Paraoxonase-1 Q192R polymorphism and its association with hs-CRP and fasting blood glucose levels and risk of coronary artery disease
Paraoxonase-1 (PON1) has been shown to protect low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) against oxidative-modification and thereby might protect against coronary-artery-disease (CAD). Here we explored the relationship of a genetic variant (a substi...
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Veröffentlicht in: | Diabetes & metabolic syndrome clinical research & reviews 2019-03, Vol.13 (2), p.1053-1057 |
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Sprache: | eng |
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Zusammenfassung: | Paraoxonase-1 (PON1) has been shown to protect low-density lipoprotein cholesterol (LDL-C) and high-density lipoprotein cholesterol (HDL-C) against oxidative-modification and thereby might protect against coronary-artery-disease (CAD). Here we explored the relationship of a genetic variant (a substitution (R) Arg with (Q) Gln at position 192) of PON1 in 250 patients with/without CAD.
Genotyping of PON1 Q192R was carried out using Real-Time-PCR TaqMan-based-probe. Demographic-characteristics and biochemical-analyses, including fasting blood sugar (FBS), HDL, LDL, triglycerides (TG) and C-reactive protein (CRP) were evaluated. Univariate/multivariate analyses were performed to determine the association of the genetic polymorphism and CAD as well as with clinical-characteristics of population.
Our findings showed that RR-genotype was more frequent in CAD-patients, compared to the wild-type genotype. Moreover, CAD patients with RR-genotype had an odd ratio of 5.0 (95% CI: 1.3–18.6; p = 0.017), versus wild-type genotype, in multivariate-analysis. Of note we also observed that CAD-patients with QQ-genotype had a significantly lower Hs-CRP level, compared to the RR-genotype.
we demonstrate that PON1-Q192R-polymorphism was associated with CRP and FBS levels; R-allele of PON1-Q192R may be an independent risk factor for CAD. Further studies are warranted to determine the value of this marker as a surrogate marker in CAD patients. |
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ISSN: | 1871-4021 1878-0334 |
DOI: | 10.1016/j.dsx.2019.01.010 |