ORIGINAL ARTICLE Olmesartan reduces arterial stiffness and serum adipocyte fatty acid-binding protein in hypertensive patients Toru Miyoshi • Masayuki Doi • Satoshi Hirohata • Shigeshi Kamikawa • Shinichi Usui • Hiroko Ogawa • Kosuke Sakane • Reishi Izumi • Yoshifumi Ninomiya • Shozo Kusachi Received: 13 July 2009 / Accepted: 30 April 2010 / Published online: 10 November 2010 Ó Springer 2010 Abstract Adipocyte fatty acid binding protein (A-FABP) has been reported to be involved in insulin resistance, lipid metabolism, and atherosclerosis; however, little is known about the effect of medication on the change in circulating A-FABP in human subjects. We evaluated the effects of angiotensin II type 1 receptor blocker (ARB) on arterial stiffness and its association with serum A-FABP in patients with hypertension. Thirty patients newly diagnosed with essential hypertension were treated with olmesartan (20 mg/day), an ARB, for 6 months. Serum levels of A-FABP and high-sensitivity C-reactive protein (hsCRP) were examined and the cardio-ankle vascular index (CAVI), which is a marker of arterial stiffness, was also determined. Serum A-FABP at baseline was significantly correlated with the body mass index (r = 0.45, P = 0.01), homeostasis model assessment as a marker of insulin resistance (r = 0.53, P \ 0.01), and systolic blood pres- sure (r = 0.37, P = 0.047), and tended to be correlated with low-density lipoprotein cholesterol, triglyceride, and CAVI. Olmesartan treatment resulted in a significant decrease in CAVI, serum A-FABP levels, and hsCRP, besides a significant reduction of blood pressure. Multiple regression analysis revealed that the change in CAVI was independently correlated with the change in serum A-FABP. Olmesartan ameliorated arterial stiffness in patients with hypertension, which may be involved in the reduction of serum A-FABP. Keywords Adipocyte Á Angiotensin II receptor antagonist Á Atherosclerosis Á Fatty acid Á Hypertension Á Inflammation Introduction Adipose tissue has been shown to be an endocrine organ that secretes various molecules, called adipokines [1]. Several adipokines, such as adiponectin, leptin, adipocyte- type fatty acid binding protein (A-FABP), and tumor necrosis factor-a, are closely involved in visceral adipose tissue [2]. Those adipokines are now considered key players not only in the role of glucose metabolism but also in vascular inflammation. Among adipokines, A-FABP, also known as aP2 or FABP4, is one of the most abundant proteins in adipocytes and activated macrophages [3]. In animal experiments, it has been shown that A-FABP- deficient mice were protected from the development of insulin resistance [4] and atherosclerosis in models of hypercholesterolemia [5]. In humans, A-FABP levels have been detected in serum [6], although A-FABP was origi- nally a cytoplasmic protein. It has been reported that the serum A-FABP level predicts the development of meta- bolic syndrome [7], and is associated with carotid intima- media thickness [8] and coronary atherosclerosis [9, 10]. Essential hypertension is associated with insulin resis- tance [11], although the underlying mechanisms remain T. Miyoshi (&) Á S. Hirohata Á S. Kamikawa Á H. Ogawa Á Y. Ninomiya Department of Molecular Biology and Biochemistry, Okayama University Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, 2-5-1 Shikata-cho, Okayama 700-8558, Japan e-mail: miyoshit@cc.okayama-u.ac.jp M. Doi Á K. Sakane Division of Cardiology, Sumitomo Besshi Hospital, Niihama, Japan S. Usui Á R. Izumi Á S. Kusachi Department of Medical Technology, Okayama University Graduate School of Health Sciences, Okayama, Japan 123 Heart Vessels (2011) 26:408–413 DOI 10.1007/s00380-010-0060-x