Soluble vascular cell adhesion molecule-1 is independently associated with soluble tumor necrosis factor receptor 2 in Japanese type 2 diabetic patients

Soluble vascular cell adhesion molecule-1 is independently associated with soluble tumor necrosis factor receptor 2 in Japanese type 2 diabetic patients

Letters to the editor / Diabetes & Metabolism 33 (2006) 79–82 D.-J. Soyeur Division of cardiology, CHU Sart Tilman, University of Liège, 4000 Liège, ...

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Letters to the editor / Diabetes & Metabolism 33 (2006) 79–82

D.-J. Soyeur Division of cardiology, CHU Sart Tilman, University of Liège, 4000 Liège, Belgium M.-A. Radermecker Division of cardiovascular surgery, CHU Sart Tilman, University of Liège, 4000 Liège, Belgium A.-J. Scheen* Division of diabetes, nutrition and metabolic disorders, department of medicine, CHU Sart Tilman, University of Liège, 4000 Liège, Belgium E-mail address: [email protected] (A.-J. Scheen). Received 3 August 2006; accepted 18 October 2006 Available online 26 January 2007 *Corresponding

author.

1262-3636/$ - see front matter © 2007 Elsevier Masson SAS. All rights reserved. doi:10.1016/j.diabet.2006.10.003

Soluble vascular cell adhesion molecule-1 is independently associated with soluble tumor necrosis factor receptor 2 in Japanese type 2 diabetic patients The major clinical consequence of type 2 diabetes is mortality and morbidity from atherosclerotic vascular disease. Although it remains to be clarified which factors are responsible for the evolution of atherosclerosis, the earliest morphological evidence of atherosclerosis is the attachment of monocytes to the cell surface of vascular endothelium. Monocytes attach at the cell surface of adhesion molecules such as vascular cell adhesion molecule 1 (VCAM-1). Jager et al. [1] have shown that increased levels of soluble VCAM-1 are associated with risk of cardiovascular mortality independently of traditional risk factors, homocysteine, and C-reactive protein in type 2 diabetic patients. The mechanisms underlying the development of atherosclerosis, however, are unclear in type 2 diabetic patients. Along with insulin resistance, tumor necrosis factor (TNF) seems to account for the development of atherosclerosis in type 2 diabetes. Shai et al. [2] demonstrated that soluble TNF receptor 2 (sTNF-R2) is strongly associated with risk of coronary heart disease in type 2 diabetic patients. We recently demonstrated that soluble TNF receptors are not associated with insulin resistance but are associated with albuminuria or aortic stiffness measured by brachial-ankle pulse wave velocity in Japanese type 2 diabetic patients [3–5]. To the best of our knowledge, however, the relationships between VCAM-1 and TNF system activities including soluble TNF receptors were not yet investigated in type 2 diabetic patients. In this regard, the problem is that insulin therapy or the degree of overweight per se affects the concentrations of VCAM-1 and TNF system activities. We therefore recruited insulin naïve type 2 diabetic

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patients who were not massively obese and investigated the relationships between VCAM-1 and TNF system activity in type 2 diabetic patients. Fifty-four Japanese type 2 diabetic patients were enrolled. Their age, BMI, fasting glucose, and HbA1c were 62.5 ± 1.7 years (mean ± S.E.M.), 23.6 ± 0.4 kg/m2, 137 ± 4 mg/dl, and 6.8 ± 0.1%, respectively. Along with VCAM-1, glucose, insulin, lipids, homocysteine, TNF-α, sTNF-R1, sTNF-R2, high sensitive C-reactive protein (hsCRP), interleukin-6 (IL-6), and leptin were measured in the morning after an overnight fast as described previously in [3,6–8]. With univariate analysis, VCAM-1 was positively correlated with age (r = 0.355, P < 0.01), sTNF-R1 (r = 0.562, P < 0.0001), and sTNF-R2 (r = 0.701, P < 0.0001) in our patients. Serum levels of VCAM-1, however, were not associated with homocysteine, TNF-α, glucose, insulin, BMI, hsCRP, IL-6, or leptin. Multiple regression analyses revealed that VCAM-1 was independently predicted by sTNF-R2 (F = 38.7), which explained 38.2% of the variability of VCAM-1 in our patients. Thus, it may be suggested that VCAM-1 is associated with TNF system activity in Japanese type 2 diabetic patients. References [1] Jager A, van Hinsbergh VW, Kostense PJ, Emeis JJ, Nijpels G, Dekker JM, et al. Increased levels of soluble vascular cell adhesion molecule 1 are associated with risk of cardiovascular mortality in type 2 diabetes: the Hoorn study. Diabetes 2000;49:485–91. [2] Shai I, Schulze MB, Manson JE, Rexrode KM, Stampfer MJ, Mantzoros C, et al. A prospective study of soluble tumor necrosis factor-alpha receptor II (sTNF-RII) and risk of coronary heart disease among women with type 2 diabetes. Diabetes Care 2005;28:1376–82. [3] Ohya M, Taniguchi A, Fukushima M, Nakai Y, Kawasaki Y, Nagasaka S, et al. Three measures of tumor necrosis factor alpha activity and insulin resistance in non-obese Japanese type 2 diabetic patients. Metabolism 2005;54:1297–301. [4] Kawasaki Y, Taniguchi A, Fukushima M, Nakai Y, Kuroe A, Ohya M, et al. Soluble TNF receptors and albuminuria in non-obese Japanese type 2 diabetic patients. Horm Metab Res 2005;37:617–21. [5] Ohgushi M, Taniguchi A, Fukushima M, Kuroe A, Ohya M, Seino Y. Soluble tumor necrosis factor receptor 2 is independently associated with brachial-ankle pulse-wave velocity in non-obese Japanese type 2 diabetic patients. Diabetes Care 2006;29:1459–60 (letter). [6] Taniguchi A, Nagasaka S, Fukushima M, Sakai M, Okumura T, Yoshii S, et al. C-reactive protein and insulin resistance in non-obese Japanese type 2 diabetic patients. Metabolism 2002;51:1578–81. [7] Taniguchi A, Fukushima M, Ohya M, Nakai Y, Yoshii S, Nagasaka S, et al. Interleukin 6, adiponectin, leptin, and insulin resistance in nonobese Japanese type 2 diabetic patients. Metabolism 2006;55:258–62. [8] Okumura T, Taniguchi A, Nagasaka S, Sakai M, Fukushima M, Kuroe A, et al. Relationship of regional adiposity to serum leptin level in non-obese Japanese type 2 diabetic male patients. Diabetes Metab 2003;29:15–8.

D. Nabeya A. Taniguchi* Division of Diabetes and Clinical Nutrition, Kansai-Denryoku Hospital, 2-1-7 Fukushima, Fukushima-ku, Osaka-city, Osaka 553-0003, Japan E-mail address: [email protected] (A. Taniguchi).

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Letters to the editor / Diabetes & Metabolism 33 (2006) 79–82

M. Fukushima Department of Health Informatics Research, Kansai-Denryoku Hospital, Osaka, Japan Y. Nakai Translational Research Informatics Center, Karasuma-Oike-Nakai Clinic, Kobe, Japan K. Matsumoto Diabetes Center, Kyoto, Japan A. Kuroe M. Ohgushi M. Ohya Division of Diabetes and Clinical Nutrition, Kansai-Denryoku Hospital, 2-1-7 Fukushima, Fukushima-ku, Osaka-city, Osaka 553-0003, Japan S. Nagasaka Division of Endocrinology and Metabolism, Sasebo-Chyuoh Hospital, Nagasaki, Japan

N. Inagaki Department of Diabetes and Clinical Nutrition, Jichi Medical School, Tochigi, Kyoto University Graduate School of Medicine, Kyoto, Japan Y. Seino Division of Diabetes and Clinical Nutrition, Kansai-Denryoku Hospital, 2-1-7 Fukushima, Fukushima-ku, Osaka-city, Osaka 553-0003, Japan Received 7 September 2006; accepted 26 October 2006 Available online 26 January 2007 *Corresponding

author.

1262-3636/$ - see front matter © 2007 Elsevier Masson SAS. All rights reserved. doi:10.1016/j.diabet.2006.10.002