当前位置: X-MOL 学术Metabolites › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Mucosal Metabolomic Profiling and Pathway Analysis Reveal the Metabolic Signature of Ulcerative Colitis.
Metabolites ( IF 4.1 ) Pub Date : 2019-11-27 , DOI: 10.3390/metabo9120291
Joseph Diab 1 , Terkel Hansen 1 , Rasmus Goll 2, 3 , Hans Stenlund 4 , Einar Jensen 1 , Thomas Moritz 4, 5 , Jon Florholmen 2, 3 , Guro Forsdahl 1
Affiliation  

The onset of ulcerative colitis (UC) is characterized by a dysregulated mucosal immune response triggered by several genetic and environmental factors in the context of host-microbe interaction. This complexity makes UC ideal for metabolomic studies to unravel the disease pathobiology and to improve the patient stratification strategies. This study aims to explore the mucosal metabolomic profile in UC patients, and to define the UC metabolic signature. Treatment- naïve UC patients (n = 18), UC patients in deep remission (n = 10), and healthy volunteers (n = 14) were recruited. Mucosa biopsies were collected during colonoscopies. Metabolomic analysis was performed by combined gas chromatography coupled to time-of-flight mass spectrometry (GC-TOF-MS) and ultra-high performance liquid chromatography coupled with mass spectrometry (UHPLC-MS). In total, 177 metabolites from 50 metabolic pathways were identified. The most prominent metabolome changes among the study groups were in lysophosphatidylcholine, acyl carnitine, and amino acid profiles. Several pathways were found perturbed according to the integrated pathway analysis. These pathways ranged from amino acid metabolism (such as tryptophan metabolism) to fatty acid metabolism, namely linoleic and butyrate. These metabolic changes during UC reflect the homeostatic disturbance in the gut, and highlight the importance of system biology approaches to identify key drivers of pathogenesis which prerequisite personalized medicine.

中文翻译:

粘膜代谢组学分析和途径分析揭示了溃疡性结肠炎的代谢特征。

溃疡性结肠炎(UC)的发作的特征是在宿主-微生物相互作用的背景下,由几种遗传和环境因素触发的粘膜免疫反应失调。这种复杂性使UC非常适合进行代谢组学研究,以阐明疾病的病理生物学并改善患者的分层策略。本研究旨在探讨UC患者的粘膜代谢组学特征,并定义UC代谢特征。招募了初治的UC患者(n = 18),深度缓解的UC患者(n = 10)和健康志愿者(n = 14)。在结肠镜检查期间收集粘膜活检。代谢组学分析通过结合飞行时间质谱联用的气相色谱法(GC-TOF-MS)和结合质谱联用的超高效液相色谱法(UHPLC-MS)进行。总共,从50种代谢途径中鉴定出177种代谢物。在研究组中,最显着的代谢组变化是溶血磷脂酰胆碱,酰基肉碱和氨基酸谱。根据综合途径分析发现了几种途径。这些途径的范围从氨基酸代谢(例如色氨酸代谢)到脂肪酸代谢,即亚油酸和丁酸。UC期间的这些代谢变化反映了肠道内的体内稳态紊乱,并突出了系统生物学方法对确定病因的关键驱动力的重要性,而这些驱动力是个性化医学的前提。根据综合途径分析发现了几种途径。这些途径的范围从氨基酸代谢(例如色氨酸代谢)到脂肪酸代谢,即亚油酸和丁酸。UC期间的这些代谢变化反映了肠道内的体内稳态紊乱,并突出了系统生物学方法对确定病因的关键驱动力的重要性,而这些驱动力是个性化医学的前提。根据综合途径分析发现了几种途径。这些途径的范围从氨基酸代谢(例如色氨酸代谢)到脂肪酸代谢,即亚油酸和丁酸。UC期间的这些代谢变化反映了肠道内的体内稳态紊乱,并突出了系统生物学方法对确定病因的关键驱动力的重要性,而这些驱动力是个性化医学的前提。
更新日期:2019-11-28
down
wechat
bug