Effect of interaction betweenPPARG,PPARAandADIPOQgene variants and dietary fatty acids on plasma lipid profile and adiponectin concentration in a large intervention study

AlSaleh, Aseel; Sanders, Tom; O’Dell, Sandra D.

doi:10.1017/s0029665111003181

Cited by 44 publications

(34 citation statements)

References 137 publications

(215 reference statements)

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“…Female gender was the variable with the stronger effect. Several other studies support our result that adiponectin concentration is higher in women than in men [14,27,30]. This difference is probably due to a direct effect of androgens on the synthesis of adiponectin [29].…”

Section: Discussionsupporting

confidence: 90%

“…Warodomwichit et al [16] found that -11391A allele carriers had significantly higher adiponectin levels and lower weight, BMI, and waist and hip circumferences, whereas in the study of AlSaleh et al [14] in subjects with different ethnicities there were no genotype-related differences. These discrepancies may be due to the interaction between the genetic variants and environmental factors.…”

Section: Discussionmentioning

confidence: 99%

“…This is considered a protective adipokine for its insulin-sensitizing and anti-inflammatory effects through its influence on immune and metabolic functions [13]. However, the adiponectin levels are significantly decreased in obesity and insulin-resistant states [14]. Conditions of hypoadiponectinemia may contribute to coronary heart disease, steatohepatitis, type 2 diabetes and some types of cancer [15].…”

Section: Introductionmentioning

confidence: 99%

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Effect of the ADIPOQ Gene -11391G/A Polymorphism Is Modulated by Lifestyle Factors in Mexican Subjects

et al. 2014

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Background/Aims: Single nucleotide polymorphisms (SNPs) in the ADIPOQ gene could explain the adiponectin level. However, the knowledge about the influence of genetic and lifestyle factors is not sufficient. The aim was to analyze whether the effect of the -11391G/A SNP in the ADIPOQ gene is modulated by lifestyle factors in Mexican subjects. Methods: A cross-sectional study was performed in which 394participants were analyzed. Genetic, anthropometric, biochemical, dietary, clinical and physical activity parameters were measured. Statistical analysis was performed with SPSSv19 software. Results: The distribution of the -11391G/A SNP genotypes was 55.6 and 44.4% for GG and AG, respectively. The adiponectin level was modulated by the -11391G/A SNP in response to the body mass index (BMI); A allele carriers showed a higher adiponectin level compared to G homozygous carriers but only in the minor BMI tertile group (p = 0.032). Adiponectin level variability was explained by gender [(r) = 1.5, 95% CI 1.1-1.9, p = 0.000], insulin resistance [(r) = -1.2, 95% CI -0.8 to -1.6, p = 0.000], physical activity [(r) = 0.6, 95% CI 0.2-0.9, p = 0.002] and monounsaturated fat intake [(r) = 0.5, 95% CI 0.38-1.0, p = 0.047]. Conclusions: The adiponectin level was modulated by the interaction between BMI and -11391G/A SNP; this suggests that the lifestyle rather than genetic factors modulates serum adiponectin.

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Section: Discussionsupporting

confidence: 90%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Effect of the ADIPOQ Gene -11391G/A Polymorphism Is Modulated by Lifestyle Factors in Mexican Subjects

et al. 2014

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“…However, other studies suggest that association between the genotype and BMI may depend on obesity (Ek et al 1999), age (Pihlajamaki et al 2004), dietary uptake of monounsaturated fatty acids (Garaulet et al 2011), and dietary ratio of polyunsaturated to saturated fatty acid (P/S ratio) (Luan et al 2001). Interestingly, dietary P/S ratio has also been shown to have an interaction with PPARG genotype on the effect on serum lipids in cross-sectional studies (Alsaleh et al 2011;Bouchard-Mercier et al 2011), and also in an intervention trial in which saturated fatty acid was replaced by monounsaturated fatty acid (AlSaleh et al 2012). Accordingly, animal studies suggest a complex interaction between PPARG2 and dietary fat.…”

Section: Introductionmentioning

confidence: 99%

Dietary polyunsaturated fatty acids and the Pro12Ala polymorphisms of PPARG regulate serum lipids through divergent pathways: a randomized crossover clinical trial

et al. 2015

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Human and animal studies suggest an interaction between the Pro12Ala polymorphism of PPARG and dietary fat. In this randomized crossover clinical trial, we investigated whether subjects with the Pro12Pro and Ala12Ala genotypes of PPARG respond differently to a diet supplemented with high saturated (SAFA) or polyunsaturated fatty acid (PUFA).We recruited non-diabetic men from a populationbased METSIM study (including 10,197 men) to obtain men with the Ala12Ala and the Pro12Pro genotypes matched for age and body mass index. Seventeen men with the Pro12Pro genotype and 14 with the Ala12Ala genotype were randomized to both a PUFA diet and a SAFA diet for 8 weeks in a crossover setting. Serum lipids and adipose tissue mRNA expression were measured during the diet intervention. At baseline, subjects with the Ala12Ala genotype had higher levels of HDL cholesterol and lower levels of LDL cholesterol, total triglycerides, and apolipoprotein B compared to those subjects with the Pro12Pro genotype (P \ 0.05, FDR \ 0

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“…Consistent with increased cellular proliferation, the activity of the tumour suppressors SMARCB1 (Modena, Lualdi et al 2005), RB1 and RBL2 (Villanueva 2014) and pro-apoptosis gene BNIPL3 (Diwan, Koesters et al 2008) was predicted to be inhibited. The activity of PPARA and PPARG, key regulators of fatty acid metabolism (AlSaleh, Sanders et al 2012) and transcriptional regulation (Salter and Tarling 2007) and the T-cell marker, CD3 as well as IRGM, an up-regulated gene in day 2 samples and day 7 feet, were also predicted to be inhibited in lymph nodes at day 7.…”

Section: Ingenuity Pathway Analysis Of Upstream Regulatorsmentioning

confidence: 99%

The role of type I interferon in the immunobiology of chikungunya virus

Wilson¹

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Chikungunya virus (CHIKV) is a mosquito-transmitted alphavirus that can cause explosive outbreaks of a febrile, arthritic/arthralgic disease usually lasting weeks to months, and in rare cases, more than a year. In 2004, the largest ever CHIKV outbreak began in Kenya, spreading to islands of the Indian Ocean, India, South East Asia and major outbreaks have recently occurred in the South Pacific Islands and the Caribbean.The host type I interferon (IFN) response is crucial for effective control of CHIKV infection.Herein, the dynamics, source and responses generated by the type I IFNs following CHIKV infection were investigated. RNASeq was undertaken to examine, in detail, the nature of the type I IFN responses generated in the feet and inguinal lymph nodes of mice following CHIKV infection at days 2 and 7 post-infection. High quality sequencing data was generated from III host and viral poly-adenylated RNA, permitting investigation of low level gene transcription from both sources, and the identification of novel genes/transcripts, in addition to analysis of differential gene expression.Investigation of host transcriptional activity revealed a type I IFN dominated immune response, in spite of a low induction of type I IFN mRNA transcripts at day 2 and an absence of type I IFN mRNA induction on day 7. Many type I IFN-regulated genes, including IRF7, remained up-regulated in the feet at day 7, suggesting type I IFNindependent mechanisms for maintenance of type I IFN-regulated gene expression. Six novel IRF3 isoforms and a potentially novel protein coding gene were also identified.RNA-Seq analysis of CHIKV transcriptional activity reflected the known CHIKV replication kinetics, in which virus replicates in the joints, and spreads to the draining lymph nodes, with viral titres peaking at day 2 and largely resolving at day 7. Assessment of mutations within the CHIKV genome showed an accumulation with time, with error accumulation higher in the lymph nodes than in the feet. These studies represent the first deep sequencing analysis of CHIKV genomes in tissues.The findings in this thesis substantially add to our knowledge of the role and function of the immune response after CHIKV, illustrating for the first time that type I IFNs protect against haemorrhagic shock and that expression of type I IFN inducible genes is maintained well after type I IFN induction has waned.

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Effect of interaction betweenPPARG,PPARAandADIPOQgene variants and dietary fatty acids on plasma lipid profile and adiponectin concentration in a large intervention study

Cited by 44 publications

References 137 publications

Effect of the <b><i>ADIPOQ</i></b> Gene -11391G/A Polymorphism Is Modulated by Lifestyle Factors in Mexican Subjects

Effect of the <b><i>ADIPOQ</i></b> Gene -11391G/A Polymorphism Is Modulated by Lifestyle Factors in Mexican Subjects

Dietary polyunsaturated fatty acids and the Pro12Ala polymorphisms of PPARG regulate serum lipids through divergent pathways: a randomized crossover clinical trial

The role of type I interferon in the immunobiology of chikungunya virus

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