Abstract
Diabetes mellitus is a group of metabolic diseases which result from defects in insulin secretion, or action, or both. Three main forms of diabetes are: type 1 diabetes mellitus, type 2 diabetes mellitus and type 3 or gestational diabetes mellitus. Endothelial dysfunction has been demonstrated in type 1 and type 2 diabetes. In type 1 diabetes, this alteration appears temporally linked to vascular disease and is more likely a consequence of the metabolic alterations. In type 2 diabetes, endothelial cell (EC) dysfunction is detectable very early in the course of the disease, even before overt hyperglycemia ensues, and may play a key role in the etiopathology of the vasculopathy associated with this disease. The hypothesis that endothelial dysfunction may be causative of some of the features of the syndrome of insulin resistance, however, deserves further research. Recent studies have provided evidence that adipose tissue may play a crucial role in the development of insulin resistance, type 2 diabetes, and their complications through the secretion of a variety of biologically active molecules (adipocytokines). Leptin affects insulin sensitivity and may participate in the development of hypertension. These adipocytokines may cause the atherosclerotic vascular disease in type 2 diabetes directly or through the development of insulin resistance. Therefore, the leptin-to-adiponectin ratio might serve as an atherogenic index superior to leptin or adiponectin alone. Furthermore, it has been demonstrated that endothelial progenitor cells (EPCs) are reduced in macrovascular diabetes complications. Hence, it might be interesting to study the effect of adipokines mainly leptin on EPCs from healthy individuals and patients with both type 1 and type 2 diabetes mellitus. This might provide opportunity to understand the cellular and intracellular changes in EPCs collected from patients with diabetes, and better knowledge of the molecular basis of diabetic disorders.
