Abstract

It is known that in patients with type 2 diabetes (T2D) and the metabolic syndrome (MS) there is a higher risk for atherosclerosis. The aim of this study was to investigate the relationship of non-traditional risk factors for atherosclerosis, biomarkers of lipid peroxidation measured by oxidized LDL levels (oxLDL) and markers of finbrinolisis measured by plasminogen activator inhibitor 1 (PAI-1) in patients with T2D and the MS. MS was defined according to the criteria of the International Diabetes Federation (IDF). We analyzed the following metabolic parameters: levels of oxLDL (ELISA), PAI-1 (photometric method), plasma insulin (PI) levels (RIA method). Insulin resistance (IR) was defined using the homeostasis model (HOMA-IR). Total cholesterol (h), HDL-h, h-LDL and triglycerides (Tg) (enzymatic method). In this study we included 32 patients with T2D and MS (group A), 14 patients with T2D without MS (group B), 10 nondiabetic patients with MS (group C) and 15 nondiabetic patients without MS (group D). OxLDL level are significantly higher in group A vs group B (113.5 +/−8.8 U / L vs 109.6 +/- U / L, p <0.05), as well as in group C vs group D (108.4 +/−5.2 U / L vs 97.6 + /- U / L, p <0.05). We found no difference in the level of other lipid parameters comparing groups A and B, as well as groups C and D. Also, levels of PAI-1 are significantly higher in group A vs B (4.6 +/−0.5 mg/mL vs 3.2 +/-0.3 mg/mL, p <0.05), as well as in groups C vs D (5, 5 +/−0.7 mg/mL vs 3.1 +/−0.4 mg/mL, p <0.05). At the same time, in T2D and nondiabetic patients, the group with MS had significantly higher levels of HOMA. The observed elevated levels of oxLDL in patients with T2D correlate with the level of Tg/HDL ratio as an indicator of the presence of small dense LDL particles, whereas the level of PAI-1 levels correlated with HOMA. Our results indicate that in patients with T2D and MS there is significant impairment of lipid peroxidation, which may affect the structural changes of LDL, while observed fibrinolysis disorders could be induced by increasing insulin resistance in these patients.

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