The apolipoprotein A5 (APOA5) gene predisposes Caucasian children to elevated triglycerides and vitamin E (Four Provinces Study)

Guardiola, Montse; Ribalta, Josep; Gómez-Coronado, Diego; Lasunción, Miguel A.; Oya, Manuel de; Garcés, Cármen

doi:10.1016/j.atherosclerosis.2010.07.004

Cited by 24 publications

(26 citation statements)

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“…First, circulating APOA-V can interact with lipoprotein lipase on the luminal side of endothelial cells to promote the hydrolysis of triglyceride-rich lipoproteins. Second, APOA-V, can bind the hepatic LDL-receptor to encourage the clearance of lipoprotein remnants [25]. Previous reports have shown that MetS prevalence and the risk of MetS is increased in individuals carrying the minor G allele in rs662799 (also known as –1131T>C), a SNP located in the upstream promoter region of the APOA5 gene [26-29].…”

Section: Discussionmentioning

confidence: 99%

Variants in APOA5 and ADIPOQ Moderate Improvements in Metabolic Syndrome during a One-Year Lifestyle Intervention

et al. 2018

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Background: Metabolic syndrome (MetS) comprises a cluster of risk factors including central obesity, hypertension, dyslipidemia, and impaired glucose homeostasis. Lifestyle interventions that promote improvements in diet quality and physical activity represent a first line of therapy for MetS. However, varying responses to lifestyle interventions are well documented and may be partially explained by underlying genetic differences. The aim of this study was to investigate if variants in genes previously associated with MetS influence the magnitude of change in MetS risk during a 1-year lifestyle intervention. Methods: The present study used data collected from the Canadian Health Advanced by Nutrition and Graded Exercise study cohort (n = 159 men and women) to investigate the effect of 17 candidate single nucleotide polymorphisms (SNPs) on response to a 1-year lifestyle intervention. Associations between SNPs and the continuous MetS (cMetS) score, as well as individual MetS components, were examined. Results: Reductions in cMetS score at both 3 months and 1 year were significantly associated with 2 variants: rs662799 (A/G) in apolipoprotein A5 (APOA5) and rs1501299 (G/T) in adiponectin (ADIPOQ). Individuals carrying a minor T allele in rs1501299 experienced a greater reduction in cMetS score at both 3 months and 1 year, whereas major allele AA homozygotes in rs662799 experienced greater reductions in cMetS score during the intervention. No associations were identified between the aforementioned SNPs and individual components of MetS. Both un-weighted and weighted genetic risk scores (GRS) using these 2 SNPs revealed that individuals carrying none of the risk alleles experienced significantly greater reductions in cMetS score after 1 year. Conclusions: The findings from the current study suggest that individuals with certain genotypes may benefit more from a lifestyle intervention for MetS and that specific variants, either independently or as part of a GRS, could be used as a nutrigenomic tool to tailor the intervention to reduce the risk of MetS.

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Section: Discussionmentioning

confidence: 99%

Variants in APOA5 and ADIPOQ Moderate Improvements in Metabolic Syndrome during a One-Year Lifestyle Intervention

et al. 2018

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“…Mutations in liver a-tocopherol transfer protein result in human a-tocopherol deficiency (14). It is also reported that human plasma levels of a-tocopherol but not g-tocopherol are increased in male adults and children by the apolipoprotein A5 1131T.C gene polymorphism (15,16). In mice, apoE4 mice have lower plasma a-tocopherol than apoE3 mice (17).…”

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confidence: 99%

Two Faces of Vitamin E in the Lung

Cook‐Mills

Abdala-Valencia

Hartert

2013

Am J Respir Crit Care Med

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Asthma and allergic lung disease occur as complex environmental and genetic interactions. Clinical studies of asthma indicate a number of protective dietary factors, such as vitamin E, on asthma risk. However, these studies have had seemingly conflicting outcomes. In this perspective, we discuss opposing regulatory effects of tocopherol isoforms of vitamin E, mechanisms for tocopherol isoform regulation of allergic lung inflammation, association of vitamin E isoforms with outcomes in clinical studies, and how the variation in global prevalence of asthma may be explained, at least in part, by vitamin E isoforms.Keywords: asthma; a-tocopherol; g-tocopherol; human; mouse Asthma and allergic lung disease occur as complex environmental and genetic interactions (1). The World Health Organization has reported that the prevalence of asthma from 1950 to the present has increased in many countries, including countries with high rates of asthma, intermediate rates of asthma, or low rates of asthma (2-4). The marked differences in rates of asthma within countries, in migrating populations, and over relatively short periods of time support an important role of the local environment, such as diet, in asthma inception. Prospective epidemiological studies, observational cross-sectional studies, and some randomized prevention trials have demonstrated the impact of a number of protective dietary factors, such as vitamin E, on asthma risk. However, these studies have had seemingly conflicting outcomes. We need to determine why there are low rates of allergic disease in developing countries and better understand the differences in diet and lifestyle that may really underpin allergic disease. One environmental change over the past 40 years has been an increase in the g-tocopherol isoform of vitamin E in the diet and in infant formulas (5, 6). We recently demonstrated that g-tocopherol increases allergic lung inflammation in mice (6)(7)(8). In this perspective, we discuss why we have yet to uncover the complex and potentially protective effects of isoforms of vitamin E on asthma in humans and in animal models of lung inflammation. We also review mechanisms for tocopherol isoform regulation of allergic lung inflammation in animals and discuss how the variation in global prevalence of asthma may be explained, at least in part, by country-specific plasma g-tocopherol differences.Vitamin E consists of natural isoforms and synthetic racemic isoforms. The eight natural isomers are d-a-, d-b-, d-g-, d-d-tocopherol and d-a-, d-b-, d-g-, d-d-tocotrienol. Plants synthesize the natural isoforms from tyrosine and chlorophyll (9). Then, these tocols are consumed in the diet from plant lipids. Mammals do not interconvert the tocopherol isoforms. The most abundant isoforms are a-tocopherol and g-tocopherol, which differ by one methyl group ( Figure 1A). There are approximately 10-fold higher tissue concentrations of a-tocopherol than g-tocopherol due to preferential transfer of a-tocopherol in the liver by a-tocopherol transfer protein and due to ...

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“…Indeed, blood concentrations of vitamin E can be modulated by the dietary intake of vitamin E, by oxidative stress (that may depletes vitamin E) (18), and by polymorphisms in genes involved in the metabolism of vitamin E and lipoproteins (19)(20)(21)(22)(23)(24)(25)(26)(27). Several candidate gene association studies showed that polymorphisms in genes involved in lipoprotein transport, such as APOE, APOA4, APOC3, hepatic lipase, SCARB1, CETP, TTPA, and SEC14L2 were associated with circulating vitamin E concentrations (19,(22)(23)(24)(25).…”

Section: Introductionmentioning

confidence: 99%

Polymorphisms in the CD36/FAT gene are associated with plasma vitamin E concentrations in humans

Lecompte

Edelenyi

Goumidi

et al. 2011

The American Journal of Clinical Nutrition

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Background: Blood vitamin E concentrations are modulated by dietary, metabolic, and genetic factors. CD36 (cluster of differentiation 36), a class B scavenger receptor, might be involved in tissue vitamin E uptake and thus would influence blood vitamin E concentrations. Objective: The goal of the study was to assess the association between CD36 single nucleotide polymorphisms (SNPs) and plasma a-tocopherol concentrations in humans. Design: A subsample from the adult SU.VI.MAX (SUpplementation en VItamines et Minéraux AntioXydants) cohort (n = 621) and the adolescent cross-sectional HELENA (Healthy Lifestyle in Europe by Nutrition in Adolescence) Study (n = 993) were genotyped for CD36 SNPs (4 and 10 SNPs, respectively). Fasting plasma a-tocopherol concentrations were assayed by using HPLC. Associations were determined by haplotype analyses and by general linear regression models. Results: In the SU.VI.MAX subsample, haplotype analyses showed that some haplotypes of SNPs rs1984112, rs1527479, rs7755, and rs1527483 tended to be associated with plasma a-tocopherol concentrations (P = 0.08 and P = 0.09 for haplotypes 1222 and 1122, respectively). We then investigated the whole known common genetic variability (10 SNPs) of CD36 in the HELENA Study. Three SNPs were associated with lower plasma a-tocopherol concentrations (rs1984112: 23.2%, P = 0.053; rs1761667: 22.9%, P = 0.046; rs1527479: 23.7%, P = 0.0061). After correction for multiple testing, the association between rs1527479 and a-tocopherol concentrations remained significant. This association was modulated by concentrations of fasting serum triglycerides (P for interaction = 0.006) and long-chain polyunsaturated fatty acids (P for interaction = 0.005). Conclusion: Our results suggest that CD36 can modulate blood a-tocopherol concentrations and may therefore be involved in the intestinal absorption or tissue uptake of vitamin E.Am J Clin Nutr 2011;93:644-51.

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The apolipoprotein A5 (APOA5) gene predisposes Caucasian children to elevated triglycerides and vitamin E (Four Provinces Study)

Cited by 24 publications

References 24 publications

Variants in <b><i>APOA5</i></b> and <b><i>ADIPOQ</i></b> Moderate Improvements in Metabolic Syndrome during a One-Year Lifestyle Intervention

Variants in <b><i>APOA5</i></b> and <b><i>ADIPOQ</i></b> Moderate Improvements in Metabolic Syndrome during a One-Year Lifestyle Intervention

Two Faces of Vitamin E in the Lung

Polymorphisms in the CD36/FAT gene are associated with plasma vitamin E concentrations in humans

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