J 2017

Polymorphism rs2073618 of the osteoprotegerin gene as a potential marker of subclinical carotid atherosclerosis in Caucasians with type 2 diabetes mellitus

PLESKOVIC, A., S.M. RAMUS, Z.J. PRAZNIKAR, M.S. LETONJA, A.C. VUJKOVAC et. al.

Základní údaje

Originální název

Polymorphism rs2073618 of the osteoprotegerin gene as a potential marker of subclinical carotid atherosclerosis in Caucasians with type 2 diabetes mellitus

Autoři

PLESKOVIC, A. (705 Slovinsko), S.M. RAMUS (705 Slovinsko), Z.J. PRAZNIKAR (705 Slovinsko), M.S. LETONJA (705 Slovinsko), A.C. VUJKOVAC (705 Slovinsko), K. GAZDIKOVA (703 Slovensko), M. CAPRNDA (703 Slovensko), L. GASPAR (703 Slovensko), Peter KRUŽLIAK (703 Slovensko, garant, domácí) a D. PETROVIC (705 Slovinsko)

Vydání

VASA-EUROPEAN JOURNAL OF VASCULAR MEDICINE, BERN 9, VERLAG HANS HUBER HOGREFE AG, 2017, 0301-1526

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30201 Cardiac and Cardiovascular systems

Stát vydavatele

Švýcarsko

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 1.210

Kód RIV

RIV/00216224:14110/17:00098765

Organizační jednotka

Lékařská fakulta

UT WoS

000409311400004

Klíčová slova anglicky

Subclinical carotid atherosclerosis; genetic polymorphism; osteoprotegerin; type 2 diabetes mellitus

Štítky

Příznaky

Mezinárodní význam, Recenzováno
Změněno: 21. 3. 2018 16:21, Soňa Böhmová

Anotace

V originále

Background: The OPG/RANKL/RANK (osteoprotegerin/receptor-activator of nuclear factor kappa B ligand/receptor-activator of nuclear factor kappa B) axis has been recently linked to the development of atherosclerosis and plaque destabilization. We have investigated whether polymorphism rs2073618 of the OPG gene is associated with subclinical markers of carotid atherosclerosis in subjects with type 2 diabetes mellitus (T2DM). Patients and methods: 595 subjects with T2DM were enrolled in the cross-sectional study. Subclinical markers of carotid atherosclerosis (carotid intima media thickness, plaque thickness, and plaques presence) were assessed with ultrasound at the time of recruitment. Genotyping for rs2073618 (a missense variant located in exon I of the OPG gene) was performed, and OPG serum levels were determined by ELISA. Results: Compared to the GG genotype, the CC genotype of the rs2073618 polymorphism had a significantly increased risk for the presence of carotid plaque (OR = 2.54, 95 % CI = 1.22-5.28, p = 0.01). No statistically significant difference could be detected (p = 0.68) upon comparing median values of serum OPG levels among studied genotype groups in subjects with T2DM. Multi-variable linear regression analyses in T2DM subjects demonstrated that GC and CC genotypes (p = 0.03 and p = 0.003), together with statin therapy (p = 0.009), were independent predictors of the number of carotid segments with plaques. Conclusions: Despite the fact that OPG rs2073618 genotypes failed to predict the serum OPG levels as there was no statistical difference among compared genotypes, our results demonstrate that the rs2073618 polymorphism could be a possible genetic marker for the prediction of increased risk for carotid plaque burden as a measure of advanced subclinical atherosclerosis in T2DM subjects.