Lifestyle Genomics最新文献

In mammalian species, the Fatty Acid Desaturase (FADS) gene cluster includes FADS1 (∆5-desaturase), FADS2 (∆6-desaturase), and a third gene member, named FADS3. According to its high degree of nucleotide sequence homology with both FADS1and FADS2, FADS3 was promptly suspected by researchers in the field to code for a new mammalian membrane-bound fatty acid desaturase. However, no catalytic activity was attributed to the FADS3 protein for a decade, until the rat FADS3 protein was shown in vitro to be able to catalyze the unexpected ∆13-desaturation of trans-vaccenic acid, producing the trans11,cis13-conjugated linoleic acid isomer. This review summarizes the recent investigations establishing the FADS3 enzyme as a reliable mammalian trans-vaccenate ∆13-desaturase in vivo and tries to identify further unresolved issues that need to be addressed.

Background: Recent studies have shown that depression is inversely correlated with high protein and low fat intake and positively correlated with vitamin D-binding protein (VDBP). Therefore, the aim of this study was to examine the interaction between protein/fat dietary patterns and VDBP genotypes with regard to the risk of depression in apparently healthy adults who have not been diagnosed with any chronic disease.

Methods: In this study, 265 individuals (126 males and 139 females) aged 18-55 years were recruited from the communities of central and west Tehran based on convenience sampling. Body composition was measured with a body composition analyzer and depression symptoms were categorized as normal, moderate depression, or severe depression using the Depression Anxiety Stress Scales 21 (DASS-21) questionnaire. Dietary patterns were determined by a semiquantitative food frequency questionnaire to assess typical food intake during the 12-month period. Blood samples were collected from and biochemical measurements performed on all participants. An analysis of two polymorphisms (rs7041 and rs4588) in the GC gene, which encodes VDBP, was performed by polymerase chain reaction-restriction fragment length polymorphism.

Results: A statistically significant association was found between depression and diet (p = 0.03) after having categorized the participants into three groups: a high-protein/low-fat (HP/LF) group, a moderate-protein/moderate-fat (MP/MF) group, and a low-protein/high-fat (LP/HF) group. Moreover, the findings demonstrated that depression was related to both the rs7041 and the rs4588 polymorphism (p = 0.05 and p = 0.02, respectively). We next used multinomial logistic modeling to investigate the risk of depression. A significant interaction was observed between HP/LF diet and the rs7041 polymorphism in the moderate- and severe-depression groups (β = -0.30, p = 0.05, and β = -0.48, p = 0.01, respectively).

Conclusion: This study showed that an HP/LF diet interacts with the rs7041 polymorphism, with T allele carriers having a greater prevalence of moderate and severe depression.

Background/aims: Guanidinoacetic acid (GAA) is an experimental dietary additive and has been reported to induce methyl depletion when provided by the diet. However, no study evaluated whether supplemental GAA affects DNA methylation, a critical epigenetic process for genome regulation.

Methods: In this open-label, repeated-measure interventional trial, we evaluated the impact of 12 weeks of GAA supplementation on global DNA methylation in 14 healthy participants (8 women and 6 men, age 22.2 ± 2.3 years, body mass index 24.8 ± 5.7).

Results: Dietary provision of GAA had no effect on global DNA methylation, with 5-methylcytosine (m5C) nonsignificantly increased by 13.4% at postadministration when averaged across participants (95% confidence interval -5.5 to 32.3; p = 0.26). Notable DNA hypomethylation (corresponding to a 5% drop in m5C) was found in 3 of 14 participants at follow-up.

Conclusion: Global DNA methylation seems to be unaltered by dietary provision of 3 g of GAA per day for 12 weeks in healthy men and women.

Introduction: The 5-hydroxytryptamine 2C receptor (HTR2C) rs6318 polymorphism has been associated with increased sensitivity to stress. This study investigated whether the rs6318 genotype modified the cortisol response to endurance physical activity.

Methods: The HTR2C SNP was genotyped in a population of agonistic cyclists, and salivary cortisol levels were measured before and after an endurance competition.

Results and conclusion: Salivary cortisol levels increased after the competition (from 20.72 ± 12.36 ng/mL to 33.80 ± 21.53 ng/mL; p = 3.189 × 10-5). rs6318 C carriers displayed higher baseline cortisol levels compared to G carriers (26.60 ± 9.35 ng/mL vs. 19.50 ± 12.63 ng/mL; p = 0.04). Baseline cortisol levels were able to predict the cortisol response to exercise (β = -0.846; p = 1.2 × 10-5). Although regression analysis did not identify an association between HTR2C genotype and change in cortisol levels, a secondary analysis in which the population was classified by median cortisol changes suggested that they might be weakly associated, thus warranting further investigation.

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.

The rates of obesity and its related comorbidities have increased substantially over the last 30 years, with approximately 35% of all US adults now classified as obese. Whilst the causes of obesity are both complex and multifactorial, one contributor is a reduction in leisure time physical activity, with no concurrent reduction in energy intake. Physical activity interventions have been demonstrated to promote fat loss, yet more than 50% of US adults undertake no leisure time physical activity at all, with a lack of time and enjoyment often cited as the main drivers of rising inactivity levels. Furthermore, recent evidence has demonstrated that a sub-group of individuals may experience no improvement in a given fitness or health-related measure following a specific training programme, suggesting that there may be optimal exercise types for different groups of individuals. In this paper, we introduce the concept of exercise response efficiency, whereby individuals are matched to the training type from which they are most likely to derive the greatest improvements for the least time commitment. We propose that a more precise targeting of exercise interventions is likely to drive more rapid improvements in health, thereby promoting exercise adherence and enjoyment, whilst simultaneously reducing obesity and mortality risks. Such an innovation would, we suggest, confer important public health benefits.