TY - JOUR
T1 - The potential biomarkers to identify the development of steatosis in hyperuricemia
AU - Tan, Yong
AU - Liu, Xinru
AU - Zhou, Ke
AU - He, Xiaojuan
AU - Lu, Cheng
AU - He, Bing
AU - Niu, Xuyan
AU - Xiao, Cheng
AU - Xu, Gang
AU - BIAN, Zhaoxiang
AU - Zu, Xianpeng
AU - ZHANG, Ge
AU - Zhang, Weidong
AU - Lu, Aiping
N1 - Funding Information:
This study was supported by the following sources of funding: National Science Foundation of China (no. 81230090; http://npd.nsfc.gov.cn/), the author who received the funding: WDZ; Hong Kong Baptist University Strategic Development Fund (no. SDF13-1209-P01; http://scm.hkbu.edu.hk/tc/home/ index.php), the author who received the funding: APL; Interdisciplinary Research Matching Scheme of Hong Kong Baptist University (no. RC-IRMS/12-13/02; http://scm.hkbu.edu.hk/tc/home/index.php), the author who received the funding: APL; China Postdoctoral Science Foundation (no. 2013M541158; http://www.chinapostdoctor.org.cn/), the author who received the funding: KZ; E-Institutes of the Shanghai Municipal Education Commission (no. E03008; http:// www.shmec.gov.cn/), the author who received the funding: WDZ; the Professor of Chang Jiang Scholars Program (http://www.moe.edu.cn/publicfiles/business/ htmlfiles/moe/A04_ndgzyd/), the author who received the funding: WDZ.
PY - 2016/2
Y1 - 2016/2
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=84960510131&partnerID=8YFLogxK
U2 - 10.1371/journal.pone.0149043
DO - 10.1371/journal.pone.0149043
M3 - Article
C2 - 26890003
AN - SCOPUS:84960510131
SN - 1932-6203
VL - 11
JO - PLoS ONE
JF - PLoS ONE
IS - 2
M1 - e0149043
ER -