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 Presentation

"Insulin Resistance, Inflammation and Atherosclerosis in Type 2 Diabetes, and the Emerging Role of the Glitazones"

Prof. Nikolaus Marx (biography)
English - 2005-09-11 - 40 minutes
(43 slides)
(8 questions)

Summary :
Patients with type 2 diabetes mellitus and insulin resistance exhibit an increased propensity to develop arteriosclerosis with its sequelae of acute myocardial infarction and stroke. Developing therapeutic strategies to modulate the increased cardiovascular risk in these patients is one of the major tasks in vascular biology. Amongst such approaches, the antidiabetic, peroxisome proliferator-activated receptor gamma (PPAR gamma)-activating thiazolidinediones (TZDs, glitazones) are very promising with respect to their antiatherogenic properties.

PPAR gamma is a nuclear receptor, activated by the antidiabetic glitazones, which controls the expression of transcription factors and regulation of genes involved in glucose homeostasis and adipogenesis. In addition to the metabolic effects of PPAR gamma, various groups have been interested in examining the effect of PPAR gamma activators on mechanisms of atherogenesis. Firstly, the expression of PPAR gamma in the vessel wall of arteriosclerotic lesions has been demonstrated, and it has been shown that antidiabetic PPAR gamma-activating TZDs exhibit anti-inflammatory and antiatherogenic properties in vascular cells. We and other groups have found TZDs to inhibit endothelial cell and T-cell activation, modulate the release of matrix-degrading enzymes from human monocytes and macrophages, and reduce smooth muscle cell migration. Given the critical role of these processes in lesion development, these in vitro data suggest that antidiabetic PPAR gamma activators may modulate the inflammatory response in the vessel wall and, as such, provide a potential novel therapeutic option to influence vascular disease in the high-risk population of type 2 diabetic patients. Subsequent clinical studies have shown that the treatment of patients with type 2 diabetes mellitus and coronary artery disease with PPAR gamma-activating TZDs reduces serum levels of novel inflammatory biomarkers of arteriosclerosis, improves endothelial function and reduces restenosis after coronary stenting in nondiabetic subjects, suggesting that this concept of the anti-inflammatory effects of TZDs holds true in treated patients.

Learning objectives :
After viewing this presentation the participant will be able to discuss:

- Evidence for effects of PPAR gamma activators on mechanisms of atherogenesis

Bibliographic references :
Donghoon Choi, MD, PHD, Soo-Kyung Kim, MD, Sung-Hee Choi, MD, Young-Guk Ko, MD, Chul-Woo Ahn, MD, PHD, Yangsoo Jang, MD, PHD, Sung-Kil Lim, MD, PHD, Hyun-Chul Lee, MD, PHD and Bong-Soo Cha, MD, PHDPreventative Effects of Rosiglitazone on Restenosis After Coronary Stent Implantation in Patients With Type 2 Diabetes Diabetes Care 27:2654-2660, 2004.

Steven M. Haffner, MD; Andrew S. Greenberg, MD; Wayde M. Weston, PhD; Hongzi Chen, PhD; Ken Williams, MS; Martin I. Freed, MD Effect of Rosiglitazone Treatment on Nontraditional Markers of Cardiovascular Disease in Patients With Type 2 Diabetes Mellitus Circulation. 2002;106:679.

Jürgen Hetzel; Bernd Balletshofer; Kilian Rittig; Daniel Walcher; Wolfgang Kratzer; Vinzenz Hombach; Hans-Ulrich Häring; Wolfgang Koenig; Nikolaus Marx Rapid Effects of Rosiglitazone Treatment on Endothelial Function and Inflammatory Biomarkers Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1804.

Nikolaus Marx; Johannes Froehlich; Laila Siam; Jochen Ittner; Gerhard Wierse; Arnold Schmidt; Hubert Scharnagl; Vinzenz Hombach; Wolfgang Koenig Antidiabetic PPAR-Activator Rosiglitazone Reduces MMP-9 Serum Levels in Type 2 Diabetic Patients With Coronary Artery Disease Arteriosclerosis, Thrombosis, and Vascular Biology. 2003;23:283.

Jagdip S. Sidhu; Zoltan Kaposzta; Hugh S. Markus; Juan Carlos Kaski Effect of Rosiglitazone on Common Carotid Intima-Media Thickness Progression in Coronary Artery Disease Patients Without Diabetes Mellitus Arteriosclerosis, Thrombosis, and Vascular Biology. 2004;24:930.

   


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