Journal of Nutritional Biochemistry最新文献

{"title":"Comparative study of lipophilicity, cell membrane permeability, and intracellular antioxidant capacity of resveratrol and pterostilbene","authors":"Tengteng Huang,&nbsp;Xiaoling Chen,&nbsp;Daiwen Chen,&nbsp;Bing Yu,&nbsp;Hui Yan,&nbsp;Ping Zheng,&nbsp;Junqiu Luo,&nbsp;Zhiqing Huang","doi":"10.1016/j.jnutbio.2025.110095","DOIUrl":"10.1016/j.jnutbio.2025.110095","url":null,"abstract":"<div><div>Pterostilbene (PTS), a methylated analog of resveratrol (RES), demonstrates superior bioavailability, potentially attributable to enhanced lipophilicity and cell membrane permeability compared to RES. However, this hypothesis lacked experimental validation. The objective of this study was to compare the lipophilicity, cell membrane permeability, and intracellular antioxidant capacity of RES and PTS. Lipophilicity was assessed via the shake-flask method, revealing higher lipophilicity for PTS than RES. Molecular dynamics simulations predicted stronger membrane permeability for PTS. Cellular uptake studies in IPEC-J2 cells and porcine myotubes using cyanine2-labeled RES (CY2-RES) and PTS (CY2-PTS) confirmed these predictions, with fluorescence microscopy and flow cytometry consistently demonstrating higher intracellular accumulation of CY2-PTS compared to CY2-RES. Furthermore, PTS exhibited stronger intracellular ROS-scavenging capacity than RES in IPEC-J2 cells and porcine myotubes. In conclusion, our study demonstrates that PTS exhibits superior lipophilicity, enhanced membrane permeability, and stronger intracellular antioxidant capacity compared to RES.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"147 ","pages":"Article 110095"},"PeriodicalIF":4.9,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015692","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plant sterol ester of α-linolenic acid protects against ferroptosis in metabolic dysfunction-associated fatty liver disease via activating the Nrf2 signaling pathway","authors":"Hao Han ,&nbsp;Liyuan Pei ,&nbsp;Yajing Dong ,&nbsp;Yanyang Han ,&nbsp;Shuqi Ji ,&nbsp;Xiaoman Wang ,&nbsp;Mingming Zheng","doi":"10.1016/j.jnutbio.2025.110098","DOIUrl":"10.1016/j.jnutbio.2025.110098","url":null,"abstract":"<div><div>Increasing evidence indicates that ferroptosis contributes to the occurrence and development of metabolic dysfunction-associated fatty liver disease (MAFLD). This study aimed to investigate the improvement effect of plant sterol ester of α-linolenic acid (PS-ALA) on ferroptosis in hepatocytes and further elucidate the underlying molecular mechanism, focusing on the regulation of Nrf2 signaling. We found that PS-ALA ameliorated liver iron overload and reduced ROS generation and lipid peroxides (MDA and 4-HNE) production both in mice fed a high-fat diet and HepG2 cells induced by oleic acid/erastin. In addition, our data revealed the ability of PS-ALA to protect against ferroptosis as evidenced by diminished PI staining positive cells, enhanced SLC7A11/GPX4 antioxidant system, and decreased protein expression of the key enzymes catalyzing lipid peroxidation (ACSL4, ALOX5ap, and PTGS2). Mechanistically, PS-ALA promoted the nuclear translocation of Nrf2 and enhanced the protein expression of HO-1 and NQO1. Silence of Nrf2 by siRNA markedly weakened the protected effect of PS-ALA on ferroptosis. Our findings indicate that inhibition of ferroptosis via activating the Nrf2 signal pathway is involved in the protective role of PS-ALA on MAFLD and highlight the potential of PS-ALA as a prevention and treatment strategy for MAFLD.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"147 ","pages":"Article 110098"},"PeriodicalIF":4.9,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015652","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The hidden impact of intrauterine growth restriction in the pathogenesis of metabolic syndrome: Functional and structural alterations in rat visceral adipose tissue","authors":"Hanna Coppola ,&nbsp;Khaled Al-Khalidi ,&nbsp;Sandrine Gremlich ,&nbsp;David Viertl ,&nbsp;Umberto Simeoni ,&nbsp;Jean-Baptiste Armengaud ,&nbsp;Catherine Yzydorczyk","doi":"10.1016/j.jnutbio.2025.110096","DOIUrl":"10.1016/j.jnutbio.2025.110096","url":null,"abstract":"<div><div>Individuals born after intrauterine growth restriction (IUGR) have a higher risk of developing metabolic syndrome (MetS) in adulthood. In a rat model, male IUGR offspring exhibit MetS features—including elevated systolic blood pressure, glucose intolerance, non-alcoholic fatty liver disease, and increased visceral adipose tissue (VAT)—by 6 months of age. Female offspring, however, do not. While higher VAT is associated with MetS, its role in IUGR-induced metabolic disorders remains unclear. The objective is to examine structural changes and mechanisms in VAT associated with metabolic disorders in IUGR rats. IUGR was induced <em>via</em> a maternal low-protein (9% casein) and compared to a control diet (23% casein). VAT was collected from 6-month-old offspring. Adipocyte hyperplasia and hypertrophy were analyzed using Ki-67 and hematoxylin/eosin (H/E) staining. Adipogenesis (PPAR-γ by Western blot; <em>ZFP423</em> by RT-qPCR), inflammation (<em>IL-6, TNF-α</em> by RT-qPCR), macrophage markers (<em>CD68, ITGAM, ITGAX</em> by RT-qPCR), oxidative stress (superoxide anion <em>via</em> hydroethidine; Cu/Zn SOD, catalase by Western blot), and senescence (lipofuscin via autofluorescence, crown-like structures by H/E, p16^INK4a, p21^WAF1, Sirtuin-1 by Western blot) were evaluated. IUGR males showed increased adipocyte proliferation, hypertrophy, and upregulated adipogenic markers (PPAR-γ, <em>ZFP423; P</em>&lt;.05, <em>P</em>&lt;.001). Inflammatory and macrophage markers were elevated (<em>P</em>&lt;.05), along with superoxide anion production, Cu/Zn SOD and catalase protein expression (<em>P</em>&lt;.05). Senescence indicators—including lipofuscin, crown-like structures, p16^INK4a, p21^WAF1, and Sirtuin-1 were also upregulated (all <em>P</em>&lt;.05). No significant changes were observed in females. VAT from male IUGR offspring exhibits increased adipogenesis, inflammation, oxidative stress, and premature senescence, suggesting a mechanistic link to their higher MetS susceptibility.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"147 ","pages":"Article 110096"},"PeriodicalIF":4.9,"publicationDate":"2025-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145015688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antioxidant potential of alpha-lipoic acid in mitigating progression of experimental periodontitis","authors":"Priscila Ayumi Kubota ,&nbsp;Deiweson Souza-Monteiro ,&nbsp;Zuleni Alexandre da Silva ,&nbsp;Deborah Ribeiro Frazão ,&nbsp;Vinicius Ruan Neves dos Santos ,&nbsp;Paulo Fernando Santos Mendes ,&nbsp;Jorddy Neves Cruz ,&nbsp;Cassiano Kuchenbecker Rösing ,&nbsp;Fabrício Mezzomo Collares ,&nbsp;Renata Duarte Souza-Rodrigues ,&nbsp;Rafael Rodrigues Lima","doi":"10.1016/j.jnutbio.2025.110087","DOIUrl":"10.1016/j.jnutbio.2025.110087","url":null,"abstract":"<div><div>This study aimed to evaluate the effects of alpha-lipoic acid supplementation, a well-known antioxidant with therapeutic potential, on the progression of experimental periodontitis in rats. Eighteen male Wistar rats were randomly assigned to three groups (<em>n</em>=6 per group): control, periodontitis, and periodontitis treated with alpha-lipoic acid. Periodontitis was induced by placing bandages around the lower first molars for 14 days. During this same period, the treated group received alpha-lipoic acid by gavage at a dose of 100 mg/kg/day and the control and periodontitis groups received distilled water. Biochemical analyses showed a significant increase in reduced glutathione levels in the supplemented group compared to the periodontitis group, although no significant changes were observed in Trolox-equivalent antioxidant capacity. Micro-Computed Tomography analysis revealed preservation of trabecular number and their thickness, along with an increase in tissue volume in the supplemented animals. Histological evaluation showed less alveolar bone damage and a larger collagen area in the group that received alpha-lipoic acid. The findings suggest that alpha-lipoic acid supplementation effectively mitigates damage associated with experimental periodontitis, enhances antioxidant defenses, and improves alveolar bone integrity.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"147 ","pages":"Article 110087"},"PeriodicalIF":4.9,"publicationDate":"2025-09-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145000770","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary omega-3 alleviates copper-induced nephrotoxicity via suppression of NLRP3-mediated pyroptosis and lipid metabolism disorder in chickens","authors":"Xin Zhang ,&nbsp;Yixin Zhang ,&nbsp;Hongmin Lu,&nbsp;Hongyue Zhen,&nbsp;Yue Zhang,&nbsp;Qi Wang,&nbsp;Ruoqi Wang,&nbsp;Manhong Liu,&nbsp;Mingwei Xing","doi":"10.1016/j.jnutbio.2025.110086","DOIUrl":"10.1016/j.jnutbio.2025.110086","url":null,"abstract":"<div><div>Excessive use of copper (Cu) in poultry farming induces nephrotoxicity closely related to inflammatory response and lipid metabolism disorder, but the mechanism remains unclear. Omega-3 (Ω-3), a natural polyunsaturated fatty acid with anti-inflammatory and antioxidative stress properties, has been demonstrated to exert protective effects on the kidneys. However, whether Ω-3 can alleviate Cu-induced renal injury and the underlying mechanisms remain unclear. Therefore, we investigated the effects of Cu exposure on chicken kidney tissues and CEK cells in this study. Subsequent dietary supplementation with Ω-3 was administered to evaluate its ameliorative effects on Cu-induced renal injury. Cu exposure significantly disrupted mitochondrial homeostasis. This was evidenced by downregulated mRNA levels of OPA1 and MFN1/2, reduced ATP content, tricarboxylic acid (TCA) cycle dysfunction, mitochondrial membrane depolarization, and excessive ROS accumulation. Electron microscopy confirmed that Cu exposure induced pyroptosis in renal cells, accompanied by activation of the NF-κB-NLRP3-GSDMD pathway, leading to significantly upregulated expression of IL-1β, IL-18, Caspase-1, ASC, and GSDMD. Additionally, Cu exposure disrupted lipid metabolism by upregulating PPARγ, SREBP1, and Fas while downregulating PGC-1α, as evidenced by abnormal lipid droplet accumulation observed under electron microscopy. Furthermore, Cu exposure significantly inhibited the Wnt3a/β-catenin signaling pathway, impairing renal repair functions. Notably, the administration of Ω-3 effectively alleviated these adverse effects. This study reveals that Ω-3 exerts its protective effects against Cu-induced nephrotoxicity by modulating the NF-κB-NLRP3-GSDMD axis, the Wnt/β-catenin signaling pathway, and lipid metabolism for the first time. This provides a dietary strategy to enhance poultry health in intensive farming.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"147 ","pages":"Article 110086"},"PeriodicalIF":4.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144992737","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Improvement of spermogenesis impairment induced by high-fat diet in obese mice through pyrroloquinoline quinone regulation of glycolysis pathway.","authors":"Qiumei Huang, Yanhong Wei, Zhenhui Fu, Rutong Wang, Runtang Zhou, Xiaocan Lei, Jianghua Le, Linlin Hu","doi":"10.1016/j.jnutbio.2025.110066","DOIUrl":"10.1016/j.jnutbio.2025.110066","url":null,"abstract":"<p><p>This study employed an obese mouse model to investigate the effects of pyrroloquinoline quinone (PQQ) intervention on reproductive physiology and glycolytic pathways. Our findings demonstrate that PQQ markedly enhanced glycolytic activity in obese mice, promoting glucose breakdown and metabolism to improve energy supply efficiency. These metabolic improvements correlated with significant support for reproductive system functionality. Mechanistic analyses revealed PQQ's potential to augment mitochondrial respiration, ameliorate mitochondrial dysfunction, and counteract obesity-associated inflammation, thereby preserving the balance between fatty acid degradation and integrated glycolysis-cholesterol metabolism. Collectively, this work provides novel insights into PQQ's molecular mechanisms for promoting glycolysis and ameliorating infertility in obese males.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110066"},"PeriodicalIF":4.9,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144992775","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Negative modulation of maternal iodine deficiency and excess on milk lipid synthesis and secretion in lactating rats","authors":"Ying Zhang ,&nbsp;Xin Zhao ,&nbsp;Ning Yu ,&nbsp;Xiru Wang ,&nbsp;Zixuan Zhang ,&nbsp;Xinbao Zhang ,&nbsp;Haohao Meng ,&nbsp;Yan Song ,&nbsp;Yuyang Cai ,&nbsp;Jingyi Wang ,&nbsp;Haozhuo Xie ,&nbsp;Wanqi Zhang ,&nbsp;Zhongna Sang","doi":"10.1016/j.jnutbio.2025.110085","DOIUrl":"10.1016/j.jnutbio.2025.110085","url":null,"abstract":"<div><div>Iodine is an essential micronutrient for developmental processes in the early stages; however, data on the effect of maternal iodine nutrition on milk lipids are limited. We aimed to explore the effect of inadequate and excessive iodine intake on milk lipid metabolism and its mechanisms preliminarily. Rats were treated with different concentrations of potassium iodide water to construct animal models of iodine deficiency and excess. Iodine excess reduced serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-C) levels during lactation. Iodine deficiency had no significant effect on blood lipid indicators. In early and late lactation, iodine deficiency and excess inhibited triglyceride (TG) levels in milk; in mid-lactation, the inhibitory effect of iodine deficiency was attenuated. Under iodine deficiency and excess, the level of TG and the expression of THRα1, THRβ1, ACC1, FAS, THRSP, BTN1A1, and ADFP proteins in the mammary gland were decreased during lactation; a decrease in LPL protein expression was observed in early and late lactation; and a decline of XOR protein expression was reported in mid and late lactation. Blood lipid metabolism was less sensitive to iodine deficiency during lactation. Iodine excess has a more profound effect on blood lipid metabolism, causing dyslipidemia in lactating rats. Long-term iodine deficiency and excess may have a negative role in the mechanisms regulating milk lipid synthesis and secretion by affecting thyroid hormones to inhibit the milk TG level.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"146 ","pages":"Article 110085"},"PeriodicalIF":4.9,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144957918","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"UDP-glucose exacerbates egg white diet-induced allergic enteritis by promoting P2Y14-mediated neutrophil chemotaxis in mice","authors":"Xing Zhang ,&nbsp;Xiao Chen ,&nbsp;Xuanyi Meng ,&nbsp;Yong Wu ,&nbsp;Hongbing Chen ,&nbsp;Xin Li","doi":"10.1016/j.jnutbio.2025.110084","DOIUrl":"10.1016/j.jnutbio.2025.110084","url":null,"abstract":"<div><div>While numerous studies have reported that exposure to food allergens can increase neutrophil counts in peripheral blood and the gastrointestinal tract, the specific roles of neutrophils in food allergy development remain unclear. By feeding an egg white diet, we investigated the contribution of neutrophil infiltration to food allergy development and explored the mechanisms driving neutrophil activity. Our results demonstrated that neutrophil depletion significantly reduced the secretion of inflammatory cytokines. Additionally, mice with food allergies exhibited widespread intestinal epithelial pyroptosis mediated by caspase-3 and Gsdmc, which subsequently promoted the release of UDP-glucose (UDPG) into the extracellular space. Increased levels of UDPG activated P2Y14R expressed on the surface of neutrophils, facilitating their chemotaxis to inflamed sites. Inhibition of P2Y14R significantly diminished mucosal neutrophil infiltration, thereby alleviating food allergy symptoms and intestinal damage in mice. We believe our findings may provide new insights for investigating the mechanisms underlying food allergy development.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"147 ","pages":"Article 110084"},"PeriodicalIF":4.9,"publicationDate":"2025-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144957893","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biotin: DNA to diet","authors":"Shivani Karalia ,&nbsp;Vinod Kumar Meena","doi":"10.1016/j.jnutbio.2025.110081","DOIUrl":"10.1016/j.jnutbio.2025.110081","url":null,"abstract":"<div><div>Biotin, also known as vitamin B7 or vitamin H, is a water-soluble vitamin that acts as an essential cofactor in many cellular metabolic processes, including fatty acid biosynthesis, fatty acid oxidation, amino acid metabolism, and gluconeogenesis. Biotin is not synthesized by human cells; they take it up from intestinal gut bacteria or dietary sources. The estimated average requirement (EAR) for biotin is uncertain, but people of different ages require biotin between 5 and 35 mcg/d. Interestingly, the chemical structure and involvement of biotin in metabolic pathways in all three domains of life have opened the possibilities of drug development against pathogenic bacteria. Moreover, biotin is a small molecule with high and robust affinity towards avidin, which makes it suitable for use as a biochemical sensor for the diagnosis of diseases. A substantial adsorption and affinity of biotin towards proteins implicated in lipid or fatty-acid synthesis directs its potential to interact with and dismantle the extracellular matrix (ECM) of bacterial biofilm. This review explores the genesis, structural outlook, and multifaceted role of biotin in genetics, healthcare, diet, and future research. This aims to provide a holistic view of biotin research, ranging from cellular and molecular levels to the dosage and food supplements.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"146 ","pages":"Article 110081"},"PeriodicalIF":4.9,"publicationDate":"2025-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144957971","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary urolithin A suppresses lung cancer via gut microbiota-mediated autophagy activation","authors":"Jiayin Zhang,&nbsp;Xiaohan Li,&nbsp;Lemei Sun,&nbsp;Bingqi Chen,&nbsp;Rong Zhang,&nbsp;Jing Duan","doi":"10.1016/j.jnutbio.2025.110080","DOIUrl":"10.1016/j.jnutbio.2025.110080","url":null,"abstract":"<div><div>Urolithin A (UA), a gut microbiota-derived metabolite of ellagic acid, exhibits diverse biological activities. Emerging evidence suggests its anti-tumor potential, possibly mediated through gut microbiota modulation, yet its role in lung cancer remains unclear. In this study, UA dose- and time-dependently suppressed lung cancer cell proliferation. Mechanistically, UA triggered autophagy, as evidenced by increased LC3-II protein levels, and transcriptome analysis revealed this effect was mediated through inhibition of the PI3K/AKT/mTOR pathway. <em>In vivo</em>, UA supplementation markedly inhibited tumor growth in H1975 xenograft models, concomitant with enhanced autophagy and downregulation of associated proteins. Notably, 16S rRNA sequencing demonstrated that UA modulated gut microbiota composition, increasing <em>Lactobacillus</em> while decreasing <em>Desulfovibrio</em> abundance. Spearman’s correlation analysis further linked these microbial shifts to altered expression of autophagy-related genes. Collectively, our findings highlight UA as a promising gut microbial metabolite for lung cancer intervention via coordinated autophagy induction and microbiota remodeling.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"146 ","pages":"Article 110080"},"PeriodicalIF":4.9,"publicationDate":"2025-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144957903","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}