PPARα L162V underlies variation in serum triglycerides and subcutaneous fat volume in young males

Uthurralt, Julieta; Gordish‐Dressman, Heather; Bradbury, Meg; Rocha, Carolina Tesi; Devaney, Joseph M.; Harmon, Brennan; Reeves, Erica K.M.; Brandoli, Cinzia; Hansen, Barbara C.; Seip, Richard L.; Thompson, Paul D.; Price, Thomas B.; Angelopoulos, Theodore J.; Clarkson, Priscilla M.; Moyna, Niall M.; Pescatello, Linda S.; Visich, Paul S.; Zoeller, Robert F.; Gordon, Paul M.; Hoffman, Eric P.

doi:10.1186/1471-2350-8-55

Cited by 39 publications

(35 citation statements)

References 23 publications

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“…The PPARα V162V genotype was found to be absent in our study, consistent with our previous study 7 and previous studies among Caucasians 13 and African Americans, 14 while the V162 allele was found to be absent among African Senegalese. 15 Meanwhile, despite having similar demographics with Malaysia, Chan et al 16 reported lower MAFs for this SNP -.005/.004/.02 in Singaporean Malays/Chinese/Indians.…”

Section: Discussionsupporting

confidence: 82%

“…Meanwhile, in Caucasian populations, MAF ranged from .06 to .08. 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.…”

Section: Discussionsupporting

confidence: 81%

“…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. 13,19 For PPARγ2 C161T SNPs, difference in the prevalence of MAF between ethnicities was noted in our current and previous 7 studies, with Indians showing significant lower MAF than Chinese. The MAF of Malaysian Indians was found to be similar with South Indians 28 and Caucasians.…”

Section: Discussionmentioning

confidence: 82%

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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: Discussionsupporting

confidence: 82%

Section: Discussionsupporting

confidence: 81%

Section: Discussionmentioning

confidence: 82%

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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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“…More precisely, the variations in total cholesterol, (apo) A-I and cholesterol concentrations in small LDL particles between individuals could be explained by the PPAR ␣ L162V polymorphism [5] . Other studies have also suggested that the PPAR ␣ L162V polymorphism was associated with increases in lipid concentrations [6][7] . These data suggest that genetic variations of the gene encoding the PPAR ␣ may also modulate the CVD risk profile [8] .…”

Section: Introductionmentioning

confidence: 99%

“…There is strong evidence that this variability in the response to diet is partly attributable to genetic factors [3] . Possible genetic variants, which may impact on the lipid response to treatment, are, among others, polymorphisms in genes encoding apolipoprotein (apo) E [4] and peroxisome proliferator-activated receptor-␣ (PPAR ␣ ) [5][6][7] . Of particular interest to the current research is an earlier study, which reported that the plasma lipoprotein/lipid responsiveness to a modification in the ratio of polyunsaturated to saturated fatty acids (FA) was influenced by the PPAR ␣ gene [5] .…”

Section: Introductionmentioning

confidence: 99%

Effect of the PPAR-Alpha L162V Polymorphism on the Cardiovascular Disease Risk Factor in Response to n–3 Polyunsaturated Fatty Acids

Caron-Dorval¹,

Paquet²,

Paradis³

et al. 2008

Lifestyle Genomics

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Background: Dietary n–3 polyunsaturated fatty acids (PUFAs) decrease the risk of cardiovascular disease (CVD). Yet, genetic variations of the gene encoding the peroxisome proliferator-activated receptor-α (PPARα) can also modulate CVD risk factors. Since fatty acids, including n–3 PUFAs, are natural ligands of PPARα, a gene-diet interaction effect could be observed. Aims: To examine whether n–3 PUFA- induced changes in CVD risk factors are influenced by the PPARα L162V polymorphism. Methods: Fourteen men, carriers of the V162 allele and 14 L162 homozygotes, were matched according to age and body mass index. Subjects followed, for 8 weeks, a low-fat diet and then were supplemented daily with 5 g of fish oil for 6 weeks. Results: Baseline characteristics were similar for both genotype groups. Independently of the genotype, the supplementation was associated with a significant decrease in plasma triacylglycerol and fasting glucose concentrations, diastolic blood pressure, and with an increase in total apolipoprotein B concentrations. The extent of the decrease in plasma triacylglycerol concentrations was comparable for both genotype groups (p < 0.03). A significant genotype-by-diet interaction effect was observed for plasma C-reactive protein concentrations (p = 0.01). Conclusions: The PPARα L162V polymorphism may contribute to the interindividual variability in the CVD risk factor response to n–3 PUFAs.

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PPARα L162V polymorphism alters the potential of n‐3 fatty acids to increase lipoprotein lipase activity

Rudkowska¹,

Caron-Dorval²,

Verreault

et al. 2010

Molecular Nutrition Food Res

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Omega-3 fatty acids (FAs) may accelerate plasma triglyceride (TG) clearance by altering lipoprotein lipase (LPL) activity. Yet, the ability of n-3 FAs to increase LPL activity is dependent on transcription factors such as peroxisome proliferator-activated receptor alpha (PPARalpha). The objective was to examine the effects of n-3 FAs on LPL activity considering the occurrence of PPARalpha L162V polymorphism. First, 14 pairs of men either L162 homozygotes or carriers of the V162 allele were supplemented with n-3 FAs. Second, transient transfections in HepG2 cells, for the L162- and V162-PPARalpha variants with the peroxisome proliferator-response element from the human LPL gene, were transactivated with n-3 FAs. In vivo results demonstrate that the LPL activity increased non-significantly by 14.4% in L162 homozygotes compared with 6.6% in carriers of the PPARalpha-V162 allele, after n-3 FA supplementation. Additionally, the L162 homozygotes tended towards an inverse correlation between LPL activities and plasma TG levels. Conversely, carriers of the V162 allele showed no such relationship. In vitro data demonstrates that transcription rates of LPL tended to be higher for the L162-PPARalpha than V162-PPARalpha after n-3 FAs activation. Overall, these results indicate that n-3 FA supplementation increases the transcription rate of LPL to a greater extent in L162-PPARalpha than V162-PPARalpha.

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PPARα L162V underlies variation in serum triglycerides and subcutaneous fat volume in young males

Cited by 39 publications

References 23 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

Effect of the PPAR-Alpha L162V Polymorphism on the Cardiovascular Disease Risk Factor in Response to n–3 Polyunsaturated Fatty Acids

PPARα L162V polymorphism alters the potential of n‐3 fatty acids to increase lipoprotein lipase activity

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