Cholesteryl Ester Transfer Protein I405V Polymorphism Influences Apolipoprotein A-I Response to a Change in Dietary Fatty Acid Composition

Abolfathi, Ali Akbar; Noori, Mohammad; Kazemi, Asma; Ostadrahimi, Alireza; Rahimipour, Ali; Darabi, Masoud; Ghatreh‐Samani, Keihan

doi:10.1055/s-0029-1192034

Cited by 14 publications

(9 citation statements)

References 22 publications

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“…Most studies included both sexes, but two studies assessed CETP gene and diet interaction only in male subjects [ 23 , 42 ]. These studies were conducted in several different countries, including New Zealand [ 23 , 26 , 39 , 41 ], Israel [ 6 , 22 ], the United States [ 7 , 38 , 42 , 49 ], Europe [ 30 , 33 , 35 , 40 , 46 – 48 , 50 ], China [ 34 , 51 ], Brazil [ 43 , 44 ], Japan [ 21 ], Iran [ 36 ], and Canada [ 37 , 45 ]. The studies examined the effects of the following individual or combinations of polymorphisms: Taq1B (17 studies), I405V (7 studies), rs3764261 (2 studies), C > T/In9 (one study), and rs183130 (1 study).…”

Section: Resultsmentioning

confidence: 99%

Genetic variations of cholesteryl ester transfer protein and diet interactions in relation to lipid profiles and coronary heart disease: a systematic review

et al. 2017

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Data on diet–genotype interactions in the prevention or treatment of dyslipidemia have increased remarkably. This systematic review aimed to assess nutrigenetic studies regarding the modulating effect of diet on cholesteryl ester transfer protein (CETP) polymorphisms in relation to metabolic traits.Data were collected through studies published between 2000 and SEP. 2016 using five electronic databases. The quality of eligible studies was assessed using a 12-item quality checklist, derived from the STrengthening the REporting of Genetic Association Studies (STREGA) statement. CETP variants that had associations with lipid profiles in previous studies were extracted for drawing of the linkage disequilibrium (LD) plot.Among CETP variants, the rs9989419 best represented this genome wide association signal across all populations, based on LD r2 estimates from 1000 genomes references. In the 23 found eligible studies (clinical trials and observational), the TaqIB and I405V polymorphisms were the two most intensively studied. Two studies reported the effect of interaction between rs3764261 and diet on lipid levels. Regarding the rs708272 (Taq1B), individuals with the B1 risk allele showed better responses to dietary interventions than those with B2B2 genotype, whereas with I405V, inconsistent results have been reported. Modest alcohol consumption was associated with decreased risk of coronary heart disease among B2 carriers of rs708272.It is concluded that variations in the CETP gene may modulate the effects of dietary components on metabolic traits. These results have been controversial, indicating complex polygenic factors in metabolic response to diet and lack of uniformity in the study conditions and designs.Electronic supplementary materialThe online version of this article (10.1186/s12986-017-0231-1) contains supplementary material, which is available to authorized users.

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Section: Resultsmentioning

confidence: 99%

Genetic variations of cholesteryl ester transfer protein and diet interactions in relation to lipid profiles and coronary heart disease: a systematic review

et al. 2017

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“…The altered expression of cat (catalase) is associated with oxidative DNA damage and subsequent cancer susceptibility [92], [93]. Cetp (Cholesteryl ester transfer protein), also called plasma lipid transfer protein [94], [95] and Abca1 (ATP-binding cassette transporter sub-family) are major regulators of cellular cholesterol and phospholipid homeostasis. Abca1functions as a cholesterol efflux pump in the cellular lipid removal pathway [96].…”

Section: Discussionmentioning

confidence: 99%

Genome-Wide Identification of Molecular Pathways and Biomarkers in Response to Arsenic Exposure in Zebrafish Liver

Lam

Shen

et al. 2013

PLoS ONE

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Inorganic arsenic is a worldwide metalloid pollutant in environment. Although extensive studies on arsenic-induced toxicity have been conducted using in vivo and in vitro models, the exact molecular mechanism of arsenate toxicity remains elusive. Here, the RNA-SAGE (serial analysis of gene expression) sequencing technology was used to analyse hepatic response to arsenic exposure at the transcriptome level. Based on more than 12 million SAGE tags mapped to zebrafish genes, 1,444 differentially expressed genes (750 up-regulated and 694 down-regulated) were identified from a relatively abundant transcripts (>10 TPM [transcripts per million]) based on minimal two-fold change. By gene ontology analyses, these differentially expressed genes were significantly enriched in several major biological processes including oxidation reduction, translation, iron ion transport, cell redox, homeostasis, etc. Accordingly, the main pathways disturbed include metabolic pathways, proteasome, oxidative phosphorylation, cancer, etc. Ingenity Pathway Analysis further revealed a network with four important upstream factors or hub genes, including Jun, Kras, APoE and Nr2f2. The network indicated apparent molecular events involved in oxidative stress, carcinogenesis, and metabolism. In order to identify potential biomarker genes for arsenic exposure, 27 out of 29 up-regulated transcripts were validated by RT-qPCR analysis in pooled RNA samples. Among these, 14 transcripts were further confirmed for up-regulation by a lower dosage of arsenic in majority of individual zebrafish. Finally, at least four of these genes, frh3 (ferrintin H3), mgst1 (microsomal glutathione S-transferase-like), cmbl (carboxymethylenebutenolidase homolog) and slc40a1 (solute carrier family 40 [iron-regulated transporter], member 1) could be confirmed in individual medaka fish similarly treated by arsenic; thus, these four genes might be robust arsenic biomarkers across species. Thus, our work represents the first comprehensive investigation of molecular mechanism of asenic toxicity and genome-wide search for potential biomarkers for arsenic exposure.

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“…Additionally, carriers of the I405V (rs5882) polymorphism in the CETP gene had higher plasma TC levels when consuming a high-TotFat diet. Previously, Darabi et al ( 38 ) showed that subjects carrying the mutated allele had a greater reduction in plasma HDL-C levels without changes in TC compared with subjects with the other genotype after a diet low in PUFA:SatFat ratio ( 38 ) . Thus, these genetic variations may modulate the effect of dietary fat on blood lipids in the Inuit and other populations; yet, more studies are needed to validate these gene–diet interaction effects.…”

Section: Discussionmentioning

confidence: 99%

Gene–diet interactions on plasma lipid levels in the Inuit population

et al. 2012

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The Inuit population is often described as being protected against CVD due to their traditional dietary patterns and their unique genetic background. The objective of the present study was to examine gene -diet interaction effects on plasma lipid levels in the Inuit population. Data from the Qanuippitaa Nunavik Health Survey (n 553) were analysed via regression models which included the following: genotypes for thirty-five known polymorphisms (SNP) from twenty genes related to lipid metabolism; dietary fat intake including total fat (TotFat) and saturated fat (SatFat) estimated from a FFQ; plasma lipid levels, namely total cholesterol (TC), LDL-cholesterol (LDL-C), HDL-cholesterol (HDL-C) and TAG. The results demonstrate that allele frequencies were different in the Inuit population compared with the Caucasian population. Further, seven SNP (APOA1 2 75G/A (rs670), APOB XbAI (rs693), AGT M235T (rs699), LIPC 480C/T (rs1800588), APOA1 84T/C (rs5070), PPARG2 2618C/G (rs10865710) and APOE 219G/T (rs405509)) in interaction with TotFat and SatFat were significantly associated with one or two plasma lipid parameters. Another four SNP (APOC3 3238C . G (rs5128), CETP I405V (rs5882), CYP1A1 A4889G (rs1048943) and ABCA1 Arg219Lys (rs2230806)) in interaction with either TotFat or SatFat intake were significantly associated with one plasma lipid variable. Further, an additive effect of these SNP in interaction with TotFat or SatFat intake was significantly associated with higher TC, LDL-C or TAG levels, as well as with lower HDL-C levels. In conclusion, the present study supports the notion that gene -diet interactions play an important role in modifying plasma lipid levels in the Inuit population.

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Cholesteryl Ester Transfer Protein I405V Polymorphism Influences Apolipoprotein A-I Response to a Change in Dietary Fatty Acid Composition

Cited by 14 publications

References 22 publications

Genetic variations of cholesteryl ester transfer protein and diet interactions in relation to lipid profiles and coronary heart disease: a systematic review

Genetic variations of cholesteryl ester transfer protein and diet interactions in relation to lipid profiles and coronary heart disease: a systematic review

Genome-Wide Identification of Molecular Pathways and Biomarkers in Response to Arsenic Exposure in Zebrafish Liver

Gene–diet interactions on plasma lipid levels in the Inuit population

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