ASSOCIATION OF THE ACE rs4646994 AND rs4341 POLYMORPHISMS WITH THE PROGRESSION OF CAROTID ATHEROSCLEROSIS IN SLOVENIAN PATIENTS WITH TYPE 2 DIABETES MELLITUS
Merlo S1, Novák J2,3,4, Tkáčová N2, Nikolajević Starčević J5, Šantl Letonja M6, Makuc J7, Cokan Vujkovac A7, Letonja J5, Bregar D5, Zorc M5, Rojko M5, Mankoč S5, Kruzliak P8, Petrovič D5
*Corresponding Author: Professor Daniel Petrovič, M.D., Ph.D., Institute of Histology and Embryology, Faculty of Medicine University Ljubljana, Korytkova 2, SI-1000 Ljubljana, Slovenia. Tel: +386-1-543-7367. Fax: +386-1- 543-7361. E-mail: daniel.petrovic@mf.uni-lj.si
page: 37

RESULTS

Patients with T2DM had a greater waist circumference, higher fasting glucose and Hb A1c levels compared to controls, whereas there were no statistically significant differences in age, body mass index (BMI), and systolic and diastolic blood pressure between patients with T2DM and control subjects (Table 1). Patients with T2DM had lower total, high density lipoprotein (HDL) and low density lipoprotein (LDL) cholesterol levels and higher triglyceride levels compared to controls (Table 1). Plasma levels of inflammatory markers (i.e., high sensitive C-reactive protein (hs-CRP) were statistically significantly higher in patients with T2DM compared to controls (Table 1). The genotype distributions both in patients with T2DM and controls were in the Hardy-Weinberg equilibrium for both ACE gene polymorphisms [rs4646994: T2DM (genotype frequencies: II genotype 21.5%, ID genotype 46.4%, DD genotype 32.1%; χ2 = 2.27; p = 0.13) and controls (genotype frequencies: II genotype 24.0%, ID genotype 49.0%, DD genotype 27.0%; χ2 = 0.07; p = 0.78); rs4341: T2DM (genotype frequencies: GG genotype 28.1%, GC genotype 52.1%, CC genotype 19.8%; χ2 = 1.44; p = 0.23) and controls (genotype frequencies: GG genotype 23.5%, GC genotype 54.5%, CC genotype 22.0%; χ2 = 1.63; p = 0.20)]. No statistically significant differences in the ACE rs4646994 and rs4341 genotype distribution frequencies were observed between the T2DM patients and controls. Moreover, in our study, linkage disequilibrium between the two selected single nucleotide polymorphisms (SNPs) (rs4646994 and rs4341) was confirmed (dí =0.98 r2=0.82). Several parameters of carotid atherosclerosis, such as CIMT, number of involved segments, and sum of plaque thicknesses, were evaluated with regard to different genotypes of both ACE polymorphisms in subjects with T2DM at enrollment and after 3.8 years (Table 2). Moreover, the parameters of progression of atherosclerosis, i.e., annual increase in CIMT, change in number of segments with plaques and change in the sum of carotid plaque thicknesses, were analyzed with univariate and multiple linear regression analyses (Tables 3 and 4). With regard to the progression of atherosclerosis in subjects with T2DM, statistically significant differences were demonstrated in the change of the sum of carotid plaque thickness for the rs4646994 polymorphism only (Table 3). Finally, according to the results of multiple linear regression analysis, faster progression of atherosclerosis was demonstrated in subjects with T2DM with the DD genotype of the rs 4646994 (ACE I/D) polymorphism in comparison with subjects with other genotypes (Table 4).



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