Lifestyle Genomics最新文献

{"title":"One-Carbon Metabolism and Nonalcoholic Fatty Liver Disease: The Crosstalk between Nutrients, Microbiota, and Genetics.","authors":"Anna Radziejewska,&nbsp;Agata Muzsik,&nbsp;Fermín I Milagro,&nbsp;J Alfredo Martínez,&nbsp;Agata Chmurzynska","doi":"10.1159/000504602","DOIUrl":"https://doi.org/10.1159/000504602","url":null,"abstract":"<p><p>The prevalence of nonalcoholic fatty liver disease (NAFLD) is increasing worldwide. Its etiology includes nutritional, genetic, and lifestyle factors. Several mechanisms may link one-carbon metabolism - the associated metabolic pathways of folate, methionine, and choline - to the onset of NAFLD. In this review, we attempted to assess how choline, folate, methionine, and betaine affect NAFLD development, mainly through their role in the secretion of very low-density lipoproteins (VLDL) from the liver. We also reviewed recent articles that have described the relation between microbiota metabolism and NAFLD progression. Moreover, we describe the effect of single-nucleotide polymorphisms (SNP) in genes related to one-carbon metabolism and disease prevalence. We additionally seek SNP identified by genome-wide associations that may increase the risk of this disease. Even though the evidence available is not entirely consistent, it seems that the concentrations of choline, methionine, folate, and betaine may affect the progression of NAFLD. Since there is no effective therapy for NAFLD, further investigations into the link between nutrition, gut microbiota, genetic factors, and NAFLD are still necessary, with a particular emphasis on methyl donors.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000504602","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37465146","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interaction of DRD2/ANKK1 Taq1A Genotype with in-Store Retail Food Environment Exposures on Diet Quality in a Cohort of Quebec Adults.","authors":"Daiva E Nielsen,&nbsp;Yang Han,&nbsp;Catherine Paquet,&nbsp;Andre K Portella,&nbsp;Yu Ma,&nbsp;Laurette Dube","doi":"10.1159/000504603","DOIUrl":"https://doi.org/10.1159/000504603","url":null,"abstract":"<p><strong>Background/aims: </strong>Gene-environment interactions may be relevant for nutrition outcomes. This study assessed the interaction between DRD2/ANKK1 Taq1A genotype and exposures to in-store retail food environment on diet quality.</p><p><strong>Methods: </strong>CARTaGENE biobank data (n = 3,532) were linked to provincial food retail data. The Canadian adaptation of the Healthy Eating Index 2010 (HEI-C) was calculated from food frequency questionnaires. Generalized linear models adjusted for sociodemographic factors, anthropometrics, and energy intake were used to assess interactions between the Taq1A variant and retail food measures.</p><p><strong>Results: </strong>A significant inverse interaction was observed between Taq1A and ice cream store displays on HEI-C score (estimate: -15.46 [95% confidence interval (CI): -24.83, -6.10], p = 0.0012) where, among allele carriers, increasing exposure to ice cream displays was associated with a lower HEI-C score as compared to allele carriers with a lower exposure. A significant positive interaction between Taq1A and price of vegetables was also observed, where, among allele carriers, increasing exposure to a higher price was associated with a higher HEI-C score compared to allele carriers with exposure to a lower price (estimate: 2.46 [95% CI: 0.78, 4.14], p = 0.0041). The opposite pattern was observed among non-carriers.</p><p><strong>Conclusions: </strong>DRD2/ANKK1 Taq1A is associated with adaptive responses to ice cream displays and vegetable prices, suggesting a differential susceptibility to retail environment food cues.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000504603","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37469629","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Association of Parental Genetic, Lifestyle, and Social Determinants of Health with Offspring Overweight.","authors":"Catherine A M Graham,&nbsp;Charles R Pedlar,&nbsp;Gary Hearne,&nbsp;Silvia Lorente-Cebrián,&nbsp;Pedro González-Muniesa,&nbsp;Yiannis Mavrommatis","doi":"10.1159/000505749","DOIUrl":"https://doi.org/10.1159/000505749","url":null,"abstract":"<p><strong>Introduction: </strong>In the UK, the number of comorbidities seen in children has increased along with the worsening obesity rate. These comorbidities worsen into adulthood. Genome-wide association studies have highlighted single nucleotide polymorphisms associated with the weight status of adults and offspring individually. To date, in the UK, parental genetic, lifestyle, and social determinants of health have not been investigated alongside one another as influencers of offspring weight status. A comprehensive obesity prevention scheme would commence prior to conception and involve parental intervention including all known risk factors. This current study aims to identify the proportion of overweight that can be explained by known parental risk factors, including genetic, lifestyle, and social determinants of health with offspring weight status in the UK.</p><p><strong>Methods: </strong>A cross-sectional study was carried out on 123 parents. Parental and offspring anthropometric data and parental lifestyle and social determinants of health data were self-reported. Parental genetic data were collected by use of GeneFiX saliva collection vials and genotype were assessed for brain-derived neurotrophic factor (BDNF) gene rs6265, melanocortin 4 receptor (MC4R) gene rs17782313, transmembrane protein 18 (TMEM18) gene rs2867125, and serine/threonine-protein kinase (TNN13K) gene rs1514175. Associations were assessed between parental data and the weight status of offspring.</p><p><strong>Results: </strong>Maternal body mass index modestly predicted child weight status (p < 0.015; R2 = 0.15). More mothers of overweight children carried the MC4R rs17782313 risk allele (77.8%; p = 0.007) compared to mothers of normal-weight children. Additionally, fathers who were not Caucasian and parents who slept for <7 h/night had a larger percentage of overweight children when compared to their counterparts (p = 0.039; p = 0.014, respectively).</p><p><strong>Conclusion: </strong>Associations exist between the weight status of offspring based solely on parental genetic, lifestyle, and social determinants of health data. Further research is required to appropriately address future interventions based on genetic and lifestyle risk groups on a pre-parent cohort.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000505749","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37652077","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lack of Association between LCT_rs140433552*CA>del Indel Polymorphism and Lactose Intolerance in a Southern Brazilian Population.","authors":"Luana Caroline Oliveira,&nbsp;Andrey Lucas Dias Barros,&nbsp;Angelica Beate Winter Boldt,&nbsp;Gabriel Adelman Cipolla","doi":"10.1159/000508509","DOIUrl":"https://doi.org/10.1159/000508509","url":null,"abstract":"<p><strong>Background/aims: </strong>Polymorphisms in the enhancer of the lactase gene (LCT) are strongly associated with lactase persistence, but not always predictive of the phenotype. We investigated a possible association between the regulatory rs140433552*CA>del variant of LCT and lactose intolerance (LI).</p><p><strong>Methods: </strong>We genotyped 122 individuals for rs140433552 and rs4988235 (-13910*C>T).</p><p><strong>Results: </strong>Associations of rs140433552*CA>del with LI depend on -13910*C>T. Homozygous individuals for the C-CA haplotype, as well as C-CA+/C individuals, seem more likely to manifest LI (OR 3.33 [95% CI 1.32-8.35], p = 0.011, and OR 3.93 [95% CI 1.61-9.61], p = 0.003, respectively), while homozygous individuals for the T-CA haplotype seem more likely to be lactose tolerant (OR 0.04 [95% CI 0.002-0.70], p = 8 × 10-4).</p><p><strong>Conclusions: </strong>rs140433552*CA>del is not independently associated with LI.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000508509","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38150025","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Alpinia zerumbet and Its Potential Use as an Herbal Medication for Atherosclerosis: Mechanistic Insights from Cell and Rodent Studies.","authors":"Ting Xiao,&nbsp;Jiaoyan Huang,&nbsp;Xiaowei Wang,&nbsp;Linjing Wu,&nbsp;Xue Zhou,&nbsp;Feng Jiang,&nbsp;Zhiyong He,&nbsp;Qianqian Guo,&nbsp;Ling Tao,&nbsp;Xiangchun Shen","doi":"10.1159/000508818","DOIUrl":"https://doi.org/10.1159/000508818","url":null,"abstract":"<p><strong>Background/aims: </strong>Alpinia zerumbet (Pers.) Burtt. et Smith has been used as a flavor additive in food and a traditional medicine for centuries, especially in Guizhou Province, China, and it prolongs people's lives with multiple beneficial effects. Thus, one of the aims of this review was to expound the chemical constituents of this plant, especially its fruits. Since cardiovascular diseases, including atherosclerosis, pose a health threat to humans, another aim was to expound the possible mechanisms of its potential use as an herbal medication for atherosclerosis.</p><p><strong>Methods: </strong>In this study, 10 reports are cited to expound the potential bioactive compounds. Moreover, 33 reports explain the antihypertensive and antiatherosclerotic effects of the plant by ameliorating inflammation and endothelial dysfunction, increasing vasodilation, improving hyperlipidemia, downgrading the glucose status, and working as an antioxidant.</p><p><strong>Results: </strong>A. zerumbetis rich in terpenes, essential oils, flavonoids, polyphenolics, and sterols. Pharmacological experiments showed that A. zerumbet has antioxidative and anti-inflammatory effects on the NF-κB signaling pathway and can ameliorate oxidative stress in the NOS-NO signaling pathway. Moreover, A. zerumbet demonstrates antihypertensive effects by accelerating vasorelaxant response and increasing 3T3-L1 intracellular cAMP, which has promising antiobesity properties, as well as hypolipidemic and anti-diabetic complication effects.</p><p><strong>Conclusions: </strong>A. zerumbet has potential functions and applications in the prevention of atherosclerosis, but further studies are required before clinical trials.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000508818","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38342552","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ximenynic Acid Regulation of n-3 PUFA Content in Liver and Brain.","authors":"Fang Cai,&nbsp;Yandi Liu,&nbsp;Dhanushka S Hettiarachichi,&nbsp;Fenglei Wang,&nbsp;Jie Li,&nbsp;Bruce Sunderland,&nbsp;Duo Li","doi":"10.1159/000502773","DOIUrl":"https://doi.org/10.1159/000502773","url":null,"abstract":"<p><strong>Background/aims: </strong>Ximenynic acid is a rare conjugated enyne fatty acid found primarily in plants in the Santalaceae family. It has been reported that sandalwood seed oil (SWSO) affects fatty acid metabolism in animal studies; however, the effects of pure ximenynic acid remain unclear. The present study aimed to study the impact of SWSO and ximenynic acid on n-3 fatty acid metabolism in the liver and brain.</p><p><strong>Methods: </strong>Thirty C57BL/6 male mice aged 4 weeks were fed SWSO (1.0 mL/20 g bodyweight), olive oil (OO), or a combination of SWSO and OO (n = 10/group) for 8 weeks. Liver and brain fatty acid compositions were determined using gas chromatography. HepG2 cells were treated with up to 150 μM ximenynic acid and oleic acid for 48-72 h. The expression and abundance of genes and proteins relevant to n-3 fatty acid metabolism pathways were investigated.</p><p><strong>Results: </strong>The intake of SWSO in mice elevated the levels of total n-3 fatty acids and decreased total n-9 fatty acids in the liver (p < 0.05) compared with the OO group. In contrast, total n-3 fatty acids were significantly decreased in the brain (p < 0.05). HepG2 cells treated with ximenynic acid for 48 h showed significant reductions in n-9 fatty acids and docosahexaenoic acid (C22:6n-3) (p < 0.05) compared with HepG2 cells treated with oleic acid. In HepG2 cells, stearoyl-CoA desaturase (SCD) and fatty acid desaturase 2 (FADS2) gene expression, as well as FADS2 protein expression, were significantly down-regulated after a 72-h incubation with 150 μM of ximenynic acid compared with the vehicle (p < 0.05).</p><p><strong>Conclusion: </strong>Ximenynic acid may regulate fatty acid metabolism by suppressing the expression of key enzymes of lipid metabolism. In contrast, SWSO, which has a high level of C18:3n-3, positively affected n-3 fatty acid synthesis in mouse liver compared to pure ximenynic acid. We hypothesize that a high level of precursor C18:3n-3 in SWSO promotes the endogenous synthesis of C22:6n-3 despite the presence of ximenynic acid.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000502773","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"37625460","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigation of the Causal Association between Long-Chain n-6 Polyunsaturated Fatty Acid Synthesis and the Risk of Type 2 Diabetes: A Mendelian Randomization Analysis.","authors":"Michael A Zulyniak,&nbsp;Harriett Fuller,&nbsp;Mark M Iles","doi":"10.1159/000509663","DOIUrl":"https://doi.org/10.1159/000509663","url":null,"abstract":"<p><strong>Background: </strong>Globally, 1 in 11 adults has diabetes mellitus, and most of these cases are type 2 diabetes (T2D). The risk of T2D is influenced by many factors, including diet. The synthesis of long-chain n-6 polyunsaturated fatty acids (LC n-6 PUFA) has been posited as a risk factor for T2D; however, its causal role is uncertain.</p><p><strong>Aim: </strong>To test the causal effect of LC n-6 PUFA synthesis on insulin resistance and transgenerational T2D risk in a large cohort of men and women.</p><p><strong>Methods: </strong>Two-sample mendelian randomization (MR) was conducted to evaluate the effect of low or high levels of LC n-6 PUFA synthesis on glycemia and development of T2D in the UK Biobank (n = 463,010) and Meta-Analysis of Glucose- and Insulin-Related Traits Consortium (MAGIC; n = 5,130) cohorts. The increased likelihood of a predisposition to low or high LC n-6 PUFA synthesis and the risk of T2D was also investigated using the participants' siblings and parents. In MR-Base, 4 genetic variants associated with LC n-6 PUFA synthesis were found (p < 10-8). After pruning, 1 variant (rs174547) on the FADS1 gene was retained.</p><p><strong>Results: </strong>Lower LC n-6 PUFA synthesis and abundance (per % unit decrease) are associated with small reductions in the insulin disposition index (-0.038 ± 0.012 mM-1; p = 0.002) within MAGIC. In the UK Biobank, we report negligible effects of low n-6 PUFA synthesis on the odds of T2D (OR <1%; p < 0.05). Additionally, reduced LC n-6 PUFA synthesis does not appear to be a contributor to familial T2D risk. No significant association was observed between LC n-6 PUFA synthesis and BMI.</p><p><strong>Conclusion: </strong>In a primarily white European population, LC n-6 PUFA synthesis is not a major contributor to T2D risk.</p>","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2020-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000509663","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"38269689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Interaction between Vascular Endothelial Growth Factor-A (rs2010963) Gene Polymorphisms and Dietary Diversity Score on Cardiovascular Risk Factors in Patients with Metabolic Syndrome","authors":"M. Abbasalizad Farhangi, M. Vajdi, L. Nikniaz, Zeinab Nikniaz","doi":"10.1159/000503789","DOIUrl":"https://doi.org/10.1159/000503789","url":null,"abstract":"Background: The vascular endothelial growth factor-A (VEGFA) family of cytokines regulates proliferation, angiogenesis, and migration of endothelial cells, increases vascular permeability, and controls thrombogenicity. Recent studies have suggested that the VEGFA gene plays an important role in the pathogenesis of metabolic syndrome and its related disorders. Dietary diversity score (DDS) has also been shown to have potential favorable effects against features of metabolic syndrome. This study examined the interactions between +405 VEGFA C/G (rs2010963) polymorphism and DDS on the metabolic and biochemical profile of metabolic syndrome. Therefore, in the current study, we aimed to evaluate the interaction between DDS and VEGFA rs2010963 gene polymorphisms in modification of metabolic risk factors including serum lipids, blood pressure, serum adiponectin, and matrix metalloproteinase (MMP)-3 concentrations in patients with metabolic syndrome. Methods and Materials: In the current cross-sectional study, 254 patients with metabolic syndrome were recruited. Measurements of blood pressure, anthropometric parameters, and dietary intakes were performed and the DDS was calculated. Biochemical variables including serum adiponectin concentrations, lipid profile, serum glucose, and MMP-3 concentrations were measured by enzyme-linked immunosorbent assay method (ELISA) and enzymatic colorimetric methods. Determination of +405 C/G VEGFA gene polymorphisms was performed using the polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) technique. Results: Patients in the lowest DDS quartile had higher insulin and homeostatic model assessment of insulin resistance (HOMA-IR), while patients in the highest DDS quartile had higher quantitative insulin check index (QUICKI; p < 0.05). Higher serum triglyceride and systolic blood pressure (SBP) values and lower serum adiponectin concentrations were also observed in lower DDS quartiles (p < 0.05). Patients with the CC genotype in the VEGFA rs2010963 polymorphism had significantly higher body mass index (BMI), fasting blood glucose, aspartate aminotransferase (AST), and alanine aminotransferase (ALT; p < 0.05) compared to patients with the other 2 genotypes. In lower quartiles of DDS, 30% of patients with metabolic syndrome had the GG genotype, while 30.4 and 30.8% of patients with metabolic syndrome in higher DDS quartiles had GC and CC genotypes, respectively (p = 0.04). Conclusion: Our study found lower insulin resistance, serum triglyceride, and SBP and higher adiponectin concentrations among patients with metabolic syndrome in highest quartiles of DDS. Moreover, patients with the CC genotype were more likely to have higher BMI, fasting blood glucose, AST, and ALT. This significant interaction gives a possible evidence of a VEGFA-DDS association that may be relevant to metabolic syndrome. Further studies are warranted to clarify the underlying mechanisms of these interactions.","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2019-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000503789","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"47995457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nutrition Assessment and Intervention in a Pediatric Patient with Angelman Syndrome: A Case Presentation Highlighting Clinical Challenges and Evidence-Based Solutions","authors":"K. Fisher, J. Keng, J. Ziegler","doi":"10.1159/000504300","DOIUrl":"https://doi.org/10.1159/000504300","url":null,"abstract":"Background: Angelman syndrome (AS) is a rare disorder of genetic imprinting which results in intellectual and developmental disability. It meets criteria of a disorder of neurologic impairment. A deletion in the long arm of chromosome 15 (del 15q11.2–q13) is responsible for about 70% of cases of AS (deletion genotype). Summary: There is a paucity of evidence to allow algorithmic nutrition assessment and intervention in pediatric patients with AS. Therefore, our objective is to use a case presentation to provide an example of nutrition assessment and intervention in a pediatric patient with the deletion genotype of AS and then highlight common challenges to providing evidenced-based nutrition care. For the highlighted challenges, we suggest evidence-based solutions to provide a resource for clinicians who may encounter similar challenges in clinical practice. Key Messages: There are genotype-phenotype correlations in AS that can help guide clinicians regarding nutritionally relevant clinical characteristics and corresponding interventions that are patient specific. The deletion genotype in AS is associated with multiple characteristics that are relevant to nutrition care and may also be different and/or more severe than characteristics seen in other AS genetic mechanisms. There is also overlap in certain nutritionally relevant clinical characteristics between AS and other conditions, including Prader-Willi syndrome, autism spectrum disorders, and disorders of neurological impairment like cerebral palsy. Clinicians can utilize nutrition resources related to these conditions to expand the scope of relevant resources available.","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2019-11-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000504300","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49014541","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevention of Potential Adverse Metabolic Effects of a Supplementation with Omega-3 Fatty Acids Using a Genetic Score Approach","authors":"Maximilien Franck, J. de Toro-Martín, F. Guénard, I. Rudkowska, S. Lemieux, B. Lamarche, P. Couture, M. Vohl","doi":"10.1159/000504022","DOIUrl":"https://doi.org/10.1159/000504022","url":null,"abstract":"Introduction: The consumption of long-chain omega-3 polyunsaturated fatty acids (n-3 PUFA) has been reported to have beneficial health effects, notably, by reducing plasma triglyceride levels. Nonetheless, a concomitant decrease in insulin sensitivity has also been observed, but is highly variable among subjects. Herein, we aimed to determine the importance of the genetic background in the interindividual variability of the insulin sensitivity response following an n-3 PUFA supplementation. Methods: A total of 210 participants completed a 6-week n-3 PUFA supplementation with 5 g/day of fish oil (providing 1.9–2.2 g of eicosapentaenoic acid + 1.1 g of docosahexaenoic acid). Insulin resistance was estimated by the homeostatic model assessment (HOMA-IR), and participants were further classified as high-risk or low-risk depending on their HOMA-IR change following the n-3 PUFA supplementation, as compared to pre-supplementation values. Genome-wide genotyping data were obtained for 138 participants using HumanOmni-5-Quad BeadChips containing 4,301,331 single nucleotide polymorphisms. A genome-wide association analysis (GWAS) was carried out between high-risk and low-risk participants. The population study was split into training (60%) and testing (40%) datasets to assess the predictive accuracy of a genetic risk score (GRS) constructed by summing the number of risk alleles. Results: Following the n-3 PUFA supplementation, 32 participants had increased HOMA-IR as compared to initial values and were classified as high risk (23.2%), whereas remaining subjects were classified as low risk (n = 106, 76.8%). A total of 8 loci had frequency differences between high-risk and low-risk participants at a suggestive GWAS association threshold (p value <1 × 10–5). After applying 10-fold cross validation, the GRS showed a significant association with the risk of increased HOMA-IR in the testing dataset (OR = 3.16 [95% CI, 1.85–7.14]), with a predictive accuracy of 0.85, and explained 40% of variation in HOMA-IR change. Conclusions: These results suggest that the genetic background has a relevant role in the interindividual variability observed in the insulin sensitivity response following an n-3 PUFA supplementation. Subjects being at risk of insulin sensitivity lowering following an n-3 PUFA supplementation may be identified using genetic-based precision nutrition approaches.","PeriodicalId":18030,"journal":{"name":"Lifestyle Genomics","volume":null,"pages":null},"PeriodicalIF":2.6,"publicationDate":"2019-11-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1159/000504022","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"43521115","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}