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        <title>Frontiers in Nutrition | Nutrigenomics section | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/nutrition/sections/nutrigenomics</link>
        <description>RSS Feed for Nutrigenomics section in the Frontiers in Nutrition journal | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-05-15T08:14:19.522+00:00</pubDate>
        <ttl>60</ttl>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2026.1823817</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2026.1823817</link>
        <title><![CDATA[Editorial: Nutritional epigenetics and cancer prevention: mechanisms and biomarkers]]></title>
        <pubdate>2026-04-20T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Ferenc Budán</author><author>Duygu Ağagündüz</author><author>Zoltán Gyöngyi</author><author>Bence Raposa</author><author>Dávid Szép</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2026.1790304</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2026.1790304</link>
        <title><![CDATA[The role of microRNAs in cardiovascular disease associated with the consumption of ultra-processed foods: a comprehensive review]]></title>
        <pubdate>2026-04-20T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Shengzhou Wen</author><author>Dushyantha T. Jayaweera</author><author>George R. Marzouka</author><author>Chunming Dong</author>
        <description><![CDATA[Ultra-processed foods (UPFs) now dominate dietary intake in many countries and are consistently associated with higher risks of cardiovascular disease (CVD), including myocardial infarction, stroke, and heart failure. Beyond excess sodium, sugar, and unhealthy fats, UPFs may exert cardiovascular harm through food matrix disruption, processing-generated toxicants, additive exposure, and microbiome perturbation. These upstream insults converge on inflammatory, oxidative, and metabolic signaling pathways that regulate microRNAs (miRNAs), a class of small non-coding RNAs that orchestrate post-transcriptional gene expression across endothelial cells, vascular smooth muscle cells, macrophages, platelets, and metabolic tissues. In this review, we propose a unifying mechanistic framework in which UPF exposure reshapes both intracellular and extracellular vesicle (EV)-associated miRNA networks, thereby linking gut, liver, adipose tissue, and the vascular wall in a feed-forward cardiometabolic signaling loop. We synthesize evidence across epidemiology, experimental models, and human dietary intervention studies, while explicitly distinguishing established, emerging, and speculative mechanisms to avoid over-interpretation. We further discuss translational opportunities, including circulating miRNA/EV-miRNA biomarkers, nutritionally responsive miRNA signatures, and miRNA-targeted therapeutics. Together, this framework positions the UPF–miRNA/EV axis as a plausible molecular bridge between modern dietary exposure and atherosclerotic disease progression, and highlights priority areas for mechanistic validation and clinical translation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2026.1778794</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2026.1778794</link>
        <title><![CDATA[Decoding psychotropic-induced metabolic disturbances: gut-brain axis, multi-omics, and nutrition-lifestyle integration]]></title>
        <pubdate>2026-03-31T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Dhoha Dhieb</author><author>Kholoud Bastaki</author>
        <description><![CDATA[Psychotropic medications remain central to psychiatric treatment, yet their use is frequently accompanied by a substantial metabolic burden. Metabolic adverse effects, including weight gain, insulin resistance, dysglycemia, dyslipidemia, and hypertension, complicated clinical management and undermine long-term adherence. Although evidence-based monitoring and mitigation approaches exist, the molecular determinants of individual susceptibility and the drivers of interindividual variability in metabolic outcomes remain insufficiently defined. Emerging evidence identifies the gut-brain-metabolic axis as a key mechanistic interface, with psychotropic medications altering gut microbiota and associated metabolic pathways that contribute to metabolic complications. Multi-omics strategies are beginning to illuminate the complex molecular networks underlying these adverse effects; however, most findings still arise from isolated omics layers, limiting mechanistic resolution and translational utility. Integrative analytical frameworks, including artificial intelligence, now enable the synthesis of molecular, clinical, environmental, lifestyle, and dietary factors to support more precise and individualized intervention. In this narrative review, we synthesize current clinical and mechanistic advances in understanding psychotropic-induced metabolic dysfunction, with a focus on insulin resistance and the gut–brain–metabolic axis and highlight how multi-omics, environmental factors and computational strategies may advance future precision approaches in psychiatric care.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2026.1753616</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2026.1753616</link>
        <title><![CDATA[Integrative phytochemical profiling and in silico nutrigenomic predictions of Chinese tea–Saudi Mentha longifolia blend formulations]]></title>
        <pubdate>2026-03-27T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Thorya A. Fallatah</author><author>Hala M. Abdelmigid</author><author>Amal A. Alyamani</author><author>Maissa M. Morsi</author><author>Mohammed Ali</author><author>Jingmei Lu</author><author>Jian Zhao</author><author>Yasmin M. Heikal</author>
        <description><![CDATA[Medicinal plants represent valuable sources of bioactive compounds with therapeutic and economic potential. In Saudi Arabia, Mentha longifolia L. has long been used in traditional medicine, while China is renowned for its diverse teas derived from Camellia sinensis L. However, the tissue-specific genomic impact of their metabolites remains poorly understood. We tested three replicates of each blending ratio: 1:1, 1:2, and 2:1 (Tea:Mentha). Moreover, we investigated the putative expression profiles of 273 genes across human tissues using transcriptomic databases to explore the nutrigenomic effects of tea–Mentha blends. 1:2 (Tea:Mentha) Replicate 2 was dominated with 50.77% bioactive compounds, making it the strongest candidate overall. The highest Mentha aroma and bioactive compounds included eucalyptol (~17.3%), (+)-2-bornanone (~12.2%), n-hexadecanoic acid (~16.6%), and phytol (~3.2%). Lipid-derived molecules, including phytol, oleamide, and linolenic acids, showed the strongest transcriptional activation, particularly in endocrine and reproductive tissues, whereas alkaloids such as caffeine exhibited moderate effects. The preliminary integrative analysis combining experimental phytochemical profiling with computational nutrigenomic predictions is designed to generate testable hypotheses for future functional assays. Such blends may contribute to product diversification, standardization, and quality enhancement in the herbal tea industry.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2026.1778396</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2026.1778396</link>
        <title><![CDATA[From diet to brain repair: natural bioactive compounds in post-ischemic stroke recovery]]></title>
        <pubdate>2026-03-27T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Fan Bu</author><author>Zicheng Zhang</author><author>Shaohua Qi</author><author>Longsheng Xu</author>
        <description><![CDATA[Stroke represents the leading cause of disability and mortality worldwide, often resulting in long-term neurological deficits, extensive neuronal damage and inflammatory cascades. Ischemic stroke, which accounts for about 80% of stroke cases, is characterized by the sudden loss of blood circulation to an area of the brain, resulting in a corresponding loss of neurologic function. The blood supply interruption induced oxidative stress, mitochondrial dysfunction, neuroinflammation, and gut dysbiosis are involved in complex interactions within brain tissues. Moreover, the reperfusion induced inflammation produces more severe damage compared to the blood supply interruption. Current therapeutic interventions face critical limitations including narrow treatment windows, restricted patient eligibility, and significant adverse effects, underscoring the urgent need for safe, effective adjunctive strategies applicable during extended recovery periods. Recent research highlights the potential of nature biologically active substances, here we referred to food-derived and natural bioactive compounds, as promising therapeutic agents for post-stroke recovery. Administration of these compound by dietary route has the potential to support cellular repair processes via reducing oxidative stress, modulating neuroinflammation, promoting neurogenesis, inhibiting ferroptosis, and enhancing synaptic plasticity. This review examines the current evidence and emerging concepts on the roles of these bioactive compounds in post-stroke recovery and synthesizing mechanistic evidence. We discussed specific dietary sources and pharmacokinetics of selected compounds, providing insights into their bioavailability and potential synergistic effects with conventional therapies. Additionally, we examined clinical studies and evaluated the efficacy and safety of these interventions, offering a translational perspective on their integration into post-stroke rehabilitation. These findings underscore the therapeutic potential of dietary bioactive compounds as adjunctive treatments in post-stroke recovery and highlight the need for dose–response optimization, biomarker-guided precision nutrition approaches for patient stratification, and large-scale trials to validate long-term efficacy and safety in diverse stroke populations.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2026.1769818</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2026.1769818</link>
        <title><![CDATA[Association between apolipoprotein E gene polymorphisms and the effects of high-intensity interval training on body composition in university students]]></title>
        <pubdate>2026-03-26T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Hao-Nan Chu</author><author>Wen-Wen Chu</author><author>Shan-Rong Xu</author><author>Yan Liu</author><author>Shu-Chen Liu</author><author>Teng Yao</author><author>Duo-Qi Zhou</author>
        <description><![CDATA[ObjectiveThis study examined the effects of APOE gene polymorphisms on body composition changes following high-intensity interval training (HIIT) in non-athletic Han Chinese university students from plain regions and identified genetic loci associated with HIIT sensitivity.MethodsA total of 236 Han Chinese undergraduates from non-physical education majors completed a 12-week HIIT program (three sessions/week). Body composition was assessed before and after the intervention. Genomic DNA from white blood cells was genotyped using Illumina chips. Single nucleotide polymorphism (SNP) quality control and association analyses with body composition indices were performed using PLINK (v1.09) and SPSS 25.0, applying linear regression and ANOVA with least significant difference (LSD) post hoc tests (p < 0.05).Results(1) Of 22 initial APOE SNPs, five passed quality control; the rs405509 locus was associated with HIIT-induced changes in body composition. (2) The GG genotype at rs405509 was associated with higher baseline BMI overall and with higher baseline weight, BMI, and waist-to-hip ratio in females than the TT genotype. (3) After training, GG carriers showed greater reductions in overall body fat than GT/TT carriers (p < 0.05), and female GG carriers exhibited greater improvements in weight, body fat, and BMI. (4) In the Bonferroni post hoc analysis, compared with the TT group, the GG group showed significantly lower body weight (MD = −1.95, 95% CI: −3.374 to −0.533, p = 0.003), weight percentage (MD = −3.44, 95% CI: −6.070 to −0.819, p = 0.006), and BMI (MD = −0.70, 95% CI: −1.264 to −0.139, p = 0.009), while the difference in skeletal muscle percentage was not significant (p = 0.107). Compared with the GT group, the GG group also had significantly lower body weight, weight percentage, skeletal muscle percentage, and BMI (p = 0.02–0.03). No significant differences were observed between the GT and TT groups (all p > 0.05, with 95% CIs crossing zero). (5) The rs405509 locus was significantly associated with HIIT sensitivity for body fat (p = 0.01873).ConclusionThe rs405509 locus of the APOE gene is associated with body composition responses to HIIT, and female GG carriers show heightened responsiveness.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2026.1715659</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2026.1715659</link>
        <title><![CDATA[Adipose tissue protein profiling: modulation by vitamin D receptor]]></title>
        <pubdate>2026-03-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ding Ding</author><author>Chengmei Zhang</author><author>Tiantian Xia</author><author>Yu Chen</author><author>Yang Liu</author><author>Yan Lou</author><author>Juan Kong</author>
        <description><![CDATA[BackgroundLittle is known regarding the expression patterns of adipose tissue proteins in the context of vitamin D deficiency and whether these expression patterns have adverse effects on fat-related diseases.MethodsThis study compares vitamin D receptor-knockout (VDRKO) and wild-type (WT) mice to determine whether the VDRKO affects the adipose tissue landscape. High-throughput proteomic technology and parallel reaction monitoring-based targeted proteomics were utilized to determine and verify protein level changes.ResultsIntegrated proteomic and succinylomic analyses revealed that VDR deletion profoundly reprograms the adipose tissue molecular landscape. We identified 572 differentially expressed proteins and 313 differentially succinylated proteins. In VDRKO mice, protein levels involved in biological regulation, metabolic processes, ribosome, and endoplasmic reticulum protein processing pathways were upregulated. Conversely, proteins serving as negative regulators were enriched in pathways such as complement and coagulation cascades and protein digestion and absorption. Notably, ribosomal proteins (e.g., pancreatic alpha-amylase: Amy2 and proliferation-associated protein 2G4:Pa2g4) were significantly upregulated, while collagen proteins (e.g., Col24a1, Col6a4) were identified as key downregulated regulators in the protein digestion and absorption pathway. Succinylome analysis further indicated extensive succinylation modifications on proteins associated with energy metabolism pathways, including alanine, aspartate and glutamate metabolism, and arginine biosynthesis. These modifications were prominent not only in mitochondria but also in the cytoplasm, suggesting a broad regulatory role for succinylation beyond mitochondrial metabolism in the VDR-deficient state.ConclusionThis integrated multi-omics study provides the first comprehensive proteomic and succinylomic profile of VDRKO adipose tissue, revealing succinylation as a novel regulatory layer in energy metabolism. Our findings advance the understanding of vitamin D signaling in adipose biology and highlight potential therapeutic targets for metabolic disorders.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2026.1772849</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2026.1772849</link>
        <title><![CDATA[Genetic and epigenetic determinants of vitamin D metabolism: nutrigenomic insights for precision nutrition]]></title>
        <pubdate>2026-03-06T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Fatima Qahtan</author><author>Salma Abu-Qiyas</author><author>Dimitrios Papandreou</author>
        <description><![CDATA[Vitamin D plays a pivotal role in immune regulation, metabolic balance, skeletal health, and gene expression. Growing evidence indicates that genetic and epigenetic factors contribute to interindividual differences in vitamin D status and physiological responses. This review summarizes current findings on the nutrigenomic determinants of vitamin D metabolism, with emphasis on genetic polymorphisms in vitamin D receptor (VDR), GC, CYP2R1, CYP27B1, and CYP24A1, as well as epigenetic mechanisms that modulate vitamin D related gene expression. Peer-reviewed original studies and review articles published between 2010 and 2025 were examined to highlight associations between genetic variation in the vitamin D pathway and susceptibility to cancer, autoimmune disorders, metabolic diseases, cardiovascular conditions, and neurodegenerative outcomes. Advances in omics technologies and epigenetic biomarker research have improved understanding the molecular pathways through which vitamin D acts across multiple body systems. Evidence from gene–environment interactions and genotype-specific supplementation responses highlights the conceptual relevance of precision nutrition, while underscoring substantial gaps in clinical validation. Collectively, current research suggests that genetic information may inform future personalized vitamin D strategies, although translation into clinical practice remains limited by inconsistent evidence and methodological heterogeneity.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2026.1737860</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2026.1737860</link>
        <title><![CDATA[Dysregulated high-density lipoprotein and low-density lipoprotein subfractions increase metabolic dysfunction-associated steatotic liver disease risk: a study of patients across body mass index categories]]></title>
        <pubdate>2026-02-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Hao-Yun Yu</author><author>Jia-Qi Zhang</author><author>Pei-Qi Sun</author><author>Qing-Hua Li</author><author>Hong Lin</author><author>Jia-Yang Wang</author><author>Xiao-Jing Qian</author><author>Xiao-Di Yang</author><author>Cheng Hu</author><author>Ping Tian</author><author>Yuan-Ye Jiang</author><author>Guo-Qiang Lin</author>
        <description><![CDATA[BackgroundTo investigate biomarker differences among patients with metabolic dysfunction-associated steatotic liver disease (MASLD) across body mass index (BMI) types, we analyzed clinical data from 2,013 subjects and serum samples from 402 patients. The clinical characteristics and lipoprotein subclass profiles were evaluated.MethodsParticipants were grouped based on BMI into overweight MASLD (113 participants), overweight controls (107 participants), lean MASLD (83 participants), and lean controls (99 participants). Serum samples from each group underwent nuclear magnetic resonance-based metabolomic analyses, and clinical and omics data were compared between the lean and overweight MASLD groups and paired control cohorts.ResultsOur study demonstrated distinct omics characteristics for lean MASLD compared with their overweight equivalents. Metabolomic analysis of the serum from the four groups identified six lipoprotein subclasses with significant diagnostic accuracy (area under the curve (AUC) > 0.7), unique to lean individuals with MASLD. In contrast, overweight patients with MASLD had 13 unique lipoprotein subclasses that exhibited a high diagnostic value. These lipoproteins correlate with clinical parameters, such as uric acid, urea, creatinine, eosinophils, blood glucose, and alanine aminotransferase.ConclusionLean and overweight patients with MASLD display unique lipoprotein omics characteristics in an Asian population, primarily involving high-density lipoprotein (HDL) and low-density lipoprotein (LDL) subcomponents, suggesting their potential as effective biomarkers.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2026.1749622</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2026.1749622</link>
        <title><![CDATA[Polyphenol-rich Chinese olive extracts attenuate lipid accumulation in HepG2 cells, accompanied by AMPK phosphorylation and miRNA alterations]]></title>
        <pubdate>2026-02-11T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Hong Wang</author><author>Bingqi Huang</author><author>Wenhong Zhao</author><author>Gongliang Liu</author><author>Weidong Bai</author>
        <description><![CDATA[IntroductionChinese olive (Canarium album L.) is a rich source of phenolic compounds and has been suggested to exhibit distinct lipid-lowering bioactivities from those reported for Mediterranean olive polyphenols.MethodsThis study investigated the effects of polyphenol-rich Chinese olive extracts on sodium oleate-induced lipid accumulation in HepG2 cells.ResultsTreatment with extracts was associated with a significant reduction in intracellular total lipid and triglyceride levels in a concentration-dependent manner. RT-qPCR results revealed that extract treatment was accompanied by the downregulation of lipogenesis-related genes (SREBP-1c, ACC1, FASN, and DGAT2) and the upregulation of β-oxidation-associated genes (PGC-1α, PPARα, CPT-1A, and ACOX1). Western blot analysis showed that extract treatment was associated with AMPK phosphorylation, occurring concurrently with the observed lipid-associated changes. Furthermore, treatment with extracts was accompanied by decreased expression of miR-122 and miR-21, which correlated with the expression of their respective lipid-metabolism target genes. UPLC–MS/MS analysis identified 39 phenolic compounds in the extract, including methyl brevifolincarboxylate and ellagic acid derivatives, indicating a complex phenolic composition.DiscussionThese results demonstrate that attenuation of lipid accumulation by polyphenol-rich Chinese olive extracts in HepG2 cells is accompanied by AMPK phosphorylation and miRNA modulation. This finding supports the potential of Chinese olive extracts as a natural hepatoprotective ingredient for the development of functional foods and nutraceuticals.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2026.1750030</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2026.1750030</link>
        <title><![CDATA[Epigenetic and microbiome responses to greens supplementation in obese older adults: results from a randomized crossover-controlled trial]]></title>
        <pubdate>2026-02-04T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Laura A. Robinson</author><author>Aidan M. Cavanah</author><author>Sarah Lennon</author><author>Madison L. Mattingly</author><author>William Van Der Pol</author><author>Kevin W. Huggins</author><author>Michael W. Greene</author><author>Michael D. Roberts</author><author>Andrew D. Frugé</author>
        <description><![CDATA[Aging is influenced by genetic, environmental, and lifestyle factors. Preliminary studies suggest that fruit and vegetable-based dietary supplements may reduce inflammation and oxidative stress, key factors in aging. Greens-based supplements typically contain concentrated extracts of leafy greens, fruits, vegetables, and bioactive phytochemicals, providing micronutrients and polyphenols that may influence aging-related pathways. This exploratory study evaluated the effects of a 30-day greens-based supplement on epigenetic markers of aging and metabolic health in adults aged 50–65 years with body mass index (BMI) >30 kg/m2, using a 60-day randomized crossover design. Participants were randomized to immediate or delayed supplementation. During the 30-day intervention period, participants consumed a daily greens supplement. Primary outcomes included peripheral blood mononuclear cell DNA methylation and epigenetic age (Horvath, PCGrimAge, AdaptAge, and DamAge). Secondary measures included clinical metabolic biomarkers, microbiome diversity, breath hydrogen and methane, body composition, actigraphy, dietary intake, and quality of life questionnaires [RAND 12 item short form questionnaire (SF-12), and 21-item Depression, Anxiety, and Stress Scale (DASS-21)]. Twenty-one participants began the protocol (65% female, mean age 58.4 ± 5.3 years, mean BMI 38.1 ± 8 kg/m2). Nineteen participants completed the study. Horvath clock data indicated that biological age paradoxically increased during the supplementation period, whereas newer-generation clocks (AdaptAge, DamAge) demonstrated trends toward improved outcomes. Gut microbiome alpha diversity remained stable; taxa of interest, including Bilophila (p = 0.037) and Desulfobacterota (p = 0.031) changed with supplementation. Body composition, metabolic biomarkers, dietary intake, breath gases, sleep, and psychosocial measures were unchanged during the study. Exploratory pre-to-post supplementation change score correlations found no significant associations between epigenetic clocks and secondary outcomes, except for an inverse relationship between Faith's phylogenetic diversity and fasting blood glucose (rs = −0.81, p < 0.001). In summary, 30 days of greens-based supplementation led to selective changes in epigenetic aging markers and individual gut microbial taxa, without significant effects on overall microbiome diversity, metabolic health markers, or body composition. Additionally, exploratory correlations suggest potential links between changes in microbial diversity and glycemic control following greens supplementation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2026.1730639</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2026.1730639</link>
        <title><![CDATA[Methionine restriction in cancer: a dietary insight for therapy]]></title>
        <pubdate>2026-02-03T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Xing Tian</author><author>Gengjun Zhu</author><author>Yuhua Zhang</author><author>Ning Liu</author>
        <description><![CDATA[BackgroundMethionine, one of the essential amino acids that needs to be obtained through protein-rich diet, provides important sulfur elements for the human body, which is crucial for protein synthesis, antioxidant and metabolic regulation. Many tumors develop a metabolic dependency due to the lack of a working methionine salvage pathway, which can be targeted by methionine restriction (MR).ResultsThe core mechanism of MR lies in disrupting one-carbon metabolism and epigenetic regulation that rely on methionine, depleting the crucial metabolite S-adenosylmethionine (SAM), thereby inhibiting histone/DNA methylation, disrupting redox homeostasis, and ultimately inducing cell cycle arrest and apoptosis. Substantial evidence indicates that MR, achieved by specific metabolic enzyme inhibitors or diet with special formulations, can intervene in tumor progression from a metabolic standpoint. Additionally, combining methionine restriction with existing treatments can achieve satisfactory outcomes in the clinical management of various tumors.ConclusionThis article provides insights into the research and its translational potential of methionine restriction as a promising strategy for cancer treatment, with the emphasis on the contributions that advance the field and better serve the clinical research community.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2026.1710841</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2026.1710841</link>
        <title><![CDATA[Integrating transcriptome and proteome profiles to compare carcass and meat quality traits between Songliao and Songlei black pigs]]></title>
        <pubdate>2026-01-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yunpeng Zhang</author><author>Qi Zhang</author><author>Suthar Teerath Kumar</author><author>Jing Xu</author><author>Yupeng Xie</author><author>Zhihao Wang</author><author>Wu-Sheng Sun</author><author>Li Pan</author><author>Yuan Zhao</author><author>Shu-Min Zhang</author>
        <description><![CDATA[With the ongoing upgrade in consumption patterns, the pork market is shifting from a focus on quantity to an emphasis on quality, demanding higher intramuscular fat content alongside maintained growth rates. Crossbreeding between the Chinese lean-type Songliao black pig and the high-quality local breed Leixiang pig allows rapid integration of parental superior traits, resulting in hybrid vigor that effectively improves pork quality, growth performance, and economic benefits. We conducted transcriptomic and 4D microDIA proteomic sequencing analyses on the longissimus dorsi muscle tissue from hybrid offspring of purebred Songliao black pigs and Songliao × Leixiang black pigs. Extensive phenotypic analyses were performed on Songliao black pigs and Songlei black pigs using multiple trait indicators. Six pigs were selected and categorized into relatively high and low intramuscular fat groups. Integrated analysis of transcriptomic and proteomic data identified candidate genes within significantly annotated lipid-related pathways via KEGG, including ACSL1, ACSL6, SREBF1, PLIN2, CEPT1, CPT1B, CPT1C, and ACSF3. Among these, CPT1B was significantly associated with fatty acid metabolism pathways. By analyzing all significantly differential genes and proteins, six candidate genes were identified as key determinants of genetic variation in lipid deposition: UCP3, CPT1B, LSMEM1, NEXN, PPP1R14C, and LOC100624149. This preliminary exploratory multi-omics study provides a valuable resource for probing intramuscular fat deposition, aiming to support pork-trait improvement in breeding and to establish a fresh theoretical basis for clarifying the molecular mechanisms of meat-quality heterosis in Songlei black pigs.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2025.1756703</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2025.1756703</link>
        <title><![CDATA[Pharmacological effects and mechanisms of medicine food homology species and active ingredients in ameliorating ovarian aging]]></title>
        <pubdate>2026-01-21T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Jiayi Chen</author><author>Xiaotian Li</author><author>Xinle Lai</author><author>Ruoyi Xu</author><author>Zheqi Liu</author><author>Jia Xing</author><author>Liuqing Yang</author><author>Qin Zhang</author>
        <description><![CDATA[Ovarian aging is the process of decline in ovarian reserve, endocrine function with age, leading to reduced fertility and increased risk of various related diseases. In recent years, medicine food homology (MFH) species have attracted much attention for their potential to delay ovarian aging due to their dietary and medicinal values. In this review, we have focused on the intervention of MFH species and active ingredients on ovarian aging, with an emphasis on the molecular mechanisms involved in antioxidant, anti-inflammatory, apoptosis inhibitory, balance of autophagy, maintenance of genome stability, mitochondrial function protective and estrogen-like effects through multiple signaling pathways (e.g., PI3K/Akt, Nrf2/HO-1, SIRT1/mTOR, Nrf2/ARE, etc.). Possessing the characteristics of multi-pathway and multi-target effects, MFH species and active ingredients provide new ideas for the research and development of health food and functional preparations. High-quality clinical studies are still needed for verification.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2025.1755919</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2025.1755919</link>
        <title><![CDATA[Editorial: Genome-based nutrition strategies for preventing diet-related chronic diseases: where genes, diet, and food culture meet, volume II]]></title>
        <pubdate>2026-01-19T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Sonia Roman</author><author>Claudia Ojeda-Granados</author><author>Arturo Panduro</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2025.1710613</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2025.1710613</link>
        <title><![CDATA[MTHFR 677C/T gene polymorphism and dietary habits: effects on trace element levels, amino acids, and biochemical parameters]]></title>
        <pubdate>2026-01-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Tatjana Orct</author><author>Jelena Kovačić</author><author>Ines Peremin</author><author>Zorana Kljaković-Gašpić</author><author>Daria Pašalić</author><author>Ankica Sekovanić</author><author>Adrijana Dorotić</author><author>Blanka Tariba Lovaković</author><author>Andreja Jurič</author><author>Alica Pizent</author><author>Fran Crnjac</author><author>Lora Dukić</author><author>Marko Gerić</author><author>Ivone Jakaša</author><author>Goran Gajski</author>
        <description><![CDATA[BackgroundPrevious research has identified that, in individuals with lower folate and/or vitamin B12 levels, homocysteine is associated with specific elements, while amino acids are associated with folate, thereby influencing folate availability during supplementation. This study investigates the impact of the MTHFR 677C/T polymorphism on levels of these compounds in individuals with differing meat consumption preferences, non-vegetarians and vegetarians.MethodsThe study was conducted on 162 Croatian subjects. MTHFR gene polymorphism was determined by PCR-RFLP, elements by ICP-QQQ, amino acids by GC–MS, and biochemical parameters by chemiluminescent immunoassay and enzymatic methods. Differences between the groups were tested by ANOVA, while associations between the parameters were examined by multiple regression analyses.ResultsThe CT + TT genotype had lower folate levels in comparison to the CC genotype. The influence of MTHFR 677C/T polymorphism on element levels was limited to Al and Ca: individuals with the CT + TT genotype exhibited higher plasma Ca levels than the wild-type (CC) genotype, while lower plasma Al values were observed only in vegetarians with the CT + TT genotype. The CT + TT genotype was also associated with higher levels of glutamic acid, proline, glycine (only in vegetarians), and aspartic acid.ConclusionAlthough we observed an effect of the MTHFR 677C/T polymorphism on folate, certain elements and amino acid levels, further research is required to validate our findings and establish a more comprehensive understanding of the link between elements, amino acids and the MTHFR gene polymorphism.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2025.1729915</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2025.1729915</link>
        <title><![CDATA[Correlation of supplement folic acid based on MTHFR and MTRR gene polymorphisms with preeclampsia in Chinese population: an retrospective cohort study]]></title>
        <pubdate>2025-12-15T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Xuanjun Xiong</author><author>Lin Xiao</author><author>Xiaoqin Xin</author><author>Jungao Huang</author>
        <description><![CDATA[Background and objectivesThe relationship between folic acid supplementation and preeclampsia remains a topic of ongoing debate. We aimed to investigate the correlation between folic acid and preeclampsia from a genetic perspective.MethodsThis retrospective cohort included 377 Chinese participants. We evaluated the risks of eclampsia, including placental growth factor (PIGF) indicators, and the genotypes of folate metabolism markers (MTHFR C677T, MTHFR A1298C, and MTRR A66G). Based on these polymorphisms, participants were categorized into high-risk and relatively low-risk groups, with the high-risk group receiving folic acid supplementation. Multivariate linear and logistic regressions were utilized to calculate the β-coefficients, odds ratios (ORs), and 95% confidence intervals (CIs).ResultsPlGF levels were negatively associated with preeclampsia, with each one-unit increase in PlGF corresponding to a 15% reduction in preeclampsia risk (OR = 0.85, 95% CI: 0.8–0.9), a finding that remained stable across various models. Interestingly, a significant difference was found in PIGF levels between the high-risk group for folic acid and the low-risk group (p = 0.01). Moreover, there was a significantly positive correlation (β = 11.11, 95% CI: 1.68–20.53) and the association persisted across different models, which indicated the high-risk group showed an increase in PIGF concentration when supplementing with folic acid.ConclusionTo our knowledge, limited studies have examined this association at the genetic level in the Chinese population. Our findings suggest that folic acid may mitigate the risk of preeclampsia through its effects on PIGF levels. Potentially, folic acid supplementation could serve as a preventative strategy against preeclampsia.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2025.1669528</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2025.1669528</link>
        <title><![CDATA[Ethnomedicinal validation of Telfairia occidentalis L. leaf: a dual experimental and computational approach to uterine leiomyoma therapy]]></title>
        <pubdate>2025-12-12T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Akingbolabo Daniel Ogunlakin</author><author>Gideon Ampoma Gyebi</author><author>Amel Elbasyouni</author><author>Oyindamola Esther Awosola</author><author>Moyosoluwa Mary Dada</author><author>Opeyemi Josphine Akinmurele</author><author>Abdullahi Adeyemi Adegoke</author><author>Israel Kunle Oladoja</author><author>Ajibola David Adelakun</author><author>Omolola Oluwadara</author><author>Gabriel Olalekan Banwo</author><author>Adedayo Johnson Adediran</author><author>Seun Elizabeth Kuyoro</author><author>Adewale Victor Aderemi</author><author>Oluyomi Stephen Adeyemi</author>
        <description><![CDATA[IntroductionA nutrient-dense vegetable with Ethnomedicinal use for treating oxidative and fibrotic diseases is Telfairia occidentalis L., often known as “ugu” in Nigeria. Although it has been used extensively in the past, neither experimental nor computational methods have been used to characterize its antifibrotic potential. This study investigates the antioxidant, enzyme-inhibitory, and antifibrotic effects of aqueous T. occidentalis leaf extract in albino rats with MSG-induced uterine leiomyomas, employing in silico modeling to understand the underlying molecular mechanisms.MethodsIron chelation, NO scavenging, and DPPH radical scavenging properties of T. occidentalis aqueous extract were evaluated, using quercetin serving as the standard. The inhibitory effects of the extract on α-amylase, α-glucosidase, monoamine oxidase (MAO), and acetylcholinesterase (AChE) were evaluated. Testosterone, FSH, LH, and oestradiol levels were measured in MSG-induced fibroid rats treated with T. occidentalis aqueous extract. The tissues of the uterus and ovaries of treated rats were examined histologically. Furthermore, the HPLC-identified compounds in the extract were docked against STEAP4.Results and discussionThe extract demonstrated modest antioxidant activity; however, it was less effective than quercetin at scavenging NO radicals, DPPH, and iron-chelating capacity. It demonstrated AChE and MAO inhibition that was dose-dependent, with an IC50 for MAO inhibition of 0.178 ± 0.003 μg/mL that was comparable to donepezil (0.155 ± 0.005 μg/mL). α-Amylase activity increased in a dose-dependent manner, whereas α-glucosidase inhibition remained lower than the control. Testosterone and oestradiol levels in T. occidentalis-treated fibrotic rats significantly decreased, suggesting that MSG-induced hormonal abnormalities were corrected. Despite some epithelial deterioration, histopathological results showed partial recovery of uterine integrity and restoration of ovarian architecture with growing follicles. These results may suggest that the leaf extract of T. occidentalis exhibits antifibrotic and Hormone-modulating properties. HPLC identified beta-carotene and lutein affinity for STEAP4 was discovered by computational methods, suggesting a synergistic process. Through a combination of hormone-regulating, enzyme-inhibitory, and antioxidant properties, T. occidentalis shows encouraging antifibrotic efficacy. These results support its traditional application and demonstrate its applicability in the development of phytotherapeutics for the treatment of uterine leiomyomas.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2025.1710267</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2025.1710267</link>
        <title><![CDATA[Identification of the role of sugar-sweetened beverages in the progression of a murine metabolic dysfunction-associated steatotic liver disease model]]></title>
        <pubdate>2025-12-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Yong-Qiang Li</author><author>Chen Huang</author><author>Jiawei Chen</author><author>Siqi Yang</author><author>Jiemin Cheng</author><author>Huiting Chen</author><author>Yongjian Zhou</author>
        <description><![CDATA[BackgroundRising metabolic dysfunction-associated steatotic liver disease (MASLD) prevalence parallels increased sugar-sweetened beverage (SSB) consumption. Clinical studies suggest differential metabolic effects of fructose, glucose, and sucrose, yet their distinct roles in MASLD pathogenesis remain uncharacterized in preclinical models. This study aimed to establish a murine model to dissect the specific contributions of fructose, glucose, and sucrose to MASLD progression.MethodsThis study establishes a murine model to dissect SSB-specific contributions to MASLD progression. Eight-week-old male C57BL/6N mice were fed a high-fat high-cholesterol (HFHC) diet with/without fructose-, glucose-, or sucrose-sweetened beverages for 10 weeks. Hepatic transcriptomic profiles were analyzed via microarray, followed by functional enrichment. Protein-protein interaction (PPI) network and single-cell analysis identify pathway perturbations and hub genes.ResultsFructose-SB supplementation, unlike glucose or sucrose, exacerbated HFHC-induced MASLD phenotypes, including elevated body weight, hepatic steatosis, glucose intolerance, and hepatocellular injury. Transcriptomics identified 2,195 fructose-specific differentially expressed genes (DEGs: 1,978 upregulated, 224 downregulated). Upregulated DEGs were enriched in thyroid hormone signaling, lysosomal activity, and autophagy, while downregulated DEGs implicated oxidative phosphorylation suppression. PPI analysis revealed key hub genes (Akt1, Stat3, Ctnnb1, Ep300) and mitochondrial components (mt-Nd4, mt-Cytb, Uqcrq) as central regulators of fructose-driven pathology. Fructose-SB uniquely accelerates MASLD progression in HFHC-fed mice through transcriptional reprogramming of metabolic and mitochondrial pathways. In mice fed a high-fructose diet, expression of key hub genes was elevated, particularly in Kupffer and endothelial cells, which were also enriched in proportion. These findings highlight fructose-specific mechanisms in MASLD pathogenesis and identify potential therapeutic targets for SSB-associated metabolic disorders.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fnut.2025.1659730</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fnut.2025.1659730</link>
        <title><![CDATA[MiRNA-3Age: a microRNA-based biological age model and its modulation by lifestyle and nutrition]]></title>
        <pubdate>2025-11-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jana Schneider</author><author>Clara Preyer</author><author>Marie Steil</author><author>Maruan Biazid</author><author>Angelika Pointner</author><author>Alexander G. Haslberger</author><author>Berit Hippe</author>
        <description><![CDATA[IntroductionThe extension of human longevity has intensified the search for biomarkers that capture not only chronological age but also biological aging and functional healthspan. Among molecular candidates, microRNAs (miRNAs) have emerged as promising regulators and indicators of aging-related processes. In this pilot study, we explored whether selected circulating miRNAs could serve as potential biomarkers of biological age and lifestyle-associated aging dynamics.MethodsBased on current literature, we focused on three miRNAs—miR-24, miR-21, and miR-155—previously linked to inflammation, senescence, and metabolic regulation. Capillary blood samples from a heterogeneous adult cohort were analyzed using quantitative PCR. ΔCt values were integrated into a composite “miRNA-3Age” model through multivariate regression analysis to estimate biological age. Associations between lifestyle variables (diet, exercise, stress, and smoking) and miRNA-based biological age were examined.ResultsThe miRNA-3Age model predicted biological age with moderate correlation to chronological age and revealed variability consistent with individual health profiles. Participants with favorable lifestyle factors (e.g., frequent consumption of fish, whole grains, and green tea; regular exercise) tended to exhibit lower miRNA-3Age estimates, whereas stress and smoking were associated with higher predicted biological age.DiscussionOur exploratory data suggest that integrating multiple miRNA signals may enhance the sensitivity of biological age estimation compared to single-biomarker approaches. However, variability within the small sample highlights the need for larger, longitudinal datasets to confirm predictive validity and to disentangle causal links between lifestyle, miRNA expression, and aging biology.ConclusionThis pilot study supports the feasibility of miRNA-based biological age modeling and identifies miR-24, miR-21, and miR-155 as promising components of a composite biomarker framework. The miRNA-3Age model provides a preliminary step toward a scalable, lifestyle-sensitive aging metric that warrants validation in diverse populations.]]></description>
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