Effect of Gene Polymorphisms
on Lipoprotein Levels in Patients with Dyslipidemia of Metabolic
Syndrome
A. STANČÁKOVÁ, L. BALDAUFOVÁ, M. JAVORSKÝ, M.
KOZÁROVÁ,
J. ŠALAGOVIČ 1, I. TKÁČ
Department of Internal Medicine IV, Faculty of Medicine, Šafárik
University, 1Institute of Medical Biology, Faculty of Medicine,
Šafárik University, Košice, Slovak Republic
Received date July 26, 2005
Accepted date November 25, 2005
On-line available December 12, 2005
Summary
Dyslipidemia in the metabolic syndrome (MS) is considered to be
one of the most important risk factors for atherosclerosis. It
is characterized by hypertriglyceridemia, low concentration of
plasma HDL-cholesterol, predominance of small dense LDL
particles and an increased concentration of plasma
apolipoprotein B (apoB). The pathogenesis of this type of
dyslipidemia is partially explained, but its genetic background
is still unknown. To evaluate the influence of cholesterol ester
transfer protein (CETP) TaqIB polymorphism, lipoprotein lipase
(LPL) PvuII and HindIII polymorphisms, hepatic lipase (LIPC)
G-250A polymorphism and apolipoprotein C-III (APOC3) SstI gene
polymorphism on lipid levels in dyslipidemia of the metabolic
syndrome, 150 patients with dyslipidemia of metabolic syndrome
were included. 96 % of patients had type 2 diabetes. The
patients did not take any lipid lowering treatment. The
exclusion criterion was the presence of any disease that could
affect lipid levels, such as thyroid disorder, liver disease,
proteinuria or renal failure. Gene polymorphisms were determined
using the polymerase chain reaction and restriction fragment
length polymorphisms. The genotype subgroups of patients divided
according to examined polymorphisms did not differ in plasma
lipid levels with the exception of apoB. The apoB level was
significantly higher in patients with S1S1 genotype of APOC3
SstI polymorphism when compared with S1S2 group (1.10±0.26 vs.
0.98±0.21 g/l, p=0.02). Similarly, patients with H-H- genotype
of LPL HindIII polymorphism had significantly higher mean apoB,
compared with H+H- and H+H+ group (1.35±0.30 vs. 1.10±0.26 g/l,
p=0.02). In the multiple stepwise linear regression analysis,
apoB level seemed to be influenced by APOC3 SstI genotype, which
explained 6 % of its variance. The present study has shown that
the S1 allele of APOC3 SstI polymorphism and the H- allele of
LPL HindIII polymorphism might have a small effect on apoB
levels in the Central European Caucasian population with
dyslipidemia of metabolic syndrome.
Key words
Apolipoprotein B • Dyslipidemia • Metabolic syndrome • Genetic
polymorphisms
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