Mirzoyan Koryun, Klavins Kristaps, Koal Therese, Gillet Marion, Marsal Dimitri, Denis Colette, Klein Julie, Bascands Jean-Loup, Schanstra Joost P, Saulnier-Blache Jean-Sébastien
Institut National de la Santé et de la Recherche Médicale (INSERM), U1048, Institut of Cardiovascular and Metabolic Disease, France; Université Toulouse III Paul-Sabatier Toulouse, France.
Biocrates Life Sciences AG, Austria.
Biochem Biophys Res Commun. 2017 May 20;487(1):109-115. doi: 10.1016/j.bbrc.2017.04.026. Epub 2017 Apr 7.
Hyperlipidemia is a risk factor for initiation and progression of diabetic nephropathy but the metabolic pathways altered in the diabetic kidney in a context of hyperlipidemia remain incompletely described. Assuming that changes in urine composition reflect the alteration of renal metabolism and function, we analyzed the urine metabolite composition of diabetic (streptozotocin-treatment) and control (non diabetic) ApoE-/- mice fed a high cholesterol diet using targeted quantitative metabolomics. Urine metabolome was also compared to the plasma metabolome of the same animals. As previously shown, urine albuminuria/urine creatinine ratio (uACR) and glomerular area and plasma lipids (cholesterol, triglycerides) were more elevated in diabetic mice compared to control. After adjustment to urine creatinine, the abundance of 52 urine metabolites was significantly different in diabetic mice compared to control. Among them was a unique metabolite, C14:2-OH (3-hydroxytetradecadienoylcarnitine) that, in diabetic mice, was positively and significantly correlated with uACR, glomerular hypertrophy, blood glucose and plasma lipids. That metabolite was not detected in plasma. C14:2-OH is a long-chain acylcarnitine reminiscent of altered fatty acid beta oxidation. Other acylcarnitines, particularly the short chains C3-OH, C3-DC, C4:1, C5-DC, C5-M-DC, C5-OH that are reminiscent of altered oxidation of branched and aromatic amino acids were also exclusively detected in urine but were only correlated with plasma lipids. Finally, the renal gene expression of several enzymes involved in fatty acid and/or amino acid oxidation was significantly reduced in diabetic mice compared to control. This included the bifunctional enoyl-CoA hydratase/3-hydroxyacyl-CoA (Ehhadh) that might play a central role in C14:2-OH production. This study indicate that the development of diabetes in a context of hyperlipidemia is associated with a reduced capacity of kidney to oxidize fatty acids and amino acids with the consequence of an elevation of urinary acetylcarnitines including C14:2-OH that specifically reflects diabetic nephropathy.
高脂血症是糖尿病肾病发生和进展的危险因素,但在高脂血症背景下糖尿病肾脏中改变的代谢途径仍未完全阐明。假设尿液成分的变化反映了肾脏代谢和功能的改变,我们使用靶向定量代谢组学分析了喂食高胆固醇饮食的糖尿病(链脲佐菌素处理)和对照(非糖尿病)ApoE-/-小鼠的尿液代谢物组成。尿液代谢组也与相同动物的血浆代谢组进行了比较。如先前所示,与对照相比,糖尿病小鼠的尿白蛋白尿/尿肌酐比值(uACR)、肾小球面积和血浆脂质(胆固醇、甘油三酯)升高更为明显。在根据尿肌酐进行调整后,与对照相比,糖尿病小鼠中52种尿液代谢物的丰度存在显著差异。其中有一种独特的代谢物,C14:2-OH(3-羟基十四碳二烯酰肉碱),在糖尿病小鼠中,它与uACR、肾小球肥大、血糖和血浆脂质呈正相关且具有显著相关性。该代谢物在血浆中未检测到。C14:2-OH是一种长链酰基肉碱,提示脂肪酸β氧化发生改变。其他酰基肉碱,特别是短链C3-OH、C3-DC、C4:1、C5-DC、C5-M-DC、C5-OH,提示支链和芳香族氨基酸氧化改变,也仅在尿液中检测到,但仅与血浆脂质相关。最后,与对照相比,糖尿病小鼠中几种参与脂肪酸和/或氨基酸氧化的酶的肾脏基因表达显著降低。这包括双功能烯酰辅酶A水合酶/3-羟基酰基辅酶A(Ehhadh),它可能在C14:2-OH的产生中起核心作用。这项研究表明,在高脂血症背景下糖尿病的发展与肾脏氧化脂肪酸和氨基酸的能力降低有关,其结果是尿乙酰肉碱升高,包括特异性反映糖尿病肾病的C14:2-OH。