Metabolomic analyses for atherosclerosis, diabetes, and obesity - PubMed (original) (raw)

Metabolomic analyses for atherosclerosis, diabetes, and obesity

Fuyong Du et al. Biomark Res. 2013.

Abstract

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.

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Figures

Figure 1

Figure 1

The work flow of Mass Spectrometry Schematic (MS-S) for metabolome analysis. The left panel depicts a triple-collector system arranged to analyze molecules and an example of total mass spectrum for the compounds A, B, C, D, E, F, and G in a reaction. The right panel outlines the relationship between the genome, proteome, and metabolome, as well as the significances of metabolomics.

Figure 2

Figure 2

Metabolome analysis related to hyperglycemia/insulin resistance, obesity, and hyperlipidemia which contribute to the development of endothelial dysfunction. The reciprocal effects of hyperglycemia/insulin resistance, obesity, and dyslipidemia result in mitochondria stress/dysfunction via a complex of factors including oxidative stress, inflammation, incomplete fat oxidation, etc. As a result, mitochondria dysfunction increases the production of reactive oxygen species (ROS) and decreases nitric oxide (NO), which ultimately produces endothelial dysfunction and progressively causes atherosclerosis in macrovessels and microangiopathy in microvessels.

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