The dependence of serum interleukin-6 level on PPAR-alpha polymorphism in men with coronary atherosclerosis

Skoczyńska, Anna; Dobosz, Tadeusz; Poręba, Rafał; Turczyn, Barbara; Derkacz, Arkadiusz; Żołędziewska, Magdalena; Jonkisz, Anna; Lebioda, Arleta

doi:10.1016/j.ejim.2005.04.012

Cited by 15 publications

(19 citation statements)

References 19 publications

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“…13,[18][19][20][21] In agreement with our current and previous findings, 7 PPARα L162V SNP was not associated with obesity in the Chinese Han, 17 Brazilians 22 and Caucasians. 4,[23][24][25] Furthermore, a study conducted by Robitaille et al 23 reported no association of this SNP with Met-S among Caucasian men, consistent with our current finding. The current study which also found that the lipid profile, glucose metabolism parameters and adiponectin levels were not affected by PPARα L162V SNP, is further supported by some studies, 4,18,22,24,26,27 but not others.…”

Section: Discussionsupporting

confidence: 82%

Screening of Peroxisome Proliferator-activated Receptors (PPARs) α, γ and δ Gene Polymorphisms for Obesity and Metabolic Syndrome Association in the Multi-ethnic Malaysian Population

Chia¹,

Fan²,

Say

2015

Ethn Dis

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Objective: This study aimed to investigate the association of peroxisome proliferatoractivated receptor (PPAR) genes PPARα L162V, PPARγ2 C161T and PPARδ T294C single nucleotide polymorphisms (SNPs) with obesity and metabolic syndrome (Met-S) in a multi-ethnic population in Kampar, Malaysia.Methods: Socio-demographic data, anthropometric and biochemical measurements (plasma lipid profile, adiponectin and interleukin-6 [IL-6] levels) were taken from 307 participants (124 males; 180 obese; 249 Met-S; 97 Malays, 85 ethnic Chinese, 55 ethnic Indians). Results:The overall minor allele frequencies were .08, .22 and .30 for PPAR α L162V, γ C161T, δ T294C, respectively. All SNPs were not associated with obesity, Met-S and obesity with/without Met-S by χ 2 analysis, ethnicity-stratified and logistic regression analyses. Nevertheless, participants with V162 allele of PPARα had significantly higher IL-6, while those with T161 allele of PPARγ2 had significantly lower HOMA-IR. Conclusions

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Section: Discussionsupporting

confidence: 82%

Screening of Peroxisome Proliferator-activated Receptors (PPARs) α, γ and δ Gene Polymorphisms for Obesity and Metabolic Syndrome Association in the Multi-ethnic Malaysian Population

Chia¹,

Fan²,

Say

2015

Ethn Dis

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“…On the other hand, aortic explants isolated from PPARα-null mice exhibit an exacerbated response to inflammatory stimuli such as LPS, as demonstrated by increased IL-6 secretion [19]. Furthermore, the frequency of the V allele of the L162V polymorphism in the PPARα gene is significantly elevated in men with coronary atherosclerosis when compared with healthy controls, demonstrating a positive correlation with serum IL-6 levels [95]. In PPARα-deficient mice, anti-inflammatory activity of fibrates is abolished due to enhanced expression of inhibitor of κBα (IκBα) [96].…”

Section: Pparα Limits Vascular Inflammationmentioning

confidence: 95%

Peroxisome Proliferator-Activated Receptor α in Lipid Metabolism and Atherosclerosis

Zheng

Tang

2015

Advances in Clinical Chemistry

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“…12 It is noteworthy that polymorphisms in PPAR-␣ have also been linked to effects on CRP, high-density lipoproteins, and interleukin-6. 13,14 While the technical axis of the nutrigenomic model may be of little interest to the empowered consumer, the information axis is another matter. Herein, internet-accessible authoritative statements regarding the health benefits of n-3 PUFAs approved by the Food and Drug Administration 15 or dietary guidelines offered by the American Heart Association 16 are integral to the success of the model.…”

Section: Preemptive Nutrition Modelmentioning

confidence: 99%

Preemptive Nutrition of Pro-inflammatory States: A Nutrigenomic Model

Gillies¹

2007

Nut. Rev.

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Nutrigenomics may provide the nutritional sciences with a molecular basis for positioning nutritional bioactives, functional foods, and designer diets to preemptively offset chronic disease. The preemptive model of nutrition consists of multiple interdependent parts that can be simplified into a number of principle axes. The science axis links nutrient-gene interaction with a health or disease state; the clinical axis ties in the modifying effects of genetic polymorphisms to biomarkers of clinical effect; and the information axis links empowered consumers to authoritative information and counseling resources. Despite the complexity of the model and the nascent state of the nutrigenomic sciences, there are emerging examples of how the model might be reduced to practice, such as the use of n-3 polyunsaturated fatty acids (PUFAs) in the dietary management of proinflammatory states. Although tightly controlled small-scale clinical studies with n-3 PUFAs are encouraging, what is needed are large-scale studies in free-living populations to broadly validate the molecular model of preemptive nutrition. With the expansion of research and the development of shared nutrigenomic databases, it may well become possible to define and track the influence of targeted nutrition on inflammation and the aging process.

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The dependence of serum interleukin-6 level on PPAR-alpha polymorphism in men with coronary atherosclerosis

Cited by 15 publications

References 19 publications

Screening of Peroxisome Proliferator-activated Receptors (PPARs) α, γ and δ Gene Polymorphisms for Obesity and Metabolic Syndrome Association in the Multi-ethnic Malaysian Population

Screening of Peroxisome Proliferator-activated Receptors (PPARs) α, γ and δ Gene Polymorphisms for Obesity and Metabolic Syndrome Association in the Multi-ethnic Malaysian Population

Peroxisome Proliferator-Activated Receptor α in Lipid Metabolism and Atherosclerosis

Preemptive Nutrition of Pro-inflammatory States: A Nutrigenomic Model

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