Genes and Nutrition最新文献

The integration of multi-omics technologies with computational biology has had a profound impact on nutritional science, enabling the development of precision nutrition strategies tailored to individual biochemical profiles. This review synthesizes recent advances in integrating genomic, epigenetic, transcriptomic, proteomic, metabolomic, and microbiome data for personalized dietary interventions. The present study analyzed machine learning approaches, with a particular focus on transformer and graph neural networks, for the processing of multi-omics data and prediction of metabolic outcomes. Advanced computational models have demonstrated an accuracy rate of over 90% in predicting individual metabolic responses to dietary interventions. Large-scale clinical trials (PREDICT, FOOD4ME, and PRECISION-HEALTH) have demonstrated significant improvements in weight management, glycemic control, and dietary adherence compared with conventional approaches. Digital health technologies, including continuous glucose monitoring and artificial intelligence (AI)-powered applications, facilitate real-time physiological monitoring and enable dynamic nutritional adjustments in patients with diabetes. The paradigm shift from population-based dietary recommendations to individualized interventions is represented by multi-omics-driven precision nutrition. The integration of sophisticated computational methodologies with comprehensive biological profiling provides a unique opportunity to prevent and manage chronic diseases via targeted dietary interventions. However, the successful implementation of such a system necessitates interdisciplinary collaboration among biologists, computational scientists, clinicians, and policymakers to ensure equitable access and ethical deployment of the technology. Future research should focus on developing scalable implementation frameworks, establishing evidence-based clinical practice guidelines to standardize multi-omics applications in precision nutrition, and identifying strategies to address potential disparities in access to these applications.

Background: High-density lipoprotein cholesterol (HDL-C) helps remove excess cholesterol, and low levels are a key metabolic risk factor for cardiovascular disease. Although several studies have investigated the association between kimchi consumption and HDL-C levels, these observational findings are often limited by confounding factors and reverse causality.

Objective: We aimed to assess the causal association between kimchi intake and the reduced HDL-C using Mendelian randomization (MR), with analyses stratified by sex.

Methods: We conducted this study using participants from two cohorts of the Korean Genome and Epidemiology Study (KoGES): the Health Examinees (HEXA) cohort (n = 53,060) and the Ansan/Ansung cohort (n = 4,907). Kimchi intake was assessed via a semi-quantitative food frequency questionnaire, estimating total daily consumption (g/day) of various kimchi types including baechu (cabbage) kimchi, kkakdugi/mu-kimchi, nabak-kimchi/dongchimi, and other varieties. Single nucleotide polymorphisms (SNPs) associated with kimchi consumption were identified via genome-wide association studies (GWAS), adjusting for covariates and applying a significance threshold of p < 5 × 10⁻⁵ and linkage disequilibrium cutoff (r² < 0.001). A total of 86 SNPs in men and 82 in women were selected as instrumental variables (IVs) for MR analysis. The MR analysis was conducted using inverse-variance weighted (IVW), MR-Egger, weighted median, and MR-PRESSO methods. Sensitivity analyses included heterogeneity testing, leave-one-out analysis, and funnel plot inspection.

Results: In men, a significant causal relationship between higher kimchi consumption and lower odds of reduced HDL-C was identified by both the IVW (OR = 0.997, 95% CI = 0.996-0.999, p < 0.05) and MR-PRESSO (OR = 0.998, 95% CI = 0.996-0.999, p < 0.05) analyses, with no evidence of heterogeneity or horizontal pleiotropy. No significant associations were observed in women.

Conclusion: This study provides evidence for a causal effect of kimchi consumption in preventing decreases in HDL-C levels among middle-aged Korean men. These findings support kimchi as a sex-specific dietary intervention for cardiovascular health.

Background: Nonalcoholic fatty liver disease (NAFLD) is an escalating health concern, with genetic factors playing a substantial role. This study aimed to establish and validate a polygenic risk score for East Asian populations (PRS-EA).

Methods: A meta-analysis of genome-wide association studies on NAFLD in East Asian populations was conducted to develop a PRS-EA model. This model was subsequently validated in the Kailuan cohort by exploring its association with NAFLD development and progression.

Results: A PRS-EA model involving four SNPs (rs2896019, rs3810622, rs58542926, and rs1260326) was constructed. Individuals with PRS-EA scores exceeding 2.33 were associated with a 53% (95% confidence interval, 3%-126%) increased risk of NAFLD development and 50% (95% confidence interval: 3%-120%) of NAFLD progression. A positive joint association was observed between higher PRS and lipid dysfunction in relation to NAFLD occurrence. Hypertension was found to amplify the association between higher PRS and NAFLD progression (hazard ratio: 3.07 vs. 1.22, P for interaction=0.015).

Conclusion: This study developed a PRS model specific to East Asian populations, highlighting the potential utility of PRS-EA in assessing and managing NAFLD risk, particularly in individuals with lipid metabolic dysfunction and hypertension.

Background: Caloric restriction is so far the most effective strategy for weight management. Based on their weight loss response, individuals can be classified as hypo-responders or hyper-responders. Therefore, efforts have been made to understand the molecular mechanisms underlying these differential responses to develop more effective and personalized weight loss interventions. This study aimed to identify changes in gene expression patterns between hyper- and hypo-responders selected from a dietary intervention based on caloric restriction.

Results: At the end of the intervention, both groups showed reductions in all evaluated anthropometric parameters. However, the hyper-responder group lost 82.3% more weight, 81.5% more in BMI, 68.9% more in hip circumference, and 47.97% more in waist circumference compared to the hypo-responder group, with statistically significant differences between groups. On the transcriptomic side, significant differences in gene expression (FDR ≤0.03) were observed between the hyper- and hypo-responder groups. A total of 1,581 genes were differentially expressed, of which only the GSPT1 gene (G1 to S Phase Transition 1) was upregulated, while the rest were downregulated in hypo-responders. Protein-protein interaction network analysis identified the Collagen Chain Trimerization and Collagen Biosynthesis and Modifying Enzymes pathways as significantly enriched (FDR = 0.0041), involving genes such as PLOD1, COL5A3, COL6A5, COL14A1, CRTAP, COL4A5, COL7A1, COL9A1, TLL2, COL20A1, COL4A2, COL24A1, COL16A1, COL5A2, COL15A1, COL4A1, and COL13A1. The upregulation of GSPT1 in hypo-responders may reflect an altered metabolic and inflammatory state that contributes to weight loss resistance. Many of the downregulated genes contribute directly to the mechanical properties of the extracellular matrix (ECM), suggesting a stiffer, less flexible ECM, an environment associated with fibrosis and insulin resistance in obese individuals.

Conclusions: This study provides novel evidence on how gene expression may contribute to the variability in weight loss responses, resulting in a hyper- or hypo-response to caloric restriction. The upregulation of GSPT1 and the downregulation of genes involved in collagen-related pathways are proposed as key molecular mechanisms influencing the hypo-response during caloric restriction.

Background: Postprandial metabolism plays a key role in cardiometabolic health, and its impairment with ageing is associated with increased disease risk. While yoghurt consumption has been linked to improved fasting metabolic markers, its acute postprandial effects are less well understood, particularly in older adults. This study investigated whether yoghurt consumption influences age-related postprandial metabolic dysregulation.

Methods: In a randomised crossover design, 14 young (20-35 years) and 14 older (65-80 years) healthy men consumed 600 mL of whole milk or yoghurt following an overnight fast. Biochemical markers (glucose, insulin, triglycerides, TNF-α, IL-6, GIP and ghrelin) were measured at baseline and up to six hours postprandially. Differences in lipid metabolism by age were further investigated by assessing free fatty acid (FFA) responses in the yoghurt phase only. Postprandial responses were analysed for time, age, product and interaction effects, and summarised using incremental area under the curve (iAUC) and incremental maximum concentration (iCmax).

Results: Glucose and insulin responses were influenced by product (time × product, p < 0.05), with yoghurt resulting in significantly lower iCmax values compared with milk. In contrast, triglyceride responses were influenced by age (time × age, p < 0.05), with older adults exhibiting higher iAUC and iCmax, delayed peak concentrations and slower return to baseline levels, independently of the product consumed. No significant age × product or age × product × time interactions were observed for any biochemical marker. Among the 37 FFAs quantified in the yoghurt phase, seven - predominantly saturated and abundant in yoghurt - exhibited a significant time × age interaction, accompanied by higher iAUC or iCmax in older adults.

Conclusions: Dairy fermentation improved postprandial glucose and insulin responses, whereas ageing predominantly affected lipid dynamics. Fermentation did not attenuate impairments in postprandial triglyceride metabolism in this acute setting. Profiling individual postprandial FFAs may enhance understanding of metabolic flexibility and inform personalised dietary strategies across the lifespan.

Background & aims: The current study aimed to systematically review the existing literature that investigated the modifying effect of genes on the relationship between dietary determinants and Metabolic syndrome (MetS).

Methods: A comprehensive search was performed on PubMed, Scopus, and Web of Science from inception to July 17, 2025, without any language restrictions, as long as the abstract was in English. The key keywords used were Diet, Nutrition, genetic factors, single-nucleotide polymorphisms (SNPs), and MetS.

Results: The literature included 40 observational studies. A significant interaction was identified between high intake of fat and genetic variations related to lipid metabolism, such as VEGF rs6921438 SNP, Caveolin-1 (CAV-1) rs3807992 SNP, Melanocortin-4 receptor (MC4R) rs12970134 SNP, Acetyl-CoA carboxylase (ACC2) rs4766587 SNP, PDZ domain containing 1 (PDZK1) i33968 SNP, ApoB rs512535 SNP, ApoA1 rs670 SNP, zinc transporters 8 (ZNT8) rs13266634 SNP, and circadian locomotor output cycles kaput (CLOCK) rs1801260 SNP. This interaction heightened the risk of MetS in individuals who are genetically predisposed to it. No interaction was found between alcohol consumption and the genotypes of alcohol dehydrogenase and aldehyde dehydrogenase. There are very few studies that have investigated the interaction between genes and macronutrients, micronutrients, food groups, and dietary patterns, and the results are inconsistent.

Conclusions: Due to the limited research in the nutrigenetics approach, the specific gene-nutrient interactions on MetS are not completely understood. Nevertheless, the results indicate that a high-fat diet interacts with certain genetic variations, particularly those involved in regulating lipid metabolism. This interaction is associated with an increased risk of MetS in individuals who are genetically predisposed.

Background: Oxidative stress plays a pivotal role in cellular aging, and dietary antioxidants may modulate this process through regulation of the aging-related Klotho gene. This cross-sectional study investigated the association between dietary total antioxidant capacity (DTAC) and Klotho gene expression in 50 healthy Iranian adults (aged 18-40 years).

Methods: Using validated food frequency questionnaires, we calculated DTAC (mmol Trolox equivalents/day) and assessed Klotho mRNA levels in peripheral blood mononuclear cells (PBMCs) via RT-PCR (ΔCt method). Linear regression models evaluated these associations, with Model 1 showing crude associations and Model 2 adjusting for age, sex, BMI, waist circumference, physical activity, and fiber intake.

Results: Unadjusted analysis revealed DTAC significantly predicted Klotho expression (β = -0.662, p < 0.001, R² = 0.438), with higher antioxidant intake associated with lower ΔCt values (indicating greater Klotho expression). This association remained significant after full adjustment (β = -0.599, p = 0.002, Adjusted R² = 0.381). Notably, among individual antioxidants, only zinc maintained an independent inverse relationship with ΔCt Klotho in the adjusted model (β = -0.439, p = 0.016), while other antioxidants lost significance.

Conclusion: These findings demonstrate that higher dietary antioxidant intake, particularly zinc, is significantly associated with increased Klotho gene expression, suggesting a potential mechanism by which antioxidant-rich diets may influence aging processes. This study provides novel evidence linking DTAC to Klotho expression in humans, supporting further investigation into dietary strategies for modulating aging-related pathways.

Maintaining a regular and nutritious diet has recently become a significant concern due to its impact on various health conditions. Despite following a normal diet, the presence of inflammation and oxidative stress can have negative consequences, especially in IBD (Inflammatory Bowel Disease) patients. The use of beneficial agents such as probiotics in their inactive form, known as paraprobiotics, can help counteract these adverse effects by exerting antioxidant and anti-inflammatory properties. This study aimed to evaluate and compare the antioxidant and anti-inflammatory properties of native probiotic strains and their inactive derivatives, known as paraprobiotics, in mitigating the harmful effects of DSS-induced colitis. Twenty male wild-type C57BL/6 mice were treated with native probiotic strains, including Lactobacillus reuteri RP100, Lactobacillus plantarum RP42, Lactobacillus plantarum RP119, Lactobacillus plantarum RP155, Bifidobacterium bifidum RP1001, and Bifidobacterium longum RP1044, as well as the derived paraprobiotics. The mice were divided into four experimental groups: normal diet (ND) + PBS, ND + DSS (Dextran Sodium Sulfate), ND + DSS + 10⁹ cfu/ml of probiotic strains, and ND + DSS + 10⁹ cfu/mL of paraprobiotic. Colitis indices, evaluation of oxidant/antioxidant enzymes, anti/pro inflammatory cytokines, and expression of NF-kB and Nrf2 pathways genes were assessed. A significant difference was noted among the groups exposed to DSS, where mice treated with probiotics and paraprobiotics in addition to DSS showed a decrease in the harmful effects caused by DSS, both in terms of enzymatic assessments and molecular markers like Nrf2 and NF-kB related genes, with similar outcomes between our native probiotic and paraprobiotic. The strong antioxidant and anti-inflammatory characteristics of our native probiotics and paraprobiotics at molecular and phenotypic levels suggest that these agents, especially paraprobiotics as non-living entities, could be valuable supplementary treatment options to improve the quality of life for individuals with IBD.