Metabolomic analyses for atherosclerosis, diabetes, and obesity

被引：50
作者：
Du F. [1 ,2 ,3 ]
Virtue A. [1 ,2 ,3 ]
Wang H. [1 ,2 ,3 ]
Yang X.-F. [1 ,2 ,3 ]
机构：
[1] Department of Pharmacology, Temple University School of Medicine, Philadelphia
[2] Cardiovascular Research Center and Department of Pharmacology, Temple University School of Medicine, 3500 North Broad Street, MERB 1059, Philadelphia
[3] Thrombosis Research Center, Temple University School of Medicine, Philadelphia
来源：
Biomarker Research | / 1卷 / 1期
基金：
美国国家卫生研究院;
关键词：
Atherosclerosis; Diabetes; Metabolites; Metabolomics analysis; Obesity;
D O I：
10.1186/2050-7771-1-17
中图分类号：
学科分类号：
摘要：
Insulin resistance associated with type 2 diabetes mellitus (T2DM), obesity, and atherosclerosis is a global health problem. A portfolio of abnormalities of metabolic and vascular homeostasis accompanies T2DM and obesity, which are believed to conspire to lead to accelerated atherosclerosis and premature death. The complexity of metabolic changes in the diseases presents challenges for a full understanding of the molecular pathways contributing to the development of these diseases. The recent advent of new technologies in this area termed " Metabolomics" may aid in comprehensive metabolic analysis of these diseases. Therefore, metabolomics has been extensively applied to the metabolites of T2DM, obesity, and atherosclerosis not only for the assessment of disease development and prognosis, but also for the biomarker discovery of disease diagnosis. Herein, we summarize the recent applications of metabolomics technology and the generated datasets in the metabolic profiling of these diseases, in particular, the applications of these technologies to these diseases at the cellular, animal models, and human disease levels. In addition, we also extensively discuss the mechanisms linking the metabolic profiling in insulin resistance, T2DM, obesity, and atherosclerosis, with a particular emphasis on potential roles of increased production of reactive oxygen species (ROS) and mitochondria dysfunctions. © 2013 Du et al.; licensee BioMed Central Ltd.
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