ADMA - A MEDIATOR OF ENDOTHELIAL CELL DYSFUNCTION IN TYPE 2 DIABETES MELLITUS

The number of people with diabetes mellitus has more than doubled globally, making it one of the most important public health challenges to all nations. Clinical trials show the role of ADMA as endogenous inhibitor of nitric oxide synthase and its connection to type 2 diabetes mellitus (T2DM). Several studies have provided evidence that ADMA acts as a mediator of endothelial cell dysfunction, representing the first step in the pathophysiological process of atherosclerosis. ADMA affects the integrity and the function of the vasculature itself through diverse mechanisms. The aim of our study was to analyze the association between endothelial dysfunction (measured by the ADMA) and IMT, lipids, RR, duration T2DM, duration hypertension, in patients with D2MT, compared to normal healthy individuals. We compared 43 patients with T2DM and control group of 41. Patients and control group were evaluated by clinical method (RR), ultrasound (IMT), and laboratory methods (cholesterol, HDL, LDL, triglycerides and ADMA). 42.5% of patients with T2DM had hypertension, and 11.6% were smokers. A statistically significant difference was observed between T2DM patients and the healthy controls for systolic blood pressure, cholesterol, triglycerides, HbAlc and ADMA. A positive statistical correlation was established between ADMA and T2DM duration, hypertension duration, systolic RR and cholesterol. A negative correlation was found between ADMA concentration and HDL-cholesterol. No correlation was established between ADMA and diastolic blood pressure, and to HbA1c. Serum ADMA changes confirm endothelial dysfunction in T2DM patients without condition complications. The connection between ADMA and lipids, systolic pressure, hyperglycemia, diabetes duration and hypertension is expressed at different levels. Damaged endothelium is a basis for changes, which in combination with risk factors and diabetes duration lead to atherosclerosis development.