Endothelial Dysfunction Induced by Type 2 Diabetes Mellitus and Fibrinolytic Activity

Abstract

Problem statement: Type 2 diabetes mellitus is the world's largest systemic and metabolic disease. Endothelin (ET) was first described as a peptidergic endothelium-derived constricting factor. Endothelin-1 is one of the endothelial factors that is overexpressed in cases of endothelial dysfunction. The fibrinolytic system is present in plasma with the degradation of fibrin polymers in blood clots. It is a proteolytic mechanism that results in the formation of one main enzyme, plasmin, which cleaves fibrin. Approach: A total of 20 normal white albino rats weighing between 180-200 g were used and divided into two groups each of 10 rats, one group served as a control which fed on normal chow diet, while the second group fed on high fat diet for one month, then received streptozocin (25 mg kg^-1) intraperitoneally as a single dose and continued feeding on high fat diet. Plasma was separated to determine the levels of tissue Plasminogen Activator (t-PA), Plasminogen Activator Inhibitor-1 (PAI-1), Fibrin Degradation Products (FDPs) and Euglobulin Clot Lysis Time (ECLT). Results: Data showed that diabetic rats have inhibited fibrinolytic activity as detected from the significant increase in PAI-1, significant decrease in both t-PA and TDPs with significant prolongation of the ECLT relative to the control group. Conclusion: Endothelial dysfunction is associated with a prothrombotic state.