression was associated with disturbances of phospholipase metabolism, purine nucleotide degradation and Liver X receptor/retinoic X receptor activation as characterized by up-regulated phosphatidic acid, cholesterol ester (18:0) and down-regulated inosine. These metabolic alterations may be at least partially responsible for the development of steatosis in HU. This study provides a new paradigm for better understanding and further prevention of disease progression. Public Library of Science 2016-02-18 /pmc/articles/PMC4758628/ /pubmed/26890003 http://dx.doi.org/10.1371/journal.pone.0149043 Text en © 2016 Tan et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Article Tan, Yong Liu, Xinru Zhou, Ke He, Xiaojuan Lu, Cheng He, Bing Niu, Xuyan Xiao, Cheng Xu, Gang Bian, Zhaoxiang Zu, Xianpeng Zhang, Ge Zhang, Weidong Lu, Aiping The Potential Biomarkers to Identify the Development of Steatosis in Hyperuricemia |
title | The Potential Biomarkers to Identify the Development of Steatosis in Hyperuricemia |
title_full | The Potential Biomarkers to Identify the Development of Steatosis in Hyperuricemia |
title_fullStr | The Potential Biomarkers to Identify the Development of Steatosis in Hyperuricemia |
title_full_unstemmed | The Potential Biomarkers to Identify the Development of Steatosis in Hyperuricemia |
title_short | The Potential Biomarkers to Identify the Development of Steatosis in Hyperuricemia |
title_sort | potential biomarkers to identify the development of steatosis in hyperuricemia |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4758628/ https://www.ncbi.nlm.nih.gov/pubmed/26890003 http://dx.doi.org/10.1371/journal.pone.0149043 |
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