The risk of atherosclerosis in patients with impaired glucose tolerance.
OBJECTIVE
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.
Okopien
B
B
Department of Clinical Pharmacology, Medical University of Silesia, Medykow 18, 40-752 Katowice, Poland. mbkdokop@mp.pl
Stachura-Kulach
A
A
Kulach
A
A
Kowalski
J
J
Zielinski
M
M
Wisniewska-Wanat
M
M
Sierant
M
M
Kalina
Z
Z
Herman
Z Stanislaw
ZS
D000328:Adult; D001161:Arteriosclerosis / Q000209:etiology; D016022:Case-Control Studies; D004797:Enzyme-Linked Immunosorbent Assay; D044882:Glucose Metabolism Disorders / Q000097:blood* / Q000150:complications; D006442:Glycated Hemoglobin / Q000378:metabolism*; D006801:Humans; D008077:Lipoproteins, LDL / Q000097:blood*; D008875:Middle Aged; D018945:Monocyte Chemoattractant Proteins / Q000097:blood*; D017395:Plasminogen Activator Inhibitor 1 / Q000097:blood*; D012307:Risk Factors
D006442:Glycated Hemoglobin; D008077:Lipoproteins, LDL; D018945:Monocyte Chemoattractant Proteins; D017395:Plasminogen Activator Inhibitor 1; C099252:oxidized low density lipoprotein