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BACKGROUND: The prevalence of obesity has been increasing worldwide. It has been reported that physiological and environmental factors such as diet, culture, physical activity, and genetics are the principal factors related to obesity. The fat mass and obesity-associated (FTO) gen variant (rs9939609: T>A) has been associated with class III obesity. The A variant has been correlated with anthropometric and metabolic alterations. Therefore, the purpose of this study was to analyze the association of the FTO rs9939609: T>A variant and environmental factors with clinical, anthropometric, and biochemical variables in subjects with class III obesity. RESULTS: The A variant frequency was higher in the class III obesity group compared with the normal weight group (44% vs. 25%, p < 0.001). Subjects with the AA genotype had a higher body mass index (BMI) than those with the AT genotype (35.46 kg/m2 (31-39.8) vs. 26.91 kg/m2 (23.7-30), p = 0.005). Women with the AA genotype showed higher waist circumferences than the AT group (101.07 cm (90.9-111.1) vs. 85.45 cm (77-93.8) p = 0.047). The FTO A variant increases the risk by 3.54 times and physical inactivity increases the risk by 6.37 times for class III obesity. CONCLUSIONS: Our results suggest that among the studied variables, those most related to class III obesity were the FTO risk genotype (A allele) and physical inactivity.

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To evaluate association of vitamin D with sleep quality in adults and the influence of VDR-gene polymorphism FokI (rs2228570;A > G). Cross-sectional population-based study in adults, conducted in Brazil. The outcome was sleep-quality, evaluated by the Pittsburgh Sleep Quality Index. Vitamin D was determined by indirect electrochemiluminescence and classified as deficiency (VDD), 25(OH)D < 20 ng/mL in a healthy population or 25(OH)D < 30 ng/mL for groups at risk for VDD. FokI polymorphism in the VDR-gene was genotyped by qPCR and classified as homozygous wild (FF or AA), heterozygous (Ff or AG), or homozygous mutant (ff or GG). Multivariate logistic analysis was used to estimate the association between vitamin D and FokI polymorphism with sleep-quality. In a total of 1674 individuals evaluated, 53.6% had poor-sleep-quality, 31.5% had VDD, and the genotype frequency of the FokI polymorphism was 9.9% FF, 44.6% Ff, and 45.5% ff. In multivariate analysis, individuals with VDD had 1.51 times the chance of poor-sleep-quality, and individuals with the ff genotype had 1.49 times the chance of poor-sleep-quality (OR:1.49;95%CI:1.05-2.12) when compared to individuals with the FF or Ff genotype. In the combined analysis, individuals with VDD and ff genotype had more chance of poor-sleep-quality than individuals with sufficient vitamin D and genotype Ff or FF (OR:2.19;95%CI:1.27-3.76). Our data suggest that VDD and VDR FokI gene polymorphism are associated with poor-sleep-quality, and combining the two factors increases the chance of poor-sleep-quality compared to separate groups.

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Globally, type 2 diabetes mellitus (T2DM) is one of the most common metabolic disorders. T2DM physiopathology is influenced by complex interrelationships between genetic, metabolic and lifestyle factors (including diet), which differ between populations and geographic regions. In fact, excessive consumptions of high fat/high sugar foods generally increase the risk of developing T2DM, whereas habitual intakes of plant-based healthy diets usually exert a protective effect. Moreover, genomic studies have allowed the characterization of sequence DNA variants across the human genome, some of which may affect gene expression and protein functions relevant for glucose homeostasis. This comprehensive literature review covers the impact of gene-diet interactions on T2DM susceptibility and disease progression, some of which have demonstrated a value as biomarkers of personal responses to certain nutritional interventions. Also, novel genotype-based dietary strategies have been developed for improving T2DM control in comparison to general lifestyle recommendations. Furthermore, progresses in other omics areas (epigenomics, metagenomics, proteomics, and metabolomics) are improving current understanding of genetic insights in T2DM clinical outcomes. Although more investigation is still needed, the analysis of the genetic make-up may help to decipher new paradigms in the pathophysiology of T2DM as well as offer further opportunities to personalize the screening, prevention, diagnosis, management, and prognosis of T2DM through precision nutrition.

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The impact of polyphenols in ovarian cancer is widely studied observing gene expression, epigenetic alterations, and molecular mechanisms based on new 'omics' technologies. Therefore, the combination of omics technologies with the use of phenolic compounds may represent a promising approach to precision nutrition in cancer. This article provides an updated review involving the current applications of high-throughput technologies in ovarian cancer, the role of dietary polyphenols and their mechanistic effects in ovarian cancer, and the current status and challenges of precision nutrition and their relationship with big data. High-throughput technologies in different omics science can provide relevant information from different facets for identifying biomarkers for diagnosis, prognosis, and selection of specific therapies for personalized treatment. Furthermore, the field of omics sciences can provide a better understanding of the role of polyphenols and their function as signaling molecules in the prevention and treatment of ovarian cancer. Although we observed an increase in the number of investigations, there are several approaches to data acquisition, analysis, and integration that still need to be improved, and the standardization of these practices still needs to be implemented in clinical trials.

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Hypertension is one of the primary risk factors associated with cardiovascular diseases (CVDs). It is a condition that affects people worldwide, and its prevalence is increasing due to several factors, such as lack of physical activity, population aging, and unhealthy diets. Notably, this increase has primarily occurred in low and middle-income countries (LMICs). In Latin America, approximately 40% of adults have been diagnosed with hypertension. Moreover, reports have shown that the Latin American genetic composition is highly diverse, and this genetic background can influence various biological processes, including disease predisposition and treatment effectiveness. Research has shown that Western dietary patterns, which include increased consumption of red meat, refined grains, sugar, and ultra-processed food, have spread across the globe, including Latin America, due to globalization processes. Furthermore, a higher than recommended sodium consumption, which has been associated with hypertension, has been identified across different regions, including Asia, Europe, America, Oceania, and Africa. In conclusion, hypertension is a multifactorial disease involving environmental and genetic factors. In Latin America, hypertension prevalence is increasing due to various factors, including age, the adoption of a "Westernized" diet, and potential genetic predisposition factors involving the ACE gene. Furthermore, identifying the genetic and molecular mechanisms of the disease, its association with diet, and how they interact is essential for the development of personalized treatments to increase its efficacy and reduce side effects.

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Polymorphisms in genes of leptin-melanocortin and insulin pathways have been associated with obesity and type 2 diabetes. We hypothesized that polymorphisms in IRS1, IRS2, MC3R, and MC4R influence metabolic and inflammatory markers and food intake composition in Brazilian subjects. This exploratory pilot study included 358 adult subjects. Clinical, anthropometric, and laboratory data were obtained through interview and access to medical records. The variants IRS1 rs2943634 A˃C, IRS2 rs1865434 C>T, MC3R rs3746619 C>A, and MC4R rs17782313 T>C were analyzed by real-time polymerase chain reaction. Food intake composition was assessed in a group of subjects with obesity (n = 84) before and after a short-term nutritional counseling program (9 weeks). MC4R rs17782313 was associated with increased risk of obesity (P = .034). Multivariate linear regression analysis adjusted by covariates indicated associations of IRS2 rs1865434 with reduced low-density lipoprotein cholesterol and resistin, MC3R rs3746619 with high glycated hemoglobin, and IRS1 rs2943634 and MC4R rs17782313 with increased high-sensitivity C-reactive protein (P < .05). Energy intake and carbohydrate and total fat intakes were reduced after the diet-oriented program (P < .05). Multivariate linear regression analysis showed associations of IRS2 rs1865434 with high basal fiber intake, IRS1 rs2943634 with low postprogram carbohydrate intake, and MC4R rs17782313 with low postprogram total fat and saturated fatty acid intakes (P < .05). Although significant associations did not survive correction for multiple comparisons using the Benjamini-Hochberg method in this exploratory study, polymorphisms in IRS1, IRS2, MC3R, and MC4R influence metabolic and inflammatory status in Brazilian adults. IRS1 and MC4R variants may influence carbohydrate, total fat, and saturated fatty acid intakes in response to a diet-oriented program in subjects with obesity.

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Hypertensive disorders of pregnancy (HDP) are a leading cause of maternal and perinatal morbimortality. Dietetic, phenotypic, and genotypic factors influencing HDP were analyzed during a nutrigenetic trial in Rio de Janeiro, Brazil (2016-2020). Pregnant women with pregestational diabetes mellitus (n = 70) were randomly assigned to a traditional or DASH diet group. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) were measured during prenatal visits and HDP were diagnosed using international criteria. Phenotypic data were obtained from medical records and personal interviews. Genotyping for FTO and ADRB2 polymorphisms used RT-PCR. Linear mixed-effect models and time-to-event analyses were performed. The variables with significant effect on the risk for progression to HDP were: black skin color (adjusted hazard ratio [aHR] 8.63, p = 0.01), preeclampsia in previous pregnancy (aHR 11.66, p < 0.01), SBP ≥ 114 mmHg in the third trimester (aHR 5.56, p 0.04), DBP ≥ 70 mmHg in the first trimester (aHR 70.15, p = 0.03), mean blood pressure > 100 mmHg (aHR 18.42, p = 0.03), and HbA1c ≥ 6.41% in the third trimester (aHR 4.76, p = 0.03). Dietetic and genotypic features had no significant effect on the outcome, although there was limited statistical power to test both.

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Obesity is a chronic disease characterized by abnormal or excessive fat accumulation that could impact an individual's health; moreover, the World Health Organization (WHO) has declared obesity a global epidemic since 1997. In Latin America, in 2016, reports indicated that 24.2% of the adult population was obese. The environmental factor or specific behaviors like dietary intake or physical activity have a vital role in the development of a condition like obesity, but the interaction of genes could contribute to that predisposition. Hence, it is vital to understand the relationship between genes and disease. Indeed, genetics in nutrition studies the genetic variations and their effect on dietary response; while genomics in nutrition studies the role of nutrients in gene expression. The present review represents a compendium of the dietary behaviors in the Latin American environment and the interactions of genes with their single nucleotide polymorphisms (SNPs) associated with obesity, including the risk allele frequencies in the Latin American population. Additionally, a bibliographical selection of several studies has been included; these studies examined the impact that dietary patterns in Latin American environments have on the expression of numerous genes involved in obesity-associated metabolic pathways.

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Currently, metabolic-associated fatty liver disease (MAFLD) is a leading global cause of chronic liver disease, and is expected to become one of the most common indications of liver transplantation. MAFLD is associated with obesity, involving multiple mechanisms such as alterations in lipid metabolism, insulin resistance, hyperinflammation, mitochondrial dysfunction, cell apoptosis, oxidative stress, and extracellular matrix formation. However, the onset and progression of MAFLD is variable among individuals, being influenced by intrinsic (personal) and external environmental factors. In this context, sequence structural variants across the human genome, epigenetic phenomena (i.e., DNA methylation, histone modifications, and long non-coding RNAs) affecting gene expression, gut microbiota dysbiosis, and metabolomics/lipidomic fingerprints may account for differences in MAFLD outcomes through interactions with nutritional features. This knowledge may contribute to gaining a deeper understanding of the molecular and physiological processes underlying MAFLD pathogenesis and phenotype heterogeneity, as well as facilitating the identification of biomarkers of disease progression and therapeutic targets for the implementation of tailored nutritional strategies. This comprehensive literature review highlights the potential of nutrigenetic, nutriepigenetic, nutrimetagenomic, nutritranscriptomics, and nutrimetabolomic approaches for the prevention and management of MAFLD in humans through the lens of precision nutrition.

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Resumen: En los últimos años se han realizado estudios de asociación del genoma completo, con el objetivo de identificar variantes genéticas asociadas a la interindividualidad de la respuesta a tratamientos dietéticos para la pérdida de peso. Estos esfuerzos de la genómica nutricional contribuyen con los avances de la ciencia de la nutrición 4.0: preventiva, participativa, predictiva y personalizada. Sin embargo, aunque a la fecha se ha descubierto millones de polimorfismos en el genoma humano, estos hallazgos no indican que la presencia de estas variaciones determina un efecto sobre la salud del individuo. Por lo anterior, el uso del perfil nutrigenético para la pérdida de peso conduce a un análisis sobre riesgos y beneficios a la luz de los principios bioéticos centrados en la unidad, individualidad y unicidad de la persona humana. Así, con base en pensadores clásicos como Aristóteles y Tomás de Aquino, pero con la contribución de filósofos contemporáneos, como Robert Spaemman, se define a la persona como sustancia individual de naturaleza racional, desglosando las dimensiones fundamentales para demostrar, por argumentación, que el principio de individualidad no solo incluye la dimensión biológica (naturalismo materialista), sino la unidad de la persona perteneciente a la naturaleza humana.

Abstract: In recent years, whole genome association studies have been conducted to identify genetic variants associated with the interindividuality of response to dietary treatments for weight loss. These nutritional genomics efforts contribute to the advancement of nutrition science 4.0: preventive, participatory, predictive and personalized. However, although to date more than 85 million polymorphisms have been discovered in the human genome, these findings do not indicate that the presence of these variations determines an effect on a personal health. Therefore, the use of the nutrigenetic profile for weight loss leads to analyze the risks/benefits with the bioethical principles focused on the unity, individuality and uniqueness of the human person. Thus, based on classical thinkers such as Aristotle and Thomas Aquinas, but with the contribution of contemporary philosophers, such as Robert Spaemman, the person is defined as an individual substance of a rational nature, breaking down the fundamental dimensions to demonstrate, by argumentation, that the principle individuality not only includes the biological dimension (materialistic naturalism), but the unity of the person belonging to human nature.

Resumo: Nos últimos anos tem se realizado estudos de associação do genoma completo, com o objetivo de identificar variantes genéticas associadas à inter-individualidade da resposta a tratamentos dietéticos para a perda de peso. Esses esforços da genômica nutricional contribuem para os avanços da ciência da nutrição 4.0: preventiva, participativa, preditiva e personalizada. Sem dúvida, ainda que até hoje tenham sido descobertos milhões de polimorfismos no genoma humano, esses achados não indicam que a presença dessas variações determine um efeito sobre a saúde do indivíduo. Assim, o uso do perfil nutrigenético para a perda de peso conduz a uma análise sobre os riscos/benefícios à luz dos princípios bioéticos centrados na unidade, individualidade e unicidade da pessoa humana. Assim, com base em pensadores clássicos como Aristóteles e Tomás de Aquino, porém com a contribuição de filósofos contemporâneos como Robert Spaemman, define-se a pessoa como substância individual de natureza racional, separando as dimensões fundamentais para demostrar, por argumentação, que o princípio da individualidade não somente inclui a dimensão biológica (naturalismo materialista), como também a unidade da pessoa pertencente à natureza humana.

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Given the relationship between vitamin D deficiency (VDD) and adverse outcomes of metabolic diseases, we investigated the interplay of dietary and genetic components on vitamin D levels and metabolic traits in young adults from Brazil. Genetic analysis, dietary intake, and anthropometric and biochemical measurements were performed in 187 healthy young adults (19−24 years). Genetic risk scores (GRS) from six genetic variants associated with vitamin D (vitamin D-GRS) and 10 genetic variants associated with metabolic disease (metabolic-GRS) were constructed. High vitamin D-GRS showed a significant association with low 25(OH)D concentrations (p = 0.001) and high metabolic-GRS showed a significant association with high fasting insulin concentrations (p = 0.045). A significant interaction was found between vitamin D-GRS and total protein intake (g/day) (adjusted for non-animal protein) on 25(OH)D (pinteraction = 0.006), where individuals consuming a high protein diet (≥73 g/d) and carrying >4 risk alleles for VDD had significantly lower 25(OH)D (p = 0.002) compared to individuals carrying ≤4 risk alleles. Even though our study did not support a link between metabolic-GRS and vitamin D status, our study has demonstrated a novel interaction, where participants with high vitamin D-GRS and consuming ≥73 g of protein/day had significantly lower 25(OH)D levels. Further research is necessary to evaluate the role of animal protein consumption on VDD in Brazilians.

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Excessive gestational weight gain (GWG) is associated with increased risk of maternal and neonatal complications. We investigated obesity-related polymorphisms in the FTO gene (rs9939609, rs17817449) and ADRB2 (rs1042713, rs1042714) as candidate risk factors concerning excessive GWG in pregnant women with pregestational diabetes. This nutrigenetic trial, conducted in Brazil, randomly assigned 70 pregnant women to one of the groups: traditional diet (n = 41) or DASH diet (n = 29). Excessive GWG was the total weight gain above the upper limit of the recommendation, according to the Institute of Medicine guidelines. Genotyping was performed using real-time PCR. Time-to-event analysis was performed to investigate risk factors for progression to excessive GWG. Regardless the type of diet, AT carriers of rs9939609 (FTO) and AA carriers of rs1042713 (ADRB2) had higher risk of earlier exceeding GWG compared to TT (aHR 2.44; CI 95% 1.03-5.78; p = 0.04) and GG (aHR 3.91; CI 95% 1.12-13.70; p = 0.03) genotypes, respectively, as the AG carriers for FTO haplotype rs9939609:rs17817449 compared to TT carriers (aHR 1.79; CI 95% 1.04-3.06; p = 0.02).

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The Genome-based Mexican (GENOMEX) diet is a strategy for preventing and managing obesity. Emotion and eating behavior in the context of a nutrigenetic intervention have not been thoroughly studied. We aimed to explore the influence of the GENOMEX diet on emotions, self-efficacy, and rewarding behaviors in unhealthy eating among subjects with risk factors for obesity-related chronic diseases. Twenty-eight subjects included in the six-month GENOMEX intervention answered questions regarding emotions that influence food consumption. Additionally, the Patient Health Questionnaire (PHQ-9) and the Reward-based eating drive scale (RED) were applied. In the study, minimal, mild, moderate, and severe depression were present in 46.4%, 39.3%, 10.7%, and 3.6%, respectively. RED did not change, but it correlated with a higher intake of fats (r2 = 0.684, ß = 2.066, p = 0.003). Mood influenced unhealthy eating in 71.7% of subjects, and 76.9% experienced binge episodes triggered by anxiety. Sugars were the most consumed foods during binge episodes (42.2%). Both low self-efficacy levels and binge episodes were associated with high consumption of unhealthy foods. After the intervention, 10.7% of subjects reported a high level of self-efficacy. In conclusion, a culturally acceptable and genetically compatible regional Mexican food diet reduced negative emotions and unhealthy eating while increasing self-efficacy.

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Evidence shows that genetic polymorphisms in perilipin 1 gene (PLIN1) are associated with excessive accumulation of body fat and disturbances in cardiometabolic markers. Therefore, the aim of this study was to verify whether the SNP PLIN1 11482 G>A (rs894160) interacts with nutrient intake, anthropometric, body composition and cardiometabolic markers in adults with normal-weight obesity (NWO) syndrome. A cross-sectional study was carried out with 116 individuals aged 20-59 years, with normal BMI and high percentage of body fat. Anthropometric and body composition measures, glycaemic control and serum lipid markers, SNP PLIN1 11482 G>A and nutrient intake were evaluated. Interactions between nutrient intake and the SNP were determined by regression models and adjusted for potential confounders. The SNP frequency was 56·0 % GG, 38·8 % GA and 5·2 % AA. Anthropometric measures and biochemical markers were not different according to genotype, except for total cholesterol (TC), LDL-cholesterol and non-HDL-cholesterol concentrations. However, important interactions between the SNP and dietary intake were observed. Carbohydrate intake interacted with the SNP PLIN1 11482 G>A to modulate waist circumference (WC) and the homeostatic model assessment of insulin resistance index. Interaction of lipid intake and the SNP modulated TC and LDL-cholesterol concentrations, and the interaction between protein intake and the SNP tended to modulate weight, WC and BMI. The SNP PLIN1 11482 G>A seems to modulate responses in anthropometric and lipid profile biomarkers of subjects with NWO depending on the dietary macronutrient composition, which may have long-term impact on cardiometabolic markers.

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ABSTRACT Objective: The aim of this study was to evaluate the serum activity of PON1 in women according to SNPs L55M and T-107C and diet composition. Materials and methods: Blood and serum samples from 26 women were used. DNA extraction, PCR and digestion with restriction enzymes of the PCR fragment were performed for genotyping the PON1 SNPs T-107C and L55M. Serum PON1 activity was measured in a single time point. Patients completed the semi-quantitative food frequency questionnaire and diet composition was estimated. Results: Genotypic distribution for L55M SNP was 56% for the LL genotype, 32% for LM and 12% for MM; for the PON1 C(-107)T SNP it was 28% for the TT genotype, 41% for CT and 31% for CC. Individuals with C and L alleles had higher serum PON1 activity. Combining the two SNPs, we observed that individuals carrying the LL and CC genotypes had twice the activity of carriers of the TT and MM genotypes. Considering food intake, no significant difference was observed between genotypes and intake levels. Conclusion: PON1 T(-107)C and L55M SNPs exert a strong effect on serum PON1 activity in an additive manner and are more important than diet to predict serum PON1 activity.

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OBJECTIVE: The aim of this study was to evaluate the serum activity of PON1 in women according to SNPs L55M and T-107C and diet composition. METHODS: Blood and serum samples from 26 women were used. DNA extraction, PCR and digestion with restriction enzymes of the PCR fragment were performed for genotyping the PON1 SNPs T-107C and L55M. Serum PON1 activity was measured in a single time point. Patients completed the semi-quantitative food frequency questionnaire and diet composition was estimated. RESULTS: Genotypic distribution for L55M SNP was 56% for the LL genotype, 32% for LM and 12% for MM; for the PON1 C(-107)T SNP it was 28% for the TT genotype, 41% for CT and 31% for CC. Individuals with C and L alleles had higher serum PON1 activity. Combining the two SNPs, we observed that individuals carrying the LL and CC genotypes had twice the activity of carriers of the TT and MM genotypes. Considering food intake, no significant difference was observed between genotypes and intake levels. CONCLUSION: PON1 T(-107)C and L55M SNPs exert a strong effect on serum PON1 activity in an additive manner and are more important than diet to predict serum PON1 activity.

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OBJECTIVE: The aim of this study was to develop genetic scores based on single-nucleotide polymorphisms (SNPs) related to lipid metabolism and evaluate whether they used to estimate disturbances in the circulating lipid profile biomarkers of adolescents. METHODS: In a preliminary cross-sectional approach, 113 Brazilian adolescents (10-19 y of age) with cardiovascular disease risk factors were evaluated. Genetic scores from 20 SNPs related to lipid metabolism were calculated by codifying each of them as the rescaled sum of risk allele frequencies. All scores were distributed in classes between 0 (absence of risk alleles) and 10 (presence of all risk alleles) to evaluate the additive effect of risk alleles on the lipid profile outcomes in the same interval. Multiple linear regression analyses were performed to evaluate the association between each score and blood lipid profile biomarkers. RESULTS: Significant associations between genetic scores and unfavorable outcomes in all evaluated lipid profile biomarkers were found. The mean ± SD of the genetic scores for the circulating lipid profile biomarkers in the 0 to 10 scale were 4.4 ± 2 for triacylglycerol, 5.3 ± 1.5 for total cholesterol, 5.6 ± 1.2 for high-density lipoprotein cholesterol, 4.9 ± 1.6 for low-density lipoprotein cholesterol, and 3.6 ± 1.9 for minimally modified low-density lipoprotein cholesterol. For each point obtained in each genetic score, a mean increase ± SE of 15.8 ± 4.2 mg/dL in triacylglycerol (P = 0.0001), 5.3 ± 1.7 mg/dL in total cholesterol (P = 0.0032), 4.8 ± 1.3 mg/dL in low-density lipoprotein cholesterol (P = 0.0003), and 1.1 ± 0.3 U/L in minimally modified low-density lipoprotein cholesterol (P = 0.0020) and a mean decrease of 3.7 ± 0.7 mg/dL in high-density lipoprotein cholesterol (P < 0.0001) concentrations were obtained. CONCLUSION: The calculated genetic scores could be used to estimate disturbances in circulating lipid profile biomarkers of adolescents and be applied in clinical practice to better target interventions to reduce cardiovascular disease risk throughout life.

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Mexican-origin (MO) adults have among the highest rates of nonalcoholic fatty liver disease (NAFLD) placing them at increased risk of liver cancer. Evidence suggests that a single nucleotide polymorphism (SNP) in the PNPLA3 gene, rs738409, increases the risk and progression of NAFLD and may modify the relationship between certain dietary factors and liver steatosis. The purpose of this study was to identify whether interactions exist between specific dietary factors and rs738409 genotype status among MO adults in relation to levels of liver steatosis. We analyzed cross-sectional data from a sample of 288 MO adults. Participants completed at least two 24-h dietary recalls. Multiple linear regression was performed assuming an additive genetic model to test the main effects of several dietary variables on levels of hepatic steatosis, adjusting for covariates. To test for effect modification, the product of the genotype and the dietary variable was included as a covariate in the model. No significant association between dietary intake and level of hepatic steatosis was observed, nor any significant gene-diet interactions. Our findings suggest that dietary intake may have the same magnitude of protective or deleterious effect even among MO adults with high genetic risk for NAFLD and NAFLD progression.

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A obesidade é caracterizada pelo aumento excessivo da gordura corporal e está ligada ao estilo de vida, ao meio ambiente e a genética do indivíduo. O equilíbrio entre ingestão e gasto energético é controlado por mecanismos neurais, hormonais, químicos e genéticos. Estudos sugerem que o gene FTO (Fat mass and obesity associated) atua como regulador primário do acúmulo de gordura corporal, quando associado a SNPs (Single Nucleotide Polymorphism) específicos, predispõe à obesidade. O propósito deste trabalho foi verificar a produção científica, analisar e catalogar os estudos de polimorfismos no gene FTO associados à obesidade e suas comorbidades. A busca por publicações entre 2009 e 2018 foi realizada na base de dados SciELO com a palavra-chave "FTO". Foram encontrados 23 artigos originais dentro dos critérios da pesquisa que correlacionam o FTO à obesidade. O nome do autor principal, país, idioma, ano de publicação, título, objetivo, polimorfismo associado e os resultados dos estudos foram extraídos e organizados para facilitar a tabulação dos dados. Também foram pesquisados os números de citações de cada artigo, utilizando-se a plataforma Google Acadêmico. Embora o Brasil se encontre em primeiro lugar em produção científica para o gene FTO na base de dados prospectada, o número de artigos originais ainda é muito modesto. Assim, os resultados encontrados podem servir de subsídio no delineamento de novas pesquisas sobre os polimorfismos do gene FTO e as causas da obesidade.

Obesity is characterized by the excessive increase in body fat and is correlated to the lifestyle, environment, and also to the genetics of the individual. The balance between energy intake and expenditure is controlled by neural, hormonal, chemical, and genetic mechanisms. Studies suggest that the FTO (fat mass and obesity associated), a gene associated with fat mass, plays a role as a primary regulator of body fat buildup, when associated to specific Single Nucleotide Polymorphisms (SNPs), causing predisposition to obesity. This paper aimed at reviewing, analyzing, and cataloguing the studies on FTO gene polymorphisms associated with obesity and its comorbidities. The search was carried out in SciELO database, checking articles published between 2009 and 2018 using the keyword "FTO". Twenty-three original articles, matching the research criteria, correlating FTO either positively or negatively with obesity, were found. The main author's name, country, language, year of publication, title, objective, associated polymorphism, and the study results were extracted and organized to facilitate data tabulation. The citation numbers for each article were also searched by using the Google Scholar platform. Although Brazil ranks first in scientific production on the FTO gene in the surveyed database, the number of original articles is still very modest. Therefore, the results found in this paper may be used as a basis for the design of new research on the FTO gene polymorphisms and the causes of obesity.

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Functional variants in genes of the renin-angiotensin (RAS) and kallikrein-kinin (KKS) systems have already been implicated in blood pressure (BP) modulation, but few studies have focused on a nutrigenetics approach. Thus, the aim of this study is to verify the effects of the interaction between genetic polymorphisms (rs4340-ACE, rs699-AGT, and rs1799722-BDKRB2) and micronutrient consumption (sodium, potassium, calcium, and magnesium) on BP values of normotensive adult individuals. The study included 335 adults, men and women, 25.5 (6.6) years old. Biochemical, anthropometric, BP measurements, and food intake data were assessed for all participants. Gene-nutrient interaction on BP outcome was tested by multiple linear regression with manual backward stepwise modeling. Our results indicated that individuals with G allele for rs699 polymorphism, in the increase of sodium and magnesium consumption, both in the genotypic model (sodium, p = 0.035; magnesium, p = 0.016) and in the dominant model (sodium, p = 0.009; magnesium, p = 0.006) had higher systolic BP (SBP) levels compared to AA homozygotes (sodium, p = 0.001; magnesium, p < 0.001). Also, individuals with the T allele for the rs1799722 polymorphism, with higher calcium intake, had significantly higher levels of SBP and diastolic BP (DBP) when compared to CC homozygotes (p = 0.037). In conclusion, our findings pointed for significant interactions between genetic polymorphisms (rs699-AGT and rs1799722-BDKRB2) and the consumption of micronutrients (sodium, magnesium, and calcium) on the BP variation. These findings contribute to the understanding of the complex mechanisms involved in BP regulation, which probable include several gene-nutrition interactions.

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