[Arterial wall and glitazones]

Numerous mechanisms contribute to impaired arterial wall in insulin resistant subjects and in type 2 diabetic patients. Endothelial dysfunction appears at an early stage of atherosclerosis progression, an accelerated process in diabetic patients. At a more advanced stage, arterial stiffness and thickening contribute to development of macroangiopathies. Inflammation plays a key role in these phenomena, particularly through growth factors and cytokines secretion in arterial wall cells. Thiazolidinediones, are pharmacological ligands of nuclear receptor PPARgamma and appear to act favorably on several pathophysiological mechanisms involved in these vascular dysfunctions and complications. Thiazolidinediones decrease plasma levels of C reactive protein, possess antiinflammatory effects through a reduction of inflammatory cytokines production, decrease free fatty acids levels, antagonize angiotensin II effects, increase adiponectin expression and production, etc. Pathophysiological mechanisms leading to vascular function impairment and their evaluation techniques are described, as well as the main thiazolidinediones beneficial effects on these mechanisms, which may lead to vascular prevention and/or protection in high cardiovascular risk insulin resistant and/or type 2 diabetic patients.