Dataset Information

Interaction of dietary fat intake with APOA2, APOA5 and LEPR polymorphisms and its relationship with obesity and dyslipidemia in young subjects.

ABSTRACT: Diet is an important environmental factor that interacts with genes to modulate the likelihood of developing disorders in lipid metabolism and the relationship between diet and genes in the presence of other chronic diseases such as obesity. The objective of this study was to analyze the interaction of a high fat diet with the APOA2 (rs3813627 and rs5082), APOA5 (rs662799 and rs3135506) and LEPR (rs8179183 and rs1137101) polymorphisms and its relationship with obesity and dyslipidemia in young subjects.The study included 200 young subjects aged 18 to 25 years (100 normal-weight and 100 obese subjects). Dietary fat intake was measured using the frequency food consumption questionnaire. Genotyping of polymorphisms was performed by PCR-RFLP.Individuals carrying the APOA5 56 G/G genotype with a high saturated fatty acid consumption (OR = 2.7, p = 0.006) and/or total fat (OR = 2.4, p = 0.018), associated with an increased risk of obesity. We also found that A/G + G/G genotypes of the 668 A/G polymorphism in the LEPR gene with an intake ? 12 g/d of saturated fatty acids, have 2.9 times higher risk of obesity (p = 0.002), 3.8 times higher risk of hypercholesterolemia (p = 0.002) and 2.4 times higher risk of hypertriglyceridemia (p = 0.02), than those with an intake <12 g/d of saturated fatty acids. Similarly, LEPR 668 A/G + G/G carriers with a high fat total intake had 3.0 times higher risk of obesity (p = 0.002) and 4.1 times higher risk of hypercholesterolemia (p = 0.001).Our results suggest that dietary fat intake modifies the effect of APOA5 and LEPR polymorphisms on serum triglycerides, cholesterol levels and obesity in young subjects.

SUBMITTER: Dominguez-Reyes T

PROVIDER: S-EPMC4568066 | biostudies-literature | 2015 Sep

REPOSITORIES: biostudies-literature

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Interaction of dietary fat intake with APOA2, APOA5 and LEPR polymorphisms and its relationship with obesity and dyslipidemia in young subjects.

Domínguez-Reyes Teresa T Astudillo-López Constanza C CC Salgado-Goytia Lorenzo L Muñoz-Valle José F JF Salgado-Bernabé Aralia B AB Guzmán-Guzmán Iris P IP Castro-Alarcón Natividad N Moreno-Godínez Ma E ME Parra-Rojas Isela I

Lipids in health and disease 20150913

<h4>Background</h4>Diet is an important environmental factor that interacts with genes to modulate the likelihood of developing disorders in lipid metabolism and the relationship between diet and genes in the presence of other chronic diseases such as obesity. The objective of this study was to analyze the interaction of a high fat diet with the APOA2 (rs3813627 and rs5082), APOA5 (rs662799 and rs3135506) and LEPR (rs8179183 and rs1137101) polymorphisms and its relationship with obesity and dysl ...[more]

PMID: 26365669

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Project description:BackgroundThe putative functional variant -265T>C (rs5082) within the APOA2 promoter has shown consistent interactions with saturated fatty acid (SFA) intake to influence the risk of obesity.ObjectiveThe aim of this study was to implement an integrative approach to characterize the molecular basis of this interaction.DesignWe conducted an epigenome-wide scan on 80 participants carrying either the rs5082 CC or TT genotypes and consuming either a low-SFA (<22 g/d) or high-SFA diet (≥22 g/d), matched for age, sex, BMI, and diabetes status in the Boston Puerto Rican Health Study (BPRHS). We then validated the findings in selected participants in the Genetics of Lipid Lowering Drugs and Diet Network (GOLDN) Study (n = 379) and the Framingham Heart Study (FHS) (n = 243). Transcription and metabolomics analyses were conducted to determine the relation between epigenetic status, APOA2 mRNA expression, and blood metabolites.ResultsIn the BPRHS, we identified methylation site cg04436964 as exhibiting significant differences between CC and TT participants consuming a high-SFA diet, but not among those consuming low-SFA. Similar results were observed in the GOLDN Study and the FHS. Additionally, in the FHS, cg04436964 methylation was negatively correlated with APOA2 expression in the blood of participants consuming a high-SFA diet. Furthermore, when consuming a high-SFA diet, CC carriers had lower APOA2 expression than those with the TT genotype. Lastly, metabolomic analysis identified 4 pathways as overrepresented by metabolite differences between CC and TT genotypes with high-SFA intake, including tryptophan and branched-chain amino acid (BCAA) pathways. Interestingly, these pathways were linked to rs5082-specific cg04436964 methylation differences in high-SFA consumers.ConclusionsThe epigenetic status of the APOA2 regulatory region is associated with SFA intake and APOA2 -265T>C genotype, promoting an APOA2 expression difference between APOA2 genotypes on a high-SFA diet, and modulating BCAA and tryptophan metabolic pathways. These findings identify potential mechanisms by which this highly reproducible gene-diet interaction influences obesity risk, and contribute new insights to ongoing investigations of the relation between SFA and human health. This study was registered at clinicaltrials.gov as NCT03452787.

Project description:Obesity is declared as a chronic multifaceted health problem, and young adults may be particularly vulnerable to weight gain. This study aims to identify the role of dietary calcium intake and the muscle strength index in handling excess of fat mass in young adults and to examine if the relationship between dietary calcium intake and fat mass percentage is mediated by muscle strength. A cross-sectional study including 355 Spanish college students (aged 21.05 ± 3.11) was performed during the 2017-2018 academic year. Pearson correlation coefficients were estimated to determine the relationship between dietary calcium intake, fat mass percentage, body mass index, muscle strength components, and total energy intake. ANCOVA models were used to analyze the differences in the muscle strength index by total dietary calcium intake categories, as well as the differences in % fat mass by total dietary calcium intake and muscle strength index categories, controlling for different sets of confounders. A mediator analysis was conducted to test if the relationship between dietary calcium intake and fat mass percentage was explained by muscle strength. Data on the fat mass percentage, dietary calcium intake, and muscle strength index as the sum of the standardized z-score of the standing long jump and z-score of handgrip/weight were collected. The muscle strength index was significantly better in young adults with higher dietary calcium intake. Moreover, the fat mass percentage was significantly lower in those with a higher dietary calcium intake and a better muscle strength index. Finally, the relationship between dietary calcium intake and fat mass percentage was fully mediated by muscle strength (z = -1.90; p < 0.05), explaining 33.33% of this relationship. This study suggests that both a major dietary calcium intake and muscle strength are associated with fat mass percentage. Moreover, muscle strength mediates the link between dietary calcium intake and fat mass percentage. Therefore, both high dietary calcium intake and exercise activities aimed at improving muscle strength levels may help to prevent the cardiometabolic risk associated with an excess of fat mass in young people.

Project description:Nutrigenetics studies the role of genetic variation on interactions between diet and health, aiming to provide more personalized dietary advice. However, replication has been low. Our aim was to study interaction among a functional APOA2 polymorphism, food intake, and body mass index (BMI) in independent populations to replicate findings and to increase their evidence level.Cross-sectional, follow-up (20 years), and case-control analyses were undertaken in 3 independent populations. We analyzed gene-diet interactions between the APOA2 -265T>C polymorphism and saturated fat intake on BMI and obesity in 3462 individuals from 3 populations in the United States: the Framingham Offspring Study (1454 whites), the Genetics of Lipid Lowering Drugs and Diet Network Study (1078 whites), and Boston-Puerto Rican Centers on Population Health and Health Disparities Study (930 Hispanics of Caribbean origin).Prevalence of the CC genotype in study participants ranged from 10.5% to 16.2%. We identified statistically significant interactions between the APOA2 -265T>C and saturated fat regarding BMI in all 3 populations. Thus, the magnitude of the difference in BMI between the individuals with the CC and TT+TC genotypes differed by saturated fat. A mean increase in BMI of 6.2% (range, 4.3%-7.9%; P = .01) was observed between genotypes with high- (> or =22 g/d) but not with low- saturated fat intake in all studies. Likewise, the CC genotype was significantly associated with higher obesity prevalence in all populations only in the high-saturated fat stratum. Meta-analysis estimations of obesity for individuals with the CC genotype compared with the TT+TC genotype were an odds ratio of 1.84 (95% confidence interval, 1.38-2.47; P < .001) in the high-saturated fat stratum, but no association was detected in the low-saturated fat stratum (odds ratio, 0.81; 95% confidence interval, 0.59-1.11; P = .18).For the first time to our knowledge, a gene-diet interaction influencing BMI and obesity has been strongly and consistently replicated in 3 independent populations.

Dataset Information

Interaction of dietary fat intake with APOA2, APOA5 and LEPR polymorphisms and its relationship with obesity and dyslipidemia in young subjects.

Publications

Interaction of dietary fat intake with APOA2, APOA5 and LEPR polymorphisms and its relationship with obesity and dyslipidemia in young subjects.

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