Peroxisome proliferator -: activate receptor γ agonist improves arterial stiffness in patients with type 2 diabetes mellitus and coronary artery disease

被引:40
作者
Yu, Jie
Jin, Nan
Wang, Guang [1 ]
Zhang, Fuchun
Mao, Jieming
Wang, Xian
机构
[1] Peking Univ, Hosp 3, Dept Cardiovasc Med, Beijing 100083, Peoples R China
[2] Peking Univ, Hlth Sci Ctr, Dept Physiol & Pathophysiol, Key Lab Mol Cardiovasc Sci Minist Educ, Beijing 100083, Peoples R China
来源
METABOLISM-CLINICAL AND EXPERIMENTAL | 2007年 / 56卷 / 10期
基金
中国国家自然科学基金;
关键词
D O I
10.1016/j.metabol.2007.05.011
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Arterial stiffness is an independent risk factor for cardiovascular events in diabetic patients, and it can be assessed by measuring pulse wave velocity (PWV). We investigated the degree of arterial stiffness in diabetic patients with coronary artery disease (CAD) and the effect of the proliferator-activated receptor gamma (PPAR-gamma) agonist rosiglitazone on arterial stiffness in the potential mechanism of anti-arteriosclerosis in patients with type 2 diabetes mellitus and CAD. The 123 participants were divided into 3 groups: healthy controls (n = 36), diabetic patients (n = 41), and diabetic patients with CAD (n = 46). Forty-six diabetic patients with CAD were randomly divided into 2 groups: untreated diabetic patients with CAD and diabetic patients with CAD treated with 4 mg/d of rosiglitazone (n = 25) for 12 weeks. Pulse wave velocity was measured before treatment and at 12-week follow-up. Baseline PWV was significantly higher in patients with diabetes, diabetes and CAD. and diabetes and CAD with treatment as compared with the healthy control group (1633 +/- 37.3, 1669 +/- 53.8, 1615 +/- 44.4, and 1360 +/- 39.9 cm/s. respectively. P <.001). Pulse wave velocity in the rosiglitazone-treated group was significantly reduced, from 1615 +/- 44.4 to 1525 +/- 43.1 cm/s. after 12-week treatment, Furthermore, PWV was significantly decreased in the rosiglitazone-treated group compared with untreated group after 12 weeks (1525 +/- 43.1 and 1670 +/- 41.3 cm/s, respectively). Pulse wave velocity in the untreated group did not differ from baseline levels after 12 weeks. In addition, plasma C-reactive protein level was decreased significantly in the rosiglitazone-treated group compared with values at baseline and for the untreated group after 12 weeks (0.73 +/- 0.09, 1.71 +/- 0.24, and 1.33 +/- 0.29 mg/L, respectively). Plasma level of monocyte chemoattractant protein 1 was decreased in the rosiglitazone group compared with the level at baseline (392 42 and 273 +/- 40 pg/mL, respectively). Moreover, the decrease in PWV was associated linearly both with improved homeostasis model assessment of insulin resistance and with decreased C-reactive protein level after PPAR-gamma agonist treatment. In conclusion, PPAR-gamma agonist rosiglitazone treatment may significantly decrease arterial stiffness in diabetic patients with CAD. Proliferator-activated receptor gamma agonists may play an important role in protecting against arteriosclerosis by normalizing the metabolic disorders and depressing chronic inflammation of the vascular system in patients with type 2 diabetes mellitus and serious vascular disease. (c) 2007 Elsevier Inc. All rights reserved.
引用
收藏
页码:1396 / 1401
页数:6
相关论文
共 23 条
[11]   Antidiabetic PPARγ-activator rosiglitazone reduces MMP-9 serum levels in type 2 diabetic patients with coronary artery disease [J].
Marx, N ;
Froehlich, J ;
Siam, L ;
Ittner, J ;
Wierse, G ;
Schmidt, A ;
Scharnagl, H ;
Hombach, V ;
Koenig, W .
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2003, 23 (02) :283-288
[12]   Peroxisome proliferator-activated receptor gamma activators inhibit gene expression and migration in human vascular smooth muscle cells [J].
Marx, N ;
Schönbeck, U ;
Lazar, MA ;
Libby, P ;
Plutzky, J .
CIRCULATION RESEARCH, 1998, 83 (11) :1097-1103
[13]   Macrophages in human atheroma contain PPARγ -: Differentiation-dependent peroxisomal proliferator-activated receptorγ (PPARγ) expression and reduction of MMP-9 activity through PPARγ activation in mononuclear phagocytes in vitro [J].
Marx, N ;
Sukhova, G ;
Murphy, C ;
Libby, P ;
Plutzky, J .
AMERICAN JOURNAL OF PATHOLOGY, 1998, 153 (01) :17-23
[14]   Potent inhibitory effect of troglitazone on carotid arterial wall thickness in type 2 diabetes [J].
Minamikawa, J ;
Tanaka, S ;
Yamauchi, M ;
Inoue, D ;
Koshiyama, H .
JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM, 1998, 83 (05) :1818-1820
[15]   Insulin induces upregulation of vascular AT1 receptor gene expression by posttranscriptional mechanisms [J].
Nickenig, G ;
Röling, J ;
Strehlow, K ;
Schnabel, P ;
Böhm, M .
CIRCULATION, 1998, 98 (22) :2453-2460
[16]   Modulation of vascular inflammation in vitro and in vivo by peroxisome proliferator-activated receptor-γ activators [J].
Pasceri, V ;
Wu, HD ;
Willerson, JT ;
Yeh, ETH .
CIRCULATION, 2000, 101 (03) :235-238
[17]  
Rizzoni D, 2001, CIRCULATION, V103, P1238
[18]  
RYAN K, 2007, IN PRESS ATHEROSCLER
[19]   NON-INSULIN-DEPENDENT DIABETES-MELLITUS AND FASTING GLUCOSE AND INSULIN CONCENTRATIONS ARE ASSOCIATED WITH ARTERIAL STIFFNESS INDEXES - THE ARIC STUDY [J].
SALOMAA, V ;
RILEY, W ;
KARK, JD ;
NARDO, C ;
FOLSOM, AR .
CIRCULATION, 1995, 91 (05) :1432-1443
[20]   Antiatherogenic effect of pioglitazone in type 2 diabetic patients irrespective of the responsiveness to its antidiabetic effect [J].
Satoh, N ;
Ogawa, Y ;
Usui, T ;
Tagami, T ;
Kono, S ;
Uesugi, H ;
Sugiyama, H ;
Sugawara, A ;
Yamada, K ;
Shimatsu, A ;
Kuzuya, H ;
Nakao, K .
DIABETES CARE, 2003, 26 (09) :2493-2499