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 (d’ =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).
|
|
|
|
 |
Number 27
VOL. 27 (2), 2024 |
Number 27
VOL. 27 (1), 2024 |
Number 26
Number 26 VOL. 26(2), 2023 All in one |
Number 26
VOL. 26(2), 2023 |
Number 26
VOL. 26, 2023 Supplement |
Number 26
VOL. 26(1), 2023 |
Number 25
VOL. 25(2), 2022 |
Number 25
VOL. 25 (1), 2022 |
Number 24
VOL. 24(2), 2021 |
Number 24
VOL. 24(1), 2021 |
Number 23
VOL. 23(2), 2020 |
Number 22
VOL. 22(2), 2019 |
Number 22
VOL. 22(1), 2019 |
Number 22
VOL. 22, 2019 Supplement |
Number 21
VOL. 21(2), 2018 |
Number 21
VOL. 21 (1), 2018 |
Number 21
VOL. 21, 2018 Supplement |
Number 20
VOL. 20 (2), 2017 |
Number 20
VOL. 20 (1), 2017 |
Number 19
VOL. 19 (2), 2016 |
Number 19
VOL. 19 (1), 2016 |
Number 18
VOL. 18 (2), 2015 |
Number 18
VOL. 18 (1), 2015 |
Number 17
VOL. 17 (2), 2014 |
Number 17
VOL. 17 (1), 2014 |
Number 16
VOL. 16 (2), 2013 |
Number 16
VOL. 16 (1), 2013 |
Number 15
VOL. 15 (2), 2012 |
Number 15
VOL. 15, 2012 Supplement |
Number 15
Vol. 15 (1), 2012 |
Number 14
14 - Vol. 14 (2), 2011 |
Number 14
The 9th Balkan Congress of Medical Genetics |
Number 14
14 - Vol. 14 (1), 2011 |
Number 13
Vol. 13 (2), 2010 |
Number 13
Vol.13 (1), 2010 |
Number 12
Vol.12 (2), 2009 |
Number 12
Vol.12 (1), 2009 |
Number 11
Vol.11 (2),2008 |
Number 11
Vol.11 (1),2008 |
Number 10
Vol.10 (2), 2007 |
Number 10
10 (1),2007 |
Number 9
1&2, 2006 |
Number 9
3&4, 2006 |
Number 8
1&2, 2005 |
Number 8
3&4, 2004 |
Number 7
1&2, 2004 |
Number 6
3&4, 2003 |
Number 6
1&2, 2003 |
Number 5
3&4, 2002 |
Number 5
1&2, 2002 |
Number 4
Vol.3 (4), 2000 |
Number 4
Vol.2 (4), 1999 |
Number 4
Vol.1 (4), 1998 |
Number 4
3&4, 2001 |
Number 4
1&2, 2001 |
Number 3
Vol.3 (3), 2000 |
Number 3
Vol.2 (3), 1999 |
Number 3
Vol.1 (3), 1998 |
Number 2
Vol.3(2), 2000 |
Number 2
Vol.1 (2), 1998 |
Number 2
Vol.2 (2), 1999 |
Number 1
Vol.3 (1), 2000 |
Number 1
Vol.2 (1), 1999 |
Number 1
Vol.1 (1), 1998 |
|
|
