p.Q192R SNP of PON1 seems not to be Associated with Carotid Atherosclerosis Risk Factors in na Asymptomatic and Normolipidemic Brazilian Population Sample

Scherrer, Daniel; Zago, Vanessa Helena de Souza; Vieira, Isabela Calanca; Parra, Eliane Soler; Panzoldo, Natália Baratella; Alexandre, Fernanda Antunes; Secolin, Rodrigo; Baracat, Jamal; Quintão, Eder Carlos Rocha; Faria, Eliana Cotta de

doi:10.5935/abc.20150053

Cited by 9 publications

(9 citation statements)

References 44 publications

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“…Another relationship was also observed based on ethnicity for PON1 rs662 polymorphism in young subjects from Bogalusa Heart Study [57], whereas Karvonen et al did not observe a significant association between PON1 rs662 and carotid IMT in the general Caucasian population [58]. Another study also showed a lack of association of PON1 rs662 with carotid IMT and carotid atherosclerotic plaques [59]. Our study's findings support the conclusion that PON1 SNPs were not correlated with carotid IMT.…”

Section: Plos Onesupporting

confidence: 81%

Evaluation of single nucleotide polymorphisms in 6 candidate genes and carotid intima-media thickness in community-dwelling residents

Liao

et al. 2020

PLoS ONE

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Evidence suggests the existence of association between a large panel of modifiable biomarkers representing inflammation, coagulation, paraoxonase, and endothelial activation pathways and carotid atherosclerosis. Thus, this study investigated whether CRP, FGA, FGB, FGG, PON1, and EDNRA gene variants affected plasma hs-CRP, fibrinogen levels, and thickness of carotid intima media thickness (IMT). Nineteen single-nucleotide polymorphisms of CRP, FGA, FGB, FGG, PON1, and EDNRA genes were examined in 480 participants from 160 families. Carotid IMT was measured by ultrasound. Generalized linear models with generalized estimating equation were utilized to consider the dependence of subjects within families. In the recessive model, homozygotes for the minor alleles of rs1800789, rs1800790 and rs4220 SNPs in FGB gene indicated a reduced risk of IMT (Exp. β = 0.89, 0.89, 0.88), which remained significant after adjustment for confounding factors. Significant interaction effects between CRP SNP rs1130864 and rs3093059 and gender for IMT were observed with a significant association in men only. Men carrying minor-minor genotype of CRP SNP rs1130864 and rs3093059 had 0.70-and 0.78-fold lower IMT than men carrying minor-major/major-major genotype. We also observed that the interaction of CRP SNP rs1130864 and rs3093059 with obesity on IMT, hs-CRP and fibrinogen levels. These results support the hypothesis that inflammatory genes are involved in atherosclerosis, most likely via complex gene-gender and gene-obesity interactions.

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Section: Plos Onesupporting

confidence: 81%

Evaluation of single nucleotide polymorphisms in 6 candidate genes and carotid intima-media thickness in community-dwelling residents

Liao

et al. 2020

PLoS ONE

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“…LCAT activity was determined using recombinant HDL, according to standardized method [17]. PON activity was measured using paraoxon (diethyl-p-nitrophenylphosphate, Sigma, St. Louis, MO, USA) as substrate [18].…”

Section: Methodsmentioning

confidence: 99%

Excess weight mediates changes in HDL pool that reduce cholesterol efflux capacity and increase antioxidant activity

Lima-Júnior

Virginio

Moura

et al. 2019

Preprint

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Objective: Obesity-related decline in high-density lipoprotein (HDL) functions such as cholesterol efflux capacity (CEC) has supported the notion that this lipoprotein dysfunction may contribute for atherogenesis among obese patients. Besides, potentially other HDL protective actions may be affected with weight gain and these changes may occur even before the obesity range. Methods: Lipid profile, body mass index (BMI), biochemical measurements, and carotid intima-media thickness (cIMT) were obtained in this cross-sectional study with 899 asymptomatic individuals. HDL functions were measured in a subgroup (n=101). Results: Individuals with increased HDL-C had an attenuated increase in cIMT with elevation of BMI. CEC, HDL-C, HDL size and HDL-antioxidant activity were negatively associated with cIMT. BMI was inversely associated with HDL-mediated inhibition of platelet aggregation and CEC, but surprisingly it was directly associated with the antioxidant activity. Thus, even in non-obese, non-diabetic individuals, increased BMI is associated with a wide change in protective functions of HDL, reducing CEC and increasing antioxidant activity. In these subjects, decreased HDL concentration, size or function are related to increased atherosclerotic burden. Conclusion: Our findings demonstrate that in non-obese, non-diabetic individuals, the increasing values of BMI are associated with impaired protective functions of HDL and concomitant increase in atherosclerotic burden.

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“…Few variants of the PON1 gene was commonly investigated for their association with serum lipid traits. These variants include rs662 (Q192R), rs854560 (L55 M) and rs705379 which showed the association with TC, HDL-C and LDL-C in different populations worldwide [ 215 – 219 ]. However none of the GWAS conducted to date has identified the association of the polymorphism at this locus with serum lipid traits.…”

Section: Genetic Basis Of Polygenic Hypercholesterolemia – the Genes mentioning

confidence: 99%

Genetic determinants of inherited susceptibility to hypercholesterolemia – a comprehensive literature review

2017

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Hypercholesterolemia is a strong determinant of mortality and morbidity associated with cardiovascular diseases and a major contributor to the global disease burden. Mutations in four genes (LDLR, APOB, PCSK9 and LDLRAP1) account for the majority of cases with familial hypercholesterolemia. However, a substantial proportion of adults with hypercholesterolemia do not have a mutation in any of these four genes. This indicates the probability of having other genes with a causative or contributory role in the pathogenesis of hypercholesterolemia and suggests a polygenic inheritance of this condition. Here in, we review the recent evidence of association of the genetic variants with hypercholesterolemia and the three lipid traits; total cholesterol (TC), HDL-cholesterol (HDL-C) and LDL-cholesterol (LDL-C), their biological pathways and the associated pathogenetic mechanisms. Nearly 80 genes involved in lipid metabolism (encoding structural components of lipoproteins, lipoprotein receptors and related proteins, enzymes, lipid transporters, lipid transfer proteins, and activators or inhibitors of protein function and gene transcription) with single nucleotide variants (SNVs) that are recognized to be associated with hypercholesterolemia and serum lipid traits in genome-wide association studies and candidate gene studies were identified. In addition, genome-wide association studies in different populations have identified SNVs associated with TC, HDL-C and LDL-C in nearly 120 genes within or in the vicinity of the genes that are not known to be involved in lipid metabolism. Over 90% of the SNVs in both these groups are located outside the coding regions of the genes. These findings indicates that there might be a considerable number of unrecognized processes and mechanisms of lipid homeostasis, which when disrupted, would lead to hypercholesterolemia. Knowledge of these molecular pathways will enable the discovery of novel treatment and preventive methods as well as identify the biochemical and molecular markers for the risk prediction and early detection of this common, yet potentially debilitating condition.Electronic supplementary materialThe online version of this article (doi:10.1186/s12944-017-0488-4) contains supplementary material, which is available to authorized users.

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p.Q192R SNP of PON1 seems not to be Associated with Carotid Atherosclerosis Risk Factors in na Asymptomatic and Normolipidemic Brazilian Population Sample

Cited by 9 publications

References 44 publications

Evaluation of single nucleotide polymorphisms in 6 candidate genes and carotid intima-media thickness in community-dwelling residents

Evaluation of single nucleotide polymorphisms in 6 candidate genes and carotid intima-media thickness in community-dwelling residents

Excess weight mediates changes in HDL pool that reduce cholesterol efflux capacity and increase antioxidant activity

Genetic determinants of inherited susceptibility to hypercholesterolemia – a comprehensive literature review

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