Genes and Nutrition最新文献

Background: Implementing personalized dietary interventions has become important as emerging evidence indicates that dietary and lifestyle-dependent epigenetic modifications affect insulin resistance.

Methods: An epigenome-wide association study (EWAS) was conducted on 1,684 non-diabetic adults aged 57-75 from the Framingham Offspring Study (FOS). Associations between dietary and lifestyle factors (assessed via food frequency questionnaire) and DNA methylation sites (DNA-MS) were analyzed, with adjustments for confounders (age, sex, lifestyle) and multiple testing. Significant epigenetic mediators were evaluated using causal mediation models. Validation was executed using the Genetics of Lipid-Lowering Drugs and Diet Network Study (n = 945).

Results: The EWAS identified 35 DNA-MS linked to HOMA-IR, with 13 DNA-MS showing significant associations with dietary factors in the FOS. Key DNA-MS including cg17901584 (DHCR24), influenced by brown rice (natural indirect effect: β ± SE, -0.02 ± 0.01, p = 0.0003), cg22761431 (EFNB3) by wheat germ (-0.01 ± 0.003, p = 0.001), and cg00574958 (CPT1A) associated with lactose (-0.001 ± 0.0003, p = 0.0001) intakes, all correlated with decreased HOMA-IR. Other DNA-MS, cg06808571 (KCNH2), cg06690548 (SLC7A11), and intergenic cg07504977, mediated increases in HOMA-IR linked to intakes of low-calorie cola (0.003 ± 0.001, p = 0.001), alcohol (0.01 ± 0.001, p = 9.0E-11), and palmitoleic acid (0.03 ± 0.01, p = 9.0E-05), respectively. In the GOLDN study, alcohol intake mediated by cg06690548 methylation in SLC7A11 was positively associated with HOMA-IR. Notably, the DHCR24 gene, crucial for cholesterol biosynthesis, was highlighted as a potential dietary target for reducing metabolic risk.

Conclusion: The identification of specific DNA methylation sites, such as those in DHCR24 and EFNB3, provides supportive evidence for the mechanistic basis of known dietary effects on metabolic health. These findings not only reinforce the importance of diet in managing insulin resistance but also open avenues for personalized dietary interventions tailored to an individual's epigenetic profile.

Background: Herbal compounds are widely recognized for their ​​diverse biological activities, often targeting multiple pathways simultaneously. However, the hypoglycemic effect of liensinine and its underlying mechanisms remain poorly understood. This study aims to clarify how liensinine exerts its blood glucose-lowering effects, with a focus on its impact on pancreatic function and the gut microbiota.

Methods: Thus, male C57BL/6 mice were randomly assigned to two dietary groups: a standard chow diet or a high-fat diet (HFD) for 4 weeks. Subsequently, type 2 diabetes mellitus (T2DM) was induced in HFD-fed mice using streptozotocin (STZ) injection, and the model was maintained for an additional four weeks. The mice were then further divided into four experimental groups: Control (standard chow), Negative Control (NC, chow-fed mice treated with liensinine at 60 mg/kg), Model (HFD + STZ-induced T2DM mice), and T2DM + Lien (T2DM mice treated with liensinine). The study employed Western blot, Immunofluorescence, and RT-qPCR techniques.

Results: Liensinine alleviated pancreatic injury and hepatic steatosis. It promoted islet cell proliferation, restored normal islet architecture, and balanced alpha- and beta-cell masses. Additionally, liensinine upregulated the expression of METTL3/14 (methyltransferases involved in RNA modification) and pancreatic duodenal homeobox 1 (PDX-1, a key regulator of pancreatic development). Meanwhile, liensinine reduced the abundance of Firmicutes, Lactobacillus, and Actinobacteriota, alongside increased levels of Bacteroides, Akkermansia, and norank_f_Muribaculaceae, concomitant with elevated short chain fatty acids (SCFAs) production in T2DM mice.

Conclusions: In conclusion, these findings indicate that liensinine holds promise as a natural therapeutic agent, exerting beneficial effects on T2DM by ameliorating islet β-cell dysfunction and modulating gut microbiota.

Background: Some studies indicate that psyllium supplementation may change lipid profile levels. This study assessed the impact of psyllium consumption on lipid profile (Low-Density Lipoprotein Cholesterol, Triglyceride, High-Density Lipoprotein Cholesterol, and cholesterol).

Main text: We started searching articles using Scopus, Institute for Scientific Information Web of Science, and PubMed to identify eligible publications from March 15, 2022 to August 2, 2025. The effect of psyllium on lipid profiles in adults was evaluated through Randomized Controlled Trials. We calculated Weighted Mean Differences with 95% Confidence Intervals using a random effects model. In this study, 41 Randomized Controlled Trials articles and 2049 participants were included. Psyllium showed a significant decrease in Low-Density Lipoprotein Cholesterol and total Cholesterol, a nonsignificant reduction in Triglyceride, and an insignificantly increase in High-Density Lipoprotein Cholesterol; cholesterol: (Weighted Mean Differences: -9.05; 95% Confidence Intervals: -13.71, -4.40; p-value < 0.05), High-Density Lipoprotein Cholesterol: (Weighted Mean Differences: 0.57; 95% Confidence Intervals: -0.88, 2.04; p-value > 0.05), Triglyceride: (Weighted Mean Differences: -5.29; 95% Confidence Intervals: -12.14, 1.54; p-value > 0.05), and Low-Density Lipoprotein Cholesterol: (Weighted Mean Differences: -8.55; 95% Confidence Intervals: -12.92, -4.19; p < 0.001). Considerable heterogeneity was found for cholesterol: (I-squared index = 89.30%, p-value < 0.001), High-Density Lipoprotein Cholesterol: ( I-squared index = 77.96%, p-value < 0.001), Low-Density Lipoprotein Cholesterol: (I-squared index = 88.46%, p-value < 0.001); and Triglyceride: (I-squared index = 83.25%, p-value < 0.001) and duration and dosage of psyllium had a nonsignificant linear influence on lipid profiles.

Conclusion: Results showed that psyllium can significantly decrease Low-Density Lipoprotein Cholesterol and total cholesterol, can insignificantly decrease triglyceride, and can insignificantly increase High-Density Lipoprotein Cholesterol following psyllium consumption.

Registration: The study was approved by the Medical Ethics Committee of Isfahan University of Medical Sciences (IR.MUI.

Research: REC.1402.017, Grant number: 140206). This research was registered in the PROSPERO system (CRD42023402987).

Clinical trial number: Not applicable.

Background: The intestinal epithelial barrier plays an essential role in protecting the body while allowing selective nutrient absorption. Natural bioactive compounds that strengthen this barrier contribute to gut health. However, the effects of pinoresinol, a dietary lignan known for its various bioactivities, on intestinal barrier function and underlying molecular mechanisms remain to be elucidated.

Methods: Caco-2 monolayers were treated with pinoresinol, and barrier function was evaluated using fluorescein permeability and transepithelial electrical resistance (TEER) assays. The expression and localization of tight junction (TJ)-related proteins were analyzed by RT-PCR, western blotting, and immunofluorescence. The involvement of the CaMKKβ-AMPKα1 signaling pathway was also investigated.

Results: Pinoresinol improved barrier integrity by decreasing apparent permeability coefficient (P_app) and increasing TEER. It enhanced the expression and junctional localization of TJ-related proteins, including cingulin, occludin, and claudin-1. These effects were associated with activation of the CaMKKβ-AMPKα1 pathway, suggesting a mechanism through which pinoresinol reinforces the epithelial barrier function.

Conclusions: This study identifies pinoresinol as a dietary bioactive compound that strengthens the intestinal barrier via activation of the CaMKKβ-AMPKα1 signaling axis. These findings provide mechanistic insight into its potential use as a functional ingredient for maintaining gut integrity and promoting overall intestinal health.

Obesity is a multifaceted condition involving complex interactions between genetic and environmental factors. Published studies have reported several genetic loci affecting obesity. Diet, physical activity, and their interaction with genetic variants have been assessed for their role in obesity. However, the role of epigenetic modifications with respect to nutrition, mitochondrial function, and energy homeostasis have not been investigated in depth. This narrative review explores scientific literature and assesses the role of nutrition and epigenetics (Nutri-epigenetics) in energy homeostasis and mitochondrial function and their subsequent effects on obesity. It details how mitochondrial dysfunction, driven by epigenetic changes, contributes to energy imbalance and metabolic disturbances and provides a comprehensive understanding of the underlying mechanisms driving obesity through the lens of the mitochondria and their functions.

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.