Lifestyle Genomics最新文献

Introduction: The effects of the rs822393 variant of ADIPOQ gene on metabolic parameters such as insulin resistance and adiponectin levels following weight loss through dietary intervention are still uncertain. The aim of this study was to evaluate the role of rs822393 of ADIPOQ gene on adiponectin levels and metabolic parameters after weight loss with a high-fat hypocaloric diet with Mediterranean pattern during 12 weeks.

Methods: A population of 283 patients with obesity was allocated to a dietary intervention trial with a high-fat hypocaloric diet during 12 weeks. Adiposity and biochemical parameters were determined. rs822393 was assessed with a dominant model analysis (CC vs. CT + TT).

Results: These patients had three different genotypes: CC (59.0%), CT (33.6%), and TT (7.4%). The allelic frequencies for C and T were 0.89 and 0.20, respectively. Basal and post-intervention HDL cholesterol, adiponectin levels, and adiponectin/leptin ratio were lower in T-allele than non-T-allele carriers. After dietary intervention, BMI, weight, fat mass, waist circumference, systolic blood pressure, insulin, HOMA-IR, leptin, total cholesterol, and LDL cholesterol levels improved significantly in both genotype groups. Moreover, HDL cholesterol (CC vs. CT + TT) (delta: 8.9 ± 1.1 mg/dL vs. 1.7 ± 0.8 mg/dL; p = 0.02), serum adiponectin in non-T-allele carriers (43.1 ± 5.9 ng/dL vs. 2.8 ± 3 0.0 ng/dL; p = 0.01), and adiponectin/leptin ratio (1.37 ± 0.1 units vs. 0.17 ± 0.08 units; p = 0.02) improved only in non-T-allele carriers after weight loss.

Conclusion: Individuals with obesity and without the T allele of rs822393 experienced improvements in adiponectin levels, adiponectin/leptin ratio, and HDL cholesterol levels after following a high-fat hypocaloric diet with a Mediterranean pattern.

Background: Cardiometabolic diseases pose a significant threat to global public health, with a substantial majority of cardiovascular disease mortality (more than three-quarters) occurring in low- and middle-income countries. There have been remarkable advances in recent years in identifying genetic variants that alter disease susceptibility by interacting with dietary factors. Despite the remarkable progress, several factors need to be considered before the translation of nutrigenetics insights to personalised and precision nutrition in ethnically diverse populations. Some of these factors include variations in genetic predispositions, cultural and lifestyle factors as well as socio-economic factors.

Summary: This review aimed to explore the factors that need to be considered in bridging the gap between existing nutrigenetics insights and the implementation of personalised and precision nutrition across diverse ethnicities. Several factors might influence variations among individuals with regard to dietary exposures and metabolic responses, and these include genetic diversity, cultural and lifestyle factors as well as socio-economic factors. A multi-omics approach involving disciplines such as metabolomics, epigenetics, and the gut microbiome might contribute to improved understanding of the underlying mechanisms of gene-diet interactions and the implementation of precision nutrition although more research is needed to confirm the practicality and effectiveness of this approach. Conducting gene-diet interaction studies in diverse populations is essential and studies utilising large sample sizes are required as this improves the power to detect interactions with minimal effect sizes. Future studies should focus on replicating initial findings to enhance reliability and promote comparison across studies. Once findings have been replicated in independent samples, dietary intervention studies will be required to further strengthen the evidence and facilitate their application in clinical practice.

Key messages: Nutrigenetics has a potential role to play in the prevention and management of cardiometabolic diseases. Conducting gene-diet interaction studies in diverse populations is essential giving the genetic diversity and variations in dietary patterns. Integrating data from disciplines such as metabolomics, epigenetics, and the gut microbiome could help in early identification of individuals at risk of cardiometabolic diseases as well as the implementation of precise dietary interventions for preventing and managing cardiometabolic diseases.

Introduction: It has been suggested that capsaicin (CAP), a major pungent component in chili peppers, can be used as an anti-obesity ingredient due to effects on energy metabolism, but evidence is not consistent. Genetics may account for differences in CAP tolerance and its impact on adiposity status. The aim of this study was to systematically review current evidence concerning the role of genetic polymorphisms influencing CAP tolerance.

Methods: The present systematic review analyzed and synthesized available evidence concerning associations between genetic polymorphisms and CAP tolerance following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses Protocols (PRISMA-P) guidelines. Databases such as PubMed/MEDLINE, Cochrane, Scopus, Google Scholar, SciELO, and LILACS were screened. Out of 228 publications identified, only 6 meet inclusion criteria and were finally included in the final report.

Results: Overall, a total of 28 single nucleotide polymorphisms were associated with several CAP tolerance traits including sensitivity to burning/stinging, heat pain, and cough reactions, and detection of bitter taste thresholds. These genetic variants were located within 6 genes involved in key physiological processes such synthesis of tetrahydrobiopterin and nitric oxide production (GCH1), CAP uptake and transduction of thermal stimuli (TRPV1), and bitter taste perception (TAS2R38, TAS2R3, TAS2R4, and TAS2R5).

Conclusion: There is evidence about the influence of genetic polymorphisms on CAP tolerance by affecting nociceptive signaling, CAP binding, and bitter tasting. This knowledge may facilitate the design and implementation of innovative CAP-based nutrigenetic strategies for a more precise clinical management of obesity.

Background: Women can spend up to 40% of their lives in the postmenopausal state. As women begin to transition into menopause, known as perimenopause, changes in hormonal concentrations and body composition dramatically increase overall cardiometabolic risk. Dietary patterns and interventions can be utilized to prevent and treat cardiovascular disease (CVD) and some dietary patterns over others may be more beneficial due to their specific effects on the health aspects of menopause. In this narrative review, we summarize key cardiovascular alterations that occur during the menopause transition and explore current dietary recommendations to address CVD risk as well as explore the new frontier of precision nutrition and the implications for nutrition prescription during menopause.

Summary: Popular dietary interventions for CVD such as the Dietary Approaches to Stop Hypertension (DASH) diet and the Mediterranean diet (MED) have limited data in women following menopause. However, both diets improve CVD risk biomarkers of total cholesterol and low-density lipoprotein cholesterol as well as lower oxidative stress and inflammation and improve endothelial function. As the menopause transition increases the risk for developing metabolic syndrome, insulin insensitivity, and dyslipidemia, the DASH diet and MED may be impactful dietary strategies for mediating CVD risk in menopausal women. However, these are "one-size-fits-all" approaches that neglect individual characteristics such as genetic predisposition and environmental factors. Precision nutrition considers individual factors for nutrition prescription, spanning from evaluating food intake preferences and behaviors to deep phenotyping. Data from a large-scale investigation of the menopause transition suggests nutritional strategies that address postprandial glycemic responses, and the gut microbiome may attenuate some of the unfavorable effects of menopause on CVD risk factors.

Key messages: Considering menopause, women are a clinical population that would greatly benefit from precision nutrition. Future research should explore the use of machine learning and artificial intelligence in a precision nutrition framework to modify the DASH diet and MED to address adverse effects that occur during the menopause transition are vital for supporting women's health as they age.

Introduction: Large neutral amino acids (LNAAs) tryptophan and phenylalanine have been implicated in the pathogenesis of neurodegenerative diseases. Given limited research on the effects of LNAA on brain health across different life stages, vascular risk, and genetic backgrounds, our study aimed to explore the interaction of LNAA levels, metabolic syndrome (MetS), and the presence of the apolipoprotein E ε4 (ApoE ε4) allele brain integrity at midlife.

Methods: Sixty-eight adults aged 40-61 underwent a health assessment to calculate the number of MetS components, quantify LNAA, measure white matter hyperintensity (WMH) volume, and genotype ApoE ε4. Multivariate linear regression analyses were performed to test the joint effect of LNAA, MetS, and ApoE ε4 on WMH while adjusting for sex, age, and education.

Results: Significant 3-way interactions were observed between serum tryptophan (β = 0.042, SE = 0.018, p < 0.05) and phenylalanine (β = 0.044, SE = 0.013, p < 0.01) levels, number of MetS components, and ApoE ε4 alleles status on WMH volume. Neither individual LNAA levels nor MetS components alone predicted WMH volume.

Conclusions: The study highlights significant 3-way interactions between LNAA, MetS, and genetic risk factors in the pathology of WMH, particularly in individuals genetically predisposed to Alzheimer's disease. These interactions suggest differential impacts of LNAA on WMH volume dependent on both genetic and metabolic factors. Results emphasize the need for personalized metabolic and genetic profile assessments in neurodegenerative disease management.

Introduction: This study aims to investigate if a mixture of functional lipids (FLs), containing conjugated linoleic acid (CLA), tocopherols (TPs), and phytosterols (PSs), prevents some lipid alterations induced by high-fat (HF) diets, without adverse effects.

Methods: Male CF1 mice (n = 6/group) were fed (4 weeks) with control (C), HF, or HF + FL diets.

Results: FL prevented the overweight induced by the HF diet and reduced the adipose tissue (AT) weight, associated with lower energy efficiency. After the intervention period, the serum triacylglycerol (TAG) levels in both HF diets underwent a decrease associated with an enhanced LPL activity (mainly in muscle). The beneficial effect of the FL mixture on body weight gain and AT weight might be attributed to the decreased lipogenesis, denoted by the lower mRNA levels of SREBP1-c and ACC in AT, as well as by an exacerbated lipid catabolism, reflected by increased mRNA levels of PPARα, ATGL, HSL, and UCP2 in AT. Liver TAG levels were reduced in the HF + FL group due to an elevated lipid oxidation associated with a higher CPT-1 activity and mRNA levels of PPARα and CPT-1a. Moreover, genes linked to fatty acid biosynthesis (SREBP1-c and ACC) showed decreased mRNA levels in both HF diets, this finding being more pronounced in the HF + FL group.

Conclusion: The administration of an FL mixture (CLA + TP + PS) prevented some lipid alterations induced by a HF diet, avoiding frequent deleterious effects of CLA in mice through the modulation of gene expression related to the regulation of lipid metabolism.

Background: Phenylketonuria (PKU) is an autosomal recessive genetic condition that results in reduced enzymatic functioning within the phenylalanine hydroxylase (PAH) pathway, which is involved in the metabolism of phenylalanine (Phe) into tyrosine (Tyr). Without dietary intervention, individuals with PKU exhibit significantly elevated levels of Phe, which is presumed to cause severe neurological dysfunction and other associated health risks. Carriers of PKU are heterozygotes for a PAH gene mutation and are typically described in the literature as "unaffected." However, decades of existing research challenges this classical thinking and it is plausible that these individuals currently classified as carriers may present with an intermediate phenotype or may be "moderately affected."

Summary: The purpose of this scoping review was to explore this hypothesis further, by searching for and summarizing existing literature on metabolism and health outcomes among PKU carriers. Preliminary research has suggested that some PKU carriers exhibit reduced PAH enzyme function, and relatedly, elevated circulating Phe levels compared to noncarriers. In addition, Phe dosing trials have further demonstrated that carriers have increased Phe levels and decreased Tyr levels compared to noncarriers. Because of these metabolic perturbations, it is biologically plausible for carriers to experience an intermediate phenotype in terms of metabolic consequences and clinical outcomes. While these outcomes have yet to be thoroughly explored, early research has found associations between PKU carrier status and lower IQs as well as decreased executive functioning, memory, processing speed, and inhibitory control. The PAH pathway is also involved in melanogenesis, and research has demonstrated increased melanoma risk among PKU carriers. However, there are many limitations to this research, and thus whether or not carriers are clinically impacted cannot yet be conclusively determined.

Key message: Overall, while preliminary research suggests a possible intermediate phenotype among PKU carriers, the current available research is limited and PKU carriers are still clinically considered "unaffected." This review outlines the current literature while discussing future research endeavors related to the metabolism and health of PKU carriers.

Background: Dysregulation of epigenetic processes and abnormal epigenetic profiles are associated with various metabolic disorders. Nutrition, as an environmental factor, can induce epigenetic changes through both direct exposure and transgenerational inheritance, continuously altering gene expression and shaping the phenotype. Nutrients consumed through food or supplementation, such as vitamin B12, folate, vitamin B6, and choline, play a pivotal role in DNA methylation, a critical process for gene regulation. Additionally, there is mounting evidence that the expression of non-coding RNAs (ncRNAs) can be modulated by the intake of specific nutrients and natural compounds, thereby influencing processes involved in the onset and progression of metabolic diseases.

Summary: Evidence suggests that dietary patterns, weight loss interventions, nutrients and nutritional bioactive compounds can modulate the expression of various microRNA (miRNAs) and DNA methylation levels, contributing to the development of metabolic disorders such as obesity and type 2 diabetes. Furthermore, several studies have proposed that DNA methylation and miRNA expression could serve as biomarkers for the effects of weight loss programs.

Key message: Despite ongoing debate regarding the effects of nutrient supplementation on DNA methylation levels and the expression of ncRNAs, certain DNA methylation marks and ncRNA expressions might predict the risk of metabolic disorders and act as biomarkers for forecasting the success of therapies within the framework of precision medicine and nutrition. The role of DNA methylation and miRNA expression as potential mediators of the effects of weight loss underscores their potential as biomarkers for the outcomes of weight loss programs. This highlights the influence of dietary patterns and weight loss interventions on the regulation of miRNA expression and DNA methylation levels, suggesting an interaction between these epigenetic factors and the body's response to weight loss.

Introduction: Roux-en-Y gastric bypass (RYGB) substantially alters the gut microbial composition which could be associated with the metabolic improvements seen after surgery. Few studies have been conducted in Latin American populations, such as Mexico, where obesity prevalence is above 30% in the adult population. Thus, the aim of this study was to characterize the changes in the gut microbiota structure in a Mexican cohort before and after RYGB and to explore whether surgery-related changes in the microbial community were associated with weight loss.

Methods: Biological samples from patients who underwent RYGB were examined before and 12 months after surgery. Fecal microbiota characterization was performed through 16S rRNA sequencing.

Results: Twenty patients who underwent RYGB showed a median excess weight loss of 66.8% 12 months after surgery. Surgery increased alpha diversity estimates (Chao, Shannon index, and observed operational taxonomic units, p < 0.05) and significantly altered gut microbiota composition. Abundance of four genera was significantly increased after surgery: Oscillospira, Veillonella, Streptococcus, and an unclassified genus from Enterobacteriaceae family (PFDR < 0.1). The change in Veillonella abundance was associated with lower excess weight loss (rho = -0.446, p = 0.063) and its abundance post-surgery with a greater BMI (rho = 0.732, p = 5.4 × 10-4). In subjects without type 2 diabetes, lower bacterial richness and diversity before surgery were associated with a greater Veillonella increase after surgery (p < 0.05), suggesting that a lower bacterial richness before surgery could favor the bloom of certain oral-derived bacteria that could negatively impact weight loss.

Conclusion: Presurgical microbiota profile may favor certain bacterial changes associated with less successful results.