The risk of atherosclerosis in patients with impaired glucose tolerance.

Objectives: Glucose metabolism disorders usually coexist with dyslipidemia and coagulation/fibrinolysis disturbances. Increase of insulin resistance followed by hyperinsulinemia leads to enhanced protein synthesis, including production of apolipoproteins. As a result, the structure of Low Density Lipoprotein (LDL) becomes small and dense. This augments lipid infiltration into the arterial wall. Following this process monocyte adhesion to endothelium initiates atherosclerotic injury. One of the markers of this inflammatory reaction is Monocyte Chemoattractant Peptide-1 (MCP-1). A lot of inflammatory mediators affect both oxidative modification of LDL and coagulation processes being responsible for anti-fibrinolytic predominance. Plasminogen Activator Inhibitor-1 (PAI-1) is a marker of this state. Therefore the aim of this study is to evaluate the marker of the oxidation processes (oxLDL) as well as prothrombotic (PAI-1) and inflammatory state (MCP-1) markers in patients with Impaired Glucose Tolerance (IGT).

Methods: The study was carried out on 16 subjects: 10 with biochemically confirmed IGT and 6 age-matched healthy persons without such disorders. Following tests were performed: OGTT, HbA(1c) level as well as TCh, HDL, LDL and TG. Plasma concentrations of oxLDL, PAI-1 and MCP-1 were measured using ELISA method.

Results: In patients with Impaired Glucose Tolerance plasma levels of oxLDL were significantly higher compared to control group (67.6 +/- 0.9 U/l vs. 57.8 +/- 4.0 U/l; p < 0.01) in spite of LDL levels, which did not reveal such difference. MCP-1 plasma concentration compared to control group occurred to be significantly increased in experimental group as well (156.4 +/- 9.2 ng/ml vs. 125.4 +/- 1.9 ng/ml; p < 0.05). PAI-1 level revealed most significant difference (84.0 +/- 1.8 ng/ml vs. 43.7 +/- 2.7 ng/ml; p < 0.0001).

Conclusions: It is concluded that patients with Impaired Glucose Tolerance should be considered as a group in which atherogenic modification of lipoproteins occurred. Also plasma inflammatory as well as prothrombotic markers concentration was elevated.