Huang Chi-Chang, Lou Bih-Show, Hsu Feng-Lin, Hou Chia-Chung
Graduate Institute of Sports Science, College of Exercise and Health Sciences, National Taiwan Sport University, Taoyuan 33301, Taiwan.
Chemistry Division, Center for General Education, Chang Gung University, Taoyuan 33301, Taiwan.
Food Chem Toxicol. 2014 Dec;74:35-44. doi: 10.1016/j.fct.2014.08.017. Epub 2014 Sep 6.
Clinical studies show that hyperuricemia is a risk factor in the progression and development of cardiovascular and metabolic disease. Elevated serum levels of uric acid induce renal injury via an inflammation response, but the detailed mechanism is still under study. To better understand the effect of hyperuricemia on the kidney, we used gas chromatography-mass spectrometry-based metabolomics to investigate the role of uric acid in the mouse kidney. Partial least-squares discriminant analysis revealed significant differences between control and hyperuricemia groups in urine metabolic profiles. We identified 33 metabolites from 76 highly reproducible peaks and found abnormal uric acid levels related to comprehensive kidney injury, including excretive function and energy metabolism. Additionally, inflammation induced by the interleukin 6/signal transducer and activator of transcription 3 signaling pathway participated in hyperuricemia-induced kidney injury. This study helps understand the relationship between hyperuricemia and kidney injury. Metabolomics may be a useful strategy for early diagnosis of kidney damage.
临床研究表明，高尿酸血症是心血管和代谢性疾病进展和发展的一个危险因素。血清尿酸水平升高通过炎症反应诱导肾损伤，但其详细机制仍在研究中。为了更好地了解高尿酸血症对肾脏的影响，我们使用基于气相色谱-质谱联用的代谢组学方法来研究尿酸在小鼠肾脏中的作用。偏最小二乘判别分析显示，对照组和高尿酸血症组的尿液代谢谱存在显著差异。我们从76个高度可重复的峰中鉴定出33种代谢物，发现尿酸水平异常与包括排泄功能和能量代谢在内的全面肾损伤有关。此外，白细胞介素6/信号转导和转录激活因子3信号通路诱导的炎症参与了高尿酸血症诱导的肾损伤。本研究有助于理解高尿酸血症与肾损伤之间的关系。代谢组学可能是早期诊断肾损伤的一种有用策略。
