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- May 12, 2008 |
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"Underlying Causes of Disease Progression: The Role of PPAR-gamma and the Metabolic and Vascular Actions of the TZDs"Prof. Nikolaus Marx (biography)
English - 2006-12-04 - 28 minutes
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 | (51 slides) |
Summary :
Type 2 diabetes mellitus is a complex metabolic disorder associated with various risk factors like dyslipidaemia, inflammation and hypertension. Patients with insulin resistance and type 2 diabetes mellitus exhibit an increased propensity to develop arteriosclerosis with its sequelae acute myocardial infarction and stroke. Anti-diabetic, PARγ−activating, thiazolidinediones (TZDs, glitazones) currently used to treat patients with type 2 diabetes, not only target insulin resistance and its associated risk factors but seem to have direct anti-atherogenic properties. As such, TZDs reduce blood glucose levels, modulate the typical lipid profile in these patients and reduce blood pressure.
In addition, TZDs have been shown to protect b-cell failure in experimental models and recent clinical data with rosiglitazone showed a 62% reduction in the development of type 2 diabetes in patients with increased FBG and/or impaired glucose tolerance.
With respect to anti-atherogenic effects, PPARγ expression has been found in the vessel wall in arteriosclerotic lesions and it has been demonstrated that anti-diabetic PPARg-activating TZDs exhibit direct anti-inflammatory and anti-atherogenic properties in vascular cells in all phases of atherogenesis. In the early phase, they inhibit monocyte and T-cell recruitment into the vessel wall; in the phase of fatty streak formation, TZDs modulate smooth muscle cell migration and T-cell activation, and in advanced lesion, PPARγ activators have been shown to limit the expression of matrix-degrading enzymes. Given the critical role of these processes in lesion development, these in vitro data suggested that anti-diabetic PPARg 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. Subsequently, clinical studies showed that treatment of patients with type 2 diabetes mellitus and coronary artery disease with PPARγ-activating TZDs reduces serum levels of novel inflammatory biomarkers of arteriosclerosis like CRP, improves endothelial function, and reduces restenosis after coronary stenting in non-diabetic subjects, suggesting that this concept of anti-inflammatory effects of TZDs holds true in treated patients. Moreover, recent studies have demonstrated that TZDs can directly influence inflammatory cell activation in the vessel wall, suggesting a plaque stabilizing effect of these agents.
Learning objectives :
After viewing this presentation the participant will be able to discuss:
- Metabolic and vascular aspects of insulin resistance
- Mechanism of action of the insulin-sensitizing thiazolidinedione (TZD) drugs
- Metabolic effects of TZDs, including effects on HDL-C and LDL particle size
- Vascular action of TZDs: in vitro and in vivo evidence for anti-inflammatory and anti-atherogenic properties
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