Genes and Nutrition最新文献

{"title":"Epigenetic age acceleration mediates the association between pro-inflammatory and pro-oxidant diets and the progression and mortality of cardiovascular-kidney-metabolic syndrome.","authors":"Shuang Wu, Siqi Lyu, Zhenkun Yang, Tianshu Gu, Yimeng Wang, Juan Wang, Jun Zhu, Yanmin Yang, Yang Chen, Lihui Zheng","doi":"10.1186/s12263-026-00804-0","DOIUrl":"10.1186/s12263-026-00804-0","url":null,"abstract":"<p><strong>Background: </strong>The cardiovascular-kidney-metabolic (CKM) syndrome is a major public health challenge driven by intertwined cardiometabolic and renal dysfunction. Diet-related inflammation and oxidative stress may accelerate biological aging, as reflected by DNA methylation age acceleration, thereby contributing to CKM progression and mortality. However, these pathways have not been comprehensively examined.</p><p><strong>Methods: </strong>We analysed data from the National Health and Nutrition Examination Survey (NHANES) 1999-2002, including non-pregnant adults aged ≥ 20 years with complete dietary, epigenetic, and cardiometabolic data. Dietary inflammatory potential and antioxidant capacity were assessed using the Dietary Inflammatory Index (DII) and Dietary Oxidative Balance Score (DOBS), derived from 24-hour dietary recall data. DNA methylation age acceleration (DNAmAA) was quantified using multiple established epigenetic clocks. Cardiovascular-kidney-metabolic (CKM) syndrome was defined and staged according to contemporary criteria. Associations of dietary indices with DNAmAA, CKM stages, and all-cause and cause-specific mortality were examined using weighted regression and Cox proportional hazards models. Mediation analyses were performed to evaluate the role of DNAmAA in linking dietary patterns with CKM progression and mortality. All analyses accounted for the complex NHANES survey design and relevant confounders.</p><p><strong>Results: </strong>Participants with higher dietary inflammatory potential (higher DII) and lower antioxidant capacity (lower DOBS) exhibited less favourable sociodemographic and cardiometabolic profiles and more advanced CKM stages at baseline. Higher DII was consistently associated with accelerated epigenetic aging across multiple DNAmAA measures, whereas higher DOBS showed protective associations. Pro-inflammatory and pro-oxidative dietary patterns were associated with increased odds of advanced CKM stages and higher risks of all-cause and cardiovascular mortality, while anti-inflammatory and antioxidant dietary patterns were associated with lower risks. Mediation analyses demonstrated that GrimAge acceleration and DunedinPoAm partially mediated the associations of dietary indices with CKM progression and mortality, supporting a role for biological aging in linking diet-related inflammation and oxidative stress to adverse CKM outcomes.</p><p><strong>Conclusions: </strong>Dietary inflammatory and oxidative potential is associated with epigenetic aging, CKM progression, and mortality, partly mediated by GrimAge and DunedinPoAm. Improving dietary quality may represent a modifiable strategy to reduce CKM burden.</p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13321538/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147846349","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sodium butyrate suppresses endometrial cancer cell growth by inhibiting thymidylate synthase and reprogramming pyrimidine metabolism.","authors":"Nayeon Kim, Sooyeon Park, Changwon Yang","doi":"10.1186/s12263-026-00805-z","DOIUrl":"10.1186/s12263-026-00805-z","url":null,"abstract":"<p><p>Endometrial cancer (EC) is the most common gynecologic malignancy, yet effective therapies for advanced and recurrent disease remain limited. Sodium butyrate (NaB), a gut microbiota-derived short-chain fatty acid (SCFA) with known anticancer activity, remains poorly understood in EC. In this study, we investigated the anticancer effects of NaB in two EC cell lines, HEC1A and AN3CA. NaB dose-dependently inhibited cell viability, colony formation, and migration in both cell lines, with HEC1A cells exhibiting greater sensitivity. NaB differentially modulated epithelial-mesenchymal transition (EMT)-related markers between the two cell lines. NaB markedly induced apoptosis in HEC1A cells, whereas AN3CA cells showed resistance to apoptotic cell death, despite mitochondrial membrane depolarization occurring in both cell lines. Cell cycle analysis revealed subG1-accumulation in HEC1A cells and G1 phase arrest in AN3CA cells. Notably, NaB potently suppressed thymidylate synthase (TS) at both mRNA and protein levels in both cell lines, representing the first demonstration of TS suppression by NaB in EC. NaB also broadly reprogrammed pyrimidine metabolism by downregulating de novo synthesis enzymes while upregulating salvage pathway components. Taken together, these findings suggest that TS suppression and pyrimidine metabolic reprogramming are important components of the in vitro response of EC cells to NaB. These results provide mechanistic insight into the metabolic effects of NaB in EC and support further investigation of this pathway in pharmacologically relevant and locally applicable therapeutic contexts.</p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-05-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13281650/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147823462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tfcp2l1 participates in paternal vitamin D deficiency-induced fetal lung maldevelopment in mice.","authors":"Zhongen Huang, Xiaohui Gong, Mei Tian, Guoying Sun, Jian Li","doi":"10.1186/s12263-026-00803-1","DOIUrl":"10.1186/s12263-026-00803-1","url":null,"abstract":"<p><p>BACKGROUND: Fetal lung development is crucial for neonatal respiratory function, with insufficient maturation contributing to neonatal respiratory distress syndrome. While maternal vitamin D deficiency (VDD) has been linked to adverse offspring outcomes, the impact of paternal VDD on fetal lung programming remains largely unexplored. This study investigates the effects of paternal VDD on fetal lung development and maturation, aiming to provide a theoretical basis for paternal preconception nutritional intervention and highlight the importance of paternal health in offspring respiratory outcomes. METHODS: Male C57BL/6J mice were gavaged with diets containing vitamin D₃ (0 or 1000 IU kg⁻¹/d) for 90 days. Serum vitamin D concentrations were measured by liquid chromatography–tandem mass spectrometry (LC–MS/MS). Treated males were then mated with females to generate offspring. Mating outcomes were recorded to assess reproductive success. Fetal lungs were collected at embryonic days 15.5–17.5 for H&E staining, morphometric analysis. Interrogation of a publicly available single-cell RNA sequencing (scRNA-seq) dataset delineated cell-type-specific marker gene signatures and prioritized candidate transcription factors, whose expression patterns were subsequently validated in offspring under paternal VDD conditions by quantitative real-time PCR, Western blotting, and multiplexed fluorescence immunohistochemistry. RESULTS: In mice, paternal VDD did not significantly affect mating success or pregnancy establishment. However, paternal VDD led to fetal lung dysplasia, accompanied by reduced lung weight and distal alveolar expansion. Alveolar type I (AT1) and type II (AT2) markers were markedly downregulated, reflecting delayed distal epithelial maturation. Guided by analysis of a publicly available scRNA-seq dataset, Tfcp2l1 was prioritized as a candidate transcription factor. Subsequent experimental validation revealed its predominant localization to AT1 and AT2 cells, with downregulation associated with decreased AT2 proliferation, a concomitant reduction in AT1 abundance, and limited AT1 expansion. CONCLUSIONS: Paternal VDD is associated with altered fetal lung development, characterized by reduced lineage specification of distal alveolar epithelial cells (AT1 and AT2) and diminished alveolar sacculation. The transcription factor Tfcp2l1 may be involved in this process, with its downregulation under paternal VDD correlating with reduced AT2 cell proliferation and decreased AT2-to-AT1 differentiation, ultimately relating to insufficient pulmonary maturation. </p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-04-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13251262/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147789511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Piperine-primed rat mesenchymal stem cells' secretome promotes an anti-inflammatory phenotype in the J774.1 murine macrophage cell line.","authors":"Navid Jamali, Fatemeh Rezaei Kahmini, Nasser Gholijani, Esmaeil Hashemi Shiri, Gholamreza Daryabor","doi":"10.1186/s12263-026-00799-8","DOIUrl":"10.1186/s12263-026-00799-8","url":null,"abstract":"","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13334742/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147789542","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"African-enriched SLC39A10 (ZIP10) missense variants differentially affect cellular zinc homeostasis and associate with health-related traits.","authors":"Jee-Oo Song, Seebon Cho, Juyoung Kim, Kaixiong Ye, Moon-Suhn Ryu","doi":"10.1186/s12263-026-00801-3","DOIUrl":"10.1186/s12263-026-00801-3","url":null,"abstract":"<p><p>BACKGROUND: Zinc deficiency remains a major global health concern and disproportionately affects populations in regions such as sub-Saharan Africa. Although inadequate dietary intake is a primary determinant of zinc status, genetic variation in zinc transport pathways may contribute to interindividual and interpopulation differences in zinc utilization. The SLC39A10 gene encodes the zinc importer ZIP10, which is upregulated under zinc-restricted conditions to sustain cellular zinc acquisition. This study sought to identify functional SLC39A10 variants and evaluate their potential physiological relevance, with particular attention to alleles enriched in populations of African ancestry. METHODS AND RESULTS: Missense variants in SLC39A10 were identified through analysis of sequencing data from the Genome Aggregation Database. The three most frequent minor alleles were markedly enriched in populations of African ancestry. Among these, two histidine-replacing variants, H194Q and H609Y, located near conserved histidine-rich regions of ZIP10, exhibited reduced capacity to increase cytosolic labile zinc levels and metallothionein expression in HEK293T cells, consistent with hypomorphic effects on transporter activity. These functional differences were not attributable to altered transcript abundance, protein expression, or subcellular localization. In silico variant effect prediction and evolutionary conservation analyses further supported the functional relevance of these substitutions. Phenome-wide association analyses in a large African ancestry cohort revealed nominal associations of these variants with hematologic and renal traits, suggesting potential physiological consequences of altered zinc transport capacity. CONCLUSIONS: These findings identify SLC39A10 as a locus of nutrigenetic diversity and demonstrate ancestry-linked variation in cellular zinc handling. The characterization of African-enriched hypomorphic ZIP10 variants provides mechanistic insight into genetic influences on micronutrient homeostasis. Incorporating genetic variation in zinc transport pathways may improve precision nutrition strategies and inform public health approaches aimed at reducing population-specific vulnerability to zinc deficiency. </p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-04-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13214128/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147663545","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Toward standardized personalized nutrition: a methodological scoping review and meta-analysis of randomized controlled trials in adults with overweight and obesity.","authors":"Tran Quang Duc, Nguyen Di Khanh, Dang Dang Khoa, Vu Thi Quynh Chi, Ngo Thi Huyen","doi":"10.1186/s12263-026-00800-4","DOIUrl":"10.1186/s12263-026-00800-4","url":null,"abstract":"<p><p>BACKGROUND: Personalized nutrition (PN) interventions are increasingly used to address overweight and obesity, yet randomized controlled trials (RCTs) vary widely in how personalization is defined and delivered. This scoping review synthesized methodological characteristics of PN RCTs in adults with overweight or obesity and meta-analyzed PN effects on anthropometrics. MAIN TEXT: We searched PubMed, Scopus, Web of Science, and ClinicalTrials.gov through November 20, 2025. Data were extracted using a standardized template capturing intervention characteristics. A random-effects meta-analysis was conducted, Bayesian meta-regression was used to explore the effect of intervention duration, and certainty of evidence was evaluated using GRADE. Among the 17 included RCTs, none provided a definition of PN, and substantial methodological heterogeneity was evident. Personalization inputs differed markedly in both number and type, and delivery modes ranged from digital platforms and group sessions to meal-box provision and routine dietitian consultations. PN interventions typically used the same delivery format as their control groups but layered on individualized components, with some providing higher contact frequency. Comparator structures also varied, from standardized guideline-based diets to minimal or no dietary counseling. Personalized diets were produced through algorithmic models, dietitian-guided tailoring, or continuous glucose monitoring-guided participant selection. PN produced a small but significant reduction in body weight, while effects on body mass index (BMI) were non-significant. Longer intervention duration was credibly associated with greater reductions in body weight and BMI. No publication bias was detected, and certainty of evidence was low for body weight and very low for BMI. CONCLUSIONS: PN interventions show modest effects on body weight but not BMI, within a highly heterogeneous methodological landscape. This review identifies design features to guide more effective PN interventions. Advancing toward more standardized approaches will require clearer operational definitions of personalization, better-aligned comparator diets, and greater transparency in how personalized strategies are generated and delivered. </p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13154502/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147616963","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA methylation of antiseizure medication metabolism genes and pharmacokinetic changes in adult epilepsy patients treated with the modified Atkins diet.","authors":"Kristina Gervin, Magnhild Kverneland, Karl Otto Nakken, Knut Rudi, Per Ole Iversen, Cecilie Johannessen Landmark, Kaja Kristine Selmer","doi":"10.1186/s12263-026-00796-x","DOIUrl":"10.1186/s12263-026-00796-x","url":null,"abstract":"<p><p>BACKGROUND: The modified Atkins diet is increasingly used as an adjunctive therapy for drug-resistant epilepsy. Recent evidence suggests that such dietary interventions may affect the pharmacokinetics of antiseizure medications and induce DNA methylation changes. However, it remains unclear whether epigenetic regulation of drug-metabolizing enzymes contributes to variability in medication serum levels. RESULTS: We analyzed 58 adults with drug-resistant epilepsy treated with a modified Atkins diet for 12 weeks. DNA methylation was profiled in peripheral blood before diet initiation (baseline) and after 4 weeks and 12 weeks using a genome-wide array. A total of 131 cytosine-phosphate-guanine (CpG) sites mapped to 13 candidate genes involved in antiseizure medication metabolism were assessed. One CpG in the CES1 gene showed significant methylation changes from baseline to 4 weeks, 12 weeks, and across all timepoints (FDR = 0.0018), indicating consistent longitudinal effects. Repeated measures correlation analyses were used to evaluate within-individual associations between DNA methylation and antiseizure medication serum concentrations. Two CpG–drug associations showed strong positive intra-individual correlations: CYP3A5 methylation was significantly associated with carbamazepine serum levels (repeated measures correlation coefficient = 0.81, FDR = 0.023), whereas CYP3A4 methylation showed a similarly strong but borderline association with topiramate (correlation coefficient = 0.76, FDR = 0.051). CONCLUSIONS: This study finds that a modified Atkins diet may be associated with DNA methylation variation at genes involved in drug metabolism. Furthermore, DNA methylation levels were strongly associated with individual serum concentrations of certain antiseizure medications. These findings are consistent with the concept of a diet–epigenome–drug metabolism axis and warrant further investigation in larger studies to assess clinical implications for personalized dietary and pharmacological management in epilepsy. </p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-03-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13101220/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147460927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Short-term caloric restriction partially reprograms immune and microbial networks during acute DSS-induced colitis.","authors":"Drake T D Hechter, Ilya Kisselev, Ian J McNicol, Sara V Good","doi":"10.1186/s12263-026-00798-9","DOIUrl":"10.1186/s12263-026-00798-9","url":null,"abstract":"<p><p>BACKGROUND AND AIMS: The effects of caloric restriction (CR) during active colitis remain incompletely understood. We examined whether short-term CR, initiated during dextran sodium sulfate (DSS)-induced inflammation, modulates disease severity, host transcriptional responses, and gut microbiota composition. Cross-species transcriptomic analyses were used to contextualize these effects within established human ulcerative colitis (UC) signatures. METHODS: Male C57BL/6 mice were assigned to control, CR, DSS, or DSS with concurrent CR (DSS.CR) groups. Clinical disease activity, histopathology, hematology, anxiety-like behavior, colon and spleen transcriptomes (RNA-seq), and fecal microbiota (16S rRNA) were assessed. Public UC microarray datasets were used to compare DSS and DSS.CR transcriptional profiles with human active and inactive UC. RESULTS: Compared with DSS, DSS.CR mice showed modest but consistent improvements in stool consistency and bleeding, with limited effects on overall histopathological scores, and reduced splenic enlargement and disruption. Transcriptomic analysis revealed limited differential gene expression between DSS and DSS.CR, but gene set enrichment analysis indicated reduced activation of inflammatory pathways (e.g., NF-κB, IL-17, cytokine–cytokine receptor) and relative enhancement of epithelial renewal and proteostasis programs. CR also partially mitigated DSS-associated dysbiosis, modestly preserving microbial diversity and functional pathways linked to carbohydrate metabolism and detoxification. Human microarray meta-analyses confirmed that DSS recapitulates active UC signatures, while CR shifted these toward a remission-like profile. CONCLUSIONS: Short-term CR during acute DSS-induced colitis partially attenuated mucosal and systemic inflammation and modestly shifted transcriptional and microbial profiles toward epithelial repair and metabolic resilience. These findings highlight CR’s potential as a non-pharmacological adjunct for modulating intestinal inflammation and support further translational evaluation of feasible dietary restriction strategies in IBD. </p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-02-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13049729/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147319103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary glycemic index, glycemic load, carbohydrate quality index, and low-carbohydrate diet score and their association with sperm DNA damage in unexplained male infertility.","authors":"Maryam Mehrkia, Seyed Ali Keshavarz, Mehran Nouri, Ghazaleh Eslamian, Naser Amirjannati, Negin Amirjannati","doi":"10.1186/s12263-026-00795-y","DOIUrl":"10.1186/s12263-026-00795-y","url":null,"abstract":"<p><strong>Background: </strong>Oxidative stress is a key driver of sperm DNA fragmentation (SDF), a molecular defect increasingly identified in men with idiopathic infertility, even when standard semen parameters appear normal. Dietary carbohydrate quality and glycemic properties may modulate oxidative stress, but their relationship with sperm DNA integrity remains underexplored. To examine the association between dietary glycemic index (GI), glycemic load (GL), carbohydrate quality index (CQI), and low-carbohydrate diet score (LCDS) with the odds of elevated sperm DNA fragmentation index (DFI) in men with unexplained infertility.</p><p><strong>Methods: </strong>In this case-control study, 300 Iranian men aged 18-50 years (150 with DFI > 30% and 150 with DFI < 20%) were recruited from a fertility clinic. Dietary intake was assessed using a validated 168-item food frequency questionnaire. GI, GL, CQI, and LCDS were calculated. Logistic regression models adjusted for age, BMI, physical activity, energy intake, fat intake, income, smoking, and infertility history were used to assess associations.</p><p><strong>Results: </strong>Men with higher CQI and LCDS had significantly lower odds of high sperm DNA fragmentation. Specifically, higher tertiles of CQI (Adjusted OR for highest vs. lowest tertile: 0.42; 95% CI: 0.20-0.89; P = 0.023) and LCDS (Adjusted OR: 0.19; 95% CI: 0.10-0.39; P < 0.001) were inversely associated with DFI. No significant associations were observed for GI and GL after multivariable adjustments.</p><p><strong>Conclusions: </strong>Higher dietary carbohydrate quality and adherence to a lower carbohydrate dietary pattern showed an inverse association with sperm DNA damage in men with unexplained infertility. These findings suggest a potential link between carbohydrate-related dietary patterns and sperm genomic integrity, but causal relationships cannot be inferred from this observational study.</p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-02-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12997687/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146183476","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The effect of walnut consumption on the peripheral blood mononuclear cell transcriptome.","authors":"Alan Kuo, Shan Kurkcu, John W Birk, Haleh Vaziri, Nuoxi Fan, Daniel W Rosenberg, Charles Giardina","doi":"10.1186/s12263-026-00793-0","DOIUrl":"10.1186/s12263-026-00793-0","url":null,"abstract":"<p><p>Gene expression in peripheral blood mononuclear cells (PBMCs) isolated from subjects before and after a 3-week walnut supplementation was examined for differentially expressed genes by RNA-seq. Significant gene expression changes were observed following walnut consumption with gene enrichment analysis showing significant overlap with genes previously associated with a robust memory B cell response following vaccination. An in-depth clustering analysis of the data revealed that a relatively large subpopulation of the subjects (11/19) showed a stronger and more uniform response to walnut consumption. This group of individuals showed an even more extensive overlap with genes associated with memory B cell production, with a significant overlap also observed for genes activated by an influenza vaccine adjuvant. The genes altered by walnut included numerous kinases and transcription factors, yet a deconvolution analysis did not reveal changes in the major PBMC cell types. Our findings show that a walnut supplementation can change gene expression in PBMCs in a manner consistent with a more responsive adaptive immune response without affecting the cellular composition of the blood.</p>","PeriodicalId":55123,"journal":{"name":"Genes and Nutrition","volume":" ","pages":""},"PeriodicalIF":2.8,"publicationDate":"2026-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12977753/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146137998","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}