Plasma Omentin Levels Are Associated with Atherosclerosis in Patients with Type 2 Diabetes

Abstract

Omentin is an adipokine predominantly expressed in visceral adipose tissue and has insulin-sensitizing and vasculoprotective effects, like adiponectin, in rodents. Previous studies indicated an associations of plasma omentin levels with atherosclerosis, vascular endothelial function, and coronary artery disease in nondiabetic individuals. In this study, we investigated the association between plasma omentin levels and atherosclerosis in patients with type 2 diabetes. We included 416 patients with type 2 diabetes in this study. Fasting plasma omentin levels and total adiponectin levels were measured by ELISA, and the mean intima media thickness (IMT) of the common carotid artery was measured by ultrasonography. The medians of plasma omentin level, adiponectin level, and IMT were 572 ng/mL, 6.1 µg/mL, and 0.76 mm, respectively. Eighty seven (21%) subjects had cardiovascular diseases (CVDs), including coronary artery disease, cerebrovascular disease, or peripheral artery disease, which were confirmed by medical records. Plasma omentin levels were positively correlated with adiponectin and HDL-cholesterol, and negatively correlated with BMI, IRI, HOMA-R, triglycerides, and eGFR. Multivariate analysis showed that plasma omentin levels were not significantly associated with IMT after adjustment for adiponectin levels and traditional CVD risk factors. However, subgroup analysis revealed that plasma omentin level was an independent determinant of IMT (β = -0.139, p = 0.015) in subjects without CVDs, but not in those with CVDs. Interaction analysis indicated a potential effect modification by the presence of CVDs on the association of plasma omentin levels with IMT. In conclusion, plasma omentin levels are associated with atherosclerosis, independently of adiponectin and traditional CVD risk factors, in patients with type 2 diabetes without CVDs. This study indicates a protective role of omentin in atherosclerosis among patients with type 2 diabetes without CVDs. Disclosure M. Hatamori: None. T. Morioka: Consultant; Self; Ono Pharmaceutical Co., Ltd.. Research Support; Self; Novartis Pharma K.K., MSD K.K., Eli Lilly and Company, Sanofi K.K., Mitsubishi Tanabe Pharma Corporation. Speaker's Bureau; Self; Takeda Pharmaceuticals U.S.A., Inc., Novo Nordisk Inc., Kowa Pharmaceuticals America, Inc., Astellas Pharma US, Inc., Boehringer Ingelheim Pharmaceuticals, Inc., Sumitomo Dainippon Pharma Co., Ltd.. M. Senda: None. M. Asada: None. Y. Kakutani: Speaker's Bureau; Self; Astellas Pharma US, Inc., Novo Nordisk Inc., Novartis Pharma K.K., Takeda Pharmaceuticals U.S.A., Inc.. Y. Yamazaki: None. K. Motoyama: None. K. Mori: Speaker's Bureau; Self; Boehringer Ingelheim GmbH, Eli Lilly and Company, Mitsubishi Tanabe Pharma Corporation, MSD K.K., Sanofi, AstraZeneca, Daiichi Sankyo Company, Limited. S. Fukumoto: Speaker's Bureau; Self; Astellas Pharma US, Inc.. Research Support; Self; Chugai Pharmaceutical Co., Ltd., Mitsubishi Tanabe Pharma Corporation. Speaker's Bureau; Self; Novo Nordisk Inc., Sanofi K.K.. Research Support; Self; Takeda Pharmaceuticals U.S.A., Inc., Taisho Toyama Pharmaceutical Co., Ltd.. A. Shioi: None. T. Shoji: Speaker's Bureau; Self; Astellas Pharma Inc, Bayer Yakuhin Ltd. Research Support; Self; Bayer Yakuhin Ltd. Speaker's Bureau; Self; Kowa Pharamaceutical Co Ltd, Daiichi Sankyo Company, Limited, MSD K.K., Chugai Pharmaceutical Co., Ltd.. Research Support; Self; Chugai Pharmaceutical Co., Ltd.. Speaker's Bureau; Self; Kyowa Hakko Kirin Co., Ltd., Kissei Pharmaceutical Co., Ltd. M. Emoto: Speaker's Bureau; Self; Eli Lilly and Company, Boehringer Ingelheim Pharmaceuticals, Inc., Sumitomo Dainippon Pharma Co., Ltd.. Research Support; Self; Astellas Pharma Inc, Ono Pharmaceutical Co., Ltd., Kissei Pharmaceutical Co., Ltd., Kowa Pharmaceutical Company Ltd., Taisho Toyama Pharmaceutical Co., Ltd., Mitsubishi Tanabe Pharma Corporation. M. Inaba: None.