Gene–gene interactions among PPARα/δ/γ polymorphisms for hypertriglyceridemia in Chinese Han population

Gu, Shujun; Liu, Mengmeng; Guo, Zhirong; Wu, Ming; Qiu, Changjian; Zhou, Zhengyuan; Zhang, Lijun; Luo, Wenshu

doi:10.1016/j.gene.2012.11.078

Cited by 16 publications

(20 citation statements)

References 21 publications

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“…45 The MAF in Chinese Han population was reported as. 30,42,46 which is similar to the MAF of Malaysian Chinese population in our study. Similar with our study, several studies from other populations reported the lack of association of PPARδ T294C SNP with obesity, 38,47 Met-S and their related clinical variables.…”

Section: Ppar Gene Variants and Obesity In Malaysians -Chia Et Alsupporting

confidence: 85%

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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: Ppar Gene Variants and Obesity In Malaysians -Chia Et Alsupporting

confidence: 85%

“…31,32,36,37,41 However, Gu et al 42 and Yilmaz-Aydogan et al 43 reported that the T161 allele carriers had higher serum TG.…”

Section: Ppar Gene Variants and Obesity In Malaysians -Chia Et Almentioning

confidence: 99%

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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“…Indian populations [38] [39], hypertriglyceridemia risk, dyslipidemia risk and low-density lipoprotein-cholesterol risk in Han Chinese [10] [11] [16]. The two alleles (C/G) of the SNP generates seven conserved punitive TFBS between the alleles while the common C allele generates an additional six unique TFBS and the minor G allele generates two unique TFBS (Table 2).…”

Section: ) Has Been Associated With Variation In Lipid Serum Levmentioning

confidence: 99%

“…Chinese [10] [11] [17]. The two alleles (C/G) of the rs9794 SNP generates eleven conserved punitive TFBS between the alleles while the common C allele generates eleven unique punitive TFBS and the minor G allele generates no unique TFBS (Table 2).…”

Section: ) Has Been Associated With Variation In Lipid Serum Levmentioning

confidence: 99%

Identifying Changes in Punitive Transcriptional Factor Binding Sites Created by PPAR<i>α/δ/γ</i> SNPs Associated with Disease

Buroker¹

2017

JBM

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Single nucleotide polymorphisms (SNPs) located in the PPARα/δ/γ genes that have been previously found to be significantly associated with human disease or a condition were also found to alter the genes punitive transcriptional factor binding sites (TFBS). Two alleles (C/G) of the PPARα SNP (rs1800206) were found to generate 7 common and 8 unique punitive TFBS. One of the unique TFBS created by the minor G (0.02) allele is for the T-Box 4 (TBX4) transcription factor which is associated with heritable pulmonary arterial hypertension. Two alleles (A/G) of the PPARδ SNP (rs2016520) were found to generate 20 unique punitive TFBS while the two alleles (C/G) of the PPARδ SNP (rs9794) were found to generate 11 common and 11unique punitive TFBS. The alleles of the PPARγ SNPs (rs10865710, rs12629751, rs709158, rs1805192 and rs3856806) were found to generate 15, 12, 16, 2 and 21 common and 9, 4, 12, 4 and 7 unique punitive TFBS, respectively. These changes in TFBS are discussed with relation to alterations in gene expression that may result in disease or change in human condition.

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“…The gene, which encodes PPARγ is located on chromosome 3p25. Polymorphisms in PPARγ gene may contribute to the risk of hypertriglyceridemia independently and/or in an interactive manner [146]. The rs1801282: Pro12Ala variant (MAF(E): 0.076; MAF(A): 0.056) is the most widely studied, common alteration of the PPARγ gene, which is highly prevalent in Caucasians.…”

Section: Peroxisome Proliferator-activated Receptors (Ppars)mentioning

confidence: 99%

Radioprotectors and Mitigators: Current Status

Yazlovitskaya¹

2013

J Bioequiv Availab

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Type 2 diabetes mellitus represents a significant global health problem contributing to a considerably increased atherosclerotic burden and cardio-and cerebrovascular risk. Type 2 diabetes mellitus has high incidence and prevalence affecting both genders at any time of life worldwide. Presence of diabetes related phenotypes may represent risk for other metabolic diseases, cardio-, and cerebrovascular disorders, as well. The etiology of type 2 diabetes mellitus is complex; several environmental-, and genetic factors have been identified, which can contribute to the pathogenesis of the disease. Nowadays, numerous genetic loci have been shown to associate with type 2 diabetes mellitus and other diabetic traits, and the number of the identified susceptibility variants is expected to still grow due to rapidly developing field of candidate gene -, linkage-, and genome-wide association studies. The identified genetic variants can affect various metabolic pathways like glucose-, and lipid metabolism, signal transduction and can have effects on transcriptional-and translational levels. Among these, lipid alterations especially increased levels of triglycerides have been found to correlate to various disease phenotypes. It is also well known, that genetic variants identified in triglyceride metabolism are often shared as presence of these SNPs can confer risk for various disorders equally representing a susceptibility link between disorders. The scope of the current review is to summarize shared susceptibility variants, which have effect on the circulating lipid levels and represent risk for type 2 diabetes mellitus.

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Gene–gene interactions among PPARα/δ/γ polymorphisms for hypertriglyceridemia in Chinese Han population

Cited by 16 publications

References 21 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

Identifying Changes in Punitive Transcriptional Factor Binding Sites Created by PPAR<i>α/δ/γ</i> SNPs Associated with Disease

Radioprotectors and Mitigators: Current Status

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Gene–gene interactions among PPARα/δ/γ polymorphisms for hypertriglyceridemia in Chinese Han population

Cited by 16 publications

References 21 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

Identifying Changes in Punitive Transcriptional Factor Binding Sites Created by PPAR&lt;i&gt;α/δ/γ&lt;/i&gt; SNPs Associated with Disease

Radioprotectors and Mitigators: Current Status

Contact Info

Product

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Identifying Changes in Punitive Transcriptional Factor Binding Sites Created by PPAR<i>α/δ/γ</i> SNPs Associated with Disease