Mariko Hayashi1, Tomoaki Morioka2, Masami Hatamori1, Yoshinori Kakutani1, Yuko Yamazaki1, Masafumi Kurajoh3, Koka Motoyama4, Katsuhito Mori5, Shinya Fukumoto6, Atsushi Shioi7, Tetsuo Shoji8, Masanori Emoto9, Masaaki Inaba10. 1. Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan. 2. Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan. Electronic address: m-tomo@med.osaka-cu.ac.jp. 3. Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan. Electronic address: m1155129@med.osaka-cu.ac.jp. 4. Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan. Electronic address: m1399776@med.osaka-cu.ac.jp. 5. Department of Nephrology, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan. Electronic address: ktmori@med.osaka-cu.ac.jp. 6. Department of Premier Preventive Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan. Electronic address: sfukumoto@med.osaka-cu.ac.jp. 7. Department of Vascular Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan; Vascular Science Center for Translational Research, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan. Electronic address: as@med.osaka-cu.ac.jp. 8. Department of Vascular Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan; Vascular Science Center for Translational Research, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan. Electronic address: t-shoji@med.osaka-cu.ac.jp. 9. Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan. Electronic address: memoto@med.osaka-cu.ac.jp. 10. Department of Metabolism, Endocrinology and Molecular Medicine, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan; Vascular Science Center for Translational Research, Osaka City University Graduate School of Medicine, 1-4-3, Asahi-machi, Abeno-ku, Osaka 545-8585, Japan. Electronic address: inaba-m@med.osaka-cu.ac.jp.
Abstract
AIMS: Omentin is an adipokine that has protective effects against cardiovascular damage. Previous studies showed an inverse relationship between omentin and obesity, diabetes, and cardiovascular disease. This study aimed to investigate the association between omentin and vascular endothelial function in patients with type 2 diabetes (T2D). METHODS: The subjects were 425 patients with T2D and 223 non-diabetic controls. Fasting plasma omentin levels were measured by enzyme-linked immunosorbent assay, and the endothelium-dependent, flow-mediated dilatation (FMD) was measured by ultrasonography. RESULTS: Plasma omentin levels were higher, while FMD was lower in participants with T2D than in non-diabetic controls. No significant correlation was found between plasma omentin levels and FMD in either non-diabetic controls or participants with T2D on multivariate analysis. However, stratified analysis in T2D patients revealed that plasma omentin levels were independently and positively associated with FMD in high cardiovascular risk subgroups according to age (≥65 years), estimated glomerular filtration rate (<60 mL/min/1.73 m2), or preexisting cardiovascular diseases but not in low-risk subgroups. CONCLUSIONS: Plasma omentin levels are independently associated with endothelial function in subgroups of patients with T2D at elevated cardiovascular risk. This study suggests a protective role of omentin against endothelial dysfunction, particularly in high-risk patients.
AIMS: Omentin is an adipokine that has protective effects against cardiovascular damage. Previous studies showed an inverse relationship between omentin and obesity, diabetes, and cardiovascular disease. This study aimed to investigate the association between omentin and vascular endothelial function in patients with type 2 diabetes (T2D). METHODS: The subjects were 425 patients with T2D and 223 non-diabetic controls. Fasting plasma omentin levels were measured by enzyme-linked immunosorbent assay, and the endothelium-dependent, flow-mediated dilatation (FMD) was measured by ultrasonography. RESULTS: Plasma omentin levels were higher, while FMD was lower in participants with T2D than in non-diabetic controls. No significant correlation was found between plasma omentin levels and FMD in either non-diabetic controls or participants with T2D on multivariate analysis. However, stratified analysis in T2D patients revealed that plasma omentin levels were independently and positively associated with FMD in high cardiovascular risk subgroups according to age (≥65 years), estimated glomerular filtration rate (<60 mL/min/1.73 m2), or preexisting cardiovascular diseases but not in low-risk subgroups. CONCLUSIONS: Plasma omentin levels are independently associated with endothelial function in subgroups of patients with T2D at elevated cardiovascular risk. This study suggests a protective role of omentin against endothelial dysfunction, particularly in high-risk patients.