Gene polymorphisms affecting HDL-cholesterol
levels in the normolipidemic population
George Miltiadous
a
, Marilena Hatzivassiliou
b
,
Evagelos Liberopoulos
a
, Eleni Bairaktari
c
,
Alexandros Tselepis
d
, Marios Cariolou
b
, Moses Elisaf
a,
*
a
Department of Internal medicine, Medical School, University of Ioannina,
GR 451 10 Ioannina, Greece
b
Molecular Genetics Department, B-DNA Identification Laboratory,
The Cyprus Institute of Neurology and Genetics, Nicosia, Cyprus
c
Department of Biological Chemistry, Medical School, University of Ioannina, Ioannina, Greece
d
Department of Biochemistry, University of Ioannina, Ioannina, Greece
Received 23 March 2004; received in revised form 27 May 2004; accepted 16 September 2004
KEYWORDS
HDL-cholesterol;
Genes;
Apolipoprotein E;
Apolipoprotein A IV;
Cholesterol ester
transfer protein
Summary Background and aim: HDL-cholesterol (HDL-C) is inversely related to
the risk of ischemic heart disease. Many genes are reported to affect HDL-C serum
levels in both hyperlipidemic and normolipidemic populations, though the data are
controversial. We examined the effect of common gene polymorphisms known to
interfere with HDL-C metabolism (apolipoprotein E, cholesterol ester transfer
protein and apolipoprotein A-IV gene polymorphisms) on HDL-C plasma levels in
normolipidemic subjects.
Methods and results: The study population consisted of 200 normolipidemic
individuals visiting our clinic for a routine check-up. None of the above gene
polymorphisms affected HDL-C levels in our population. However, participants
carrying the allele E4 of the apolipoprotein (apo) E gene, the allele B1 of the TaqIB
polymorphisms in the cholesterol ester transfer protein (CETP) gene and the allele
T of the apoA-IV gene (A to T polymorphism at site 347) (nZ28) had statistically
significantly lower HDL-C levels compared to those not carrying the above allele
combination (0.99G0.33 vs 1.28G0.35 mmol/L, pZ0.04).
Conclusion: In this study, we describe a subgroup of normolipidemic individuals
with low HDL-C levels due to genetic variability, and we discuss the underlying
possible mechanisms involved.
ª 2005 Elsevier Ltd. All rights reserved.
* Corresponding author. Tel.: C30 2651097509; fax: C30 2651097016.
E-mail address: me00521@cc.uoi.gr (M. Elisaf).
0939-4753/$ - see front matter ª 2005 Elsevier Ltd. All rights reserved.
doi:10.1016/j.numecd.2004.09.004
Nutrition, Metabolism & Cardiovascular Diseases (2005) 15, 219e224
www.elsevier.com/locate/nmcd