Kazuo Omori1, Naoto Katakami1,2, Yuichi Yamamoto1, Hiroyo Ninomiya1, Mitsuyoshi Takahara1,3, Taka-Aki Matsuoka1, Takeshi Bamba4, Eiichiro Fukusaki5, Iichiro Shimomura1. 1. Department of Metabolic Medicine, Osaka University Graduate School of Medicine. 2. Department of Metabolism and Atherosclerosis, Osaka University Graduate School of Medicine. 3. Department of Diabetes Care Medicine, Graduate, School of Medicine, Osaka University. 4. Division of Metabolomics, Medical Institute of Bioregulation, Kyushu University. 5. Laboratory of Bioresource Engineering, Department of Biotechnology, Graduate School of Engineering, Osaka University.
Abstract
AIM: Coronary artery disease (CAD) is the result of a complex metabolic disorder caused by various environmental and genetic factors. Metabolomics is a potential tool for identifying biomarkers for better risk classification and for understanding the pathophysiological mechanisms of CAD. With this background, we performed a pilot study to identify metabolites associated with the future onset of CAD in patients with type 2 diabetes. METHODS: Sixteen subjects who suffered from CAD event during the observation period and 39 non-CAD subjects who were matched to the CAD subjects for Framingham Coronary Heart Disease Risk Score, diabetes duration, and HbA1c were selected. Capillary electrophoresis time-of-flight mass spectrometry (CE-TOFMS) was used to perform non-targeted metabolome analysis of serum samples collected in 2005. RESULTS: A total of 104 metabolites were identified. Unsupervised principal component analysis (PCA) did not to reveal two distinct clusters of individuals. However, a significant association with CAD was found for 7 metabolites (pelargonic acid, glucosamine:galactosamine, thymine, 3-hydroxybutyric acid, creatine, 2-aminoisobutyric acid, hypoxanthine) and the levels of all these metabolites were significantly lower in the CAD group compared with the non-CAD group. CONCLUSIONS: We identified 7 metabolites related to long-term future onset of CAD in Japanese patients with diabetes. Further studies with large sample size would be necessary to confirm our findings, and future studies using in vivo or in vitro models would be necessary to elucidate whether direct relationships exist between the detected metabolites and CAD pathophysiology.
AIM: Coronary artery disease (CAD) is the result of a complex metabolic disorder caused by various environmental and genetic factors. Metabolomics is a potential tool for identifying biomarkers for better risk classification and for understanding the pathophysiological mechanisms of CAD. With this background, we performed a pilot study to identify metabolites associated with the future onset of CAD in patients with type 2 diabetes. METHODS: Sixteen subjects who suffered from CAD event during the observation period and 39 non-CAD subjects who were matched to the CAD subjects for Framingham Coronary Heart Disease Risk Score, diabetes duration, and HbA1c were selected. Capillary electrophoresis time-of-flight mass spectrometry (CE-TOFMS) was used to perform non-targeted metabolome analysis of serum samples collected in 2005. RESULTS: A total of 104 metabolites were identified. Unsupervised principal component analysis (PCA) did not to reveal two distinct clusters of individuals. However, a significant association with CAD was found for 7 metabolites (pelargonic acid, glucosamine:galactosamine, thymine, 3-hydroxybutyric acid, creatine, 2-aminoisobutyric acid, hypoxanthine) and the levels of all these metabolites were significantly lower in the CAD group compared with the non-CAD group. CONCLUSIONS: We identified 7 metabolites related to long-term future onset of CAD in Japanese patients with diabetes. Further studies with large sample size would be necessary to confirm our findings, and future studies using in vivo or in vitro models would be necessary to elucidate whether direct relationships exist between the detected metabolites and CAD pathophysiology.
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