Journal of Nutritional Biochemistry最新文献

{"title":"Dietary Rutin Mitigates Cold-Induced Oxidative Stress and Enhances Meat Quality in Broilers: Implications for Improved Antioxidant Capacity and Myofibrillar Protein Structure.","authors":"Jingyang Zhang, Xinyu Wang, Chendi Fu, Chunting Yu, Yihan Jiao, Ruoshi Zhang, Xingjun Feng","doi":"10.1016/j.jnutbio.2025.110123","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.110123","url":null,"abstract":"<p><p>This study aimed to investigate the effects of dietary rutin on meat quality, myofibrillar protein (MPs) structure, and antioxidant status in the pectoralis major of broilers exposed to cold stress. 360 one-day-old male AA broilers were randomly divided into four groups with six replicates (15 birds per replicate): a control group (CON) kept at 26 ± 2°C on a basal diet, and three cold-stressed groups exposed to 10±2°C with diets supplemented with 0, 500, and 1000 mg/kg rutin (CS, CSR500, and CSR1000, respectively). The duration of the experiment was 42 days. Results showed that dietary rutin increased pH_15min, improved meat color, tenderness, and water holding capacity (WHC). It also boosted amino acid content, and muscle flavor. Furthermore, dietary rutin attenuated protein oxidation and enhanced the structural integrity of MPs, as indicated by increased Ca²⁺-ATPase activity, reduced dityrosine content and diminished protein particle size. These alterations were attributed to enhanced antioxidant enzyme activities regulated by nuclear factor E2-related factor (Nrf2) genes and reduced lipid and protein oxidation. In conclusion, the dietary rutin enhanced meat quality in cold-stressed broilers. These findings indicate that rutin may serve as a potential dietary supplement for the production of chickens with enhanced nutritional value and improved quality in regions with cold climates.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110123"},"PeriodicalIF":4.9,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145125022","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":"Stevioside alleviates high-fat diet-induced MASLD/MASH in Apo-E^‑/‑ mice by modulating the TGF-β signaling.","authors":"Sateesh Alavala, Nidhi Sharma, Rajendra Sangaraju, Suresh Challa, Ramakrishna Sistla, Sai Balaji Andugulapati","doi":"10.1016/j.jnutbio.2025.110125","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.110125","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD) is an emerging global health issue characterized by excessive hepatic fat accumulation, which can progress to inflammation and fibrosis. This condition is closely linked to systemic metabolic disorders, including obesity, type 2 diabetes, and dyslipidemia. Due to the absence of approved pharmacological treatments, identifying effective therapeutic strategies is essential. Stevioside (STV), a natural sweetener with documented bioactive properties, was evaluated for its potential to alleviate MASLD in both in vitro and in vivo models. In vitro, STV dose-dependently suppressed transforming growth factor-beta (TGF-β)-induced fibrogenic activation in hepatic stellate cells (HSC-LX2). In the in vivo model, MASLD was induced in ApoE-deficient (ApoE⁻/⁻) mice by feeding a high-fat diet (HFD) for 10 weeks, resulting in an average body weight of approximately 45 g. Further, mice were randomized and assigned to chow control, HFD control, or STV treatment groups for another 6-week intervention. STV administration significantly attenuated HFD-induced weight gain, dyslipidemia, and liver injury markers. Histological analyses revealed substantial reductions in hepatic steatosis, inflammation, and fibrosis in STV-treated mice. Mechanistic investigations (in in vitro and in vivo models) indicated that STV mitigates disease progression by modulating the canonical TGF-β/Smad signaling pathway. Overall, these findings demonstrate that STV effectively alleviates MASLD in ApoE⁻/⁻ mice and inhibits fibrogenic activation in HSC-LX2 cells, highlighting its potential as a therapeutic agent for MASLD.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110125"},"PeriodicalIF":4.9,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145125051","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":"Fecal microbiota transplantation alleviates chronic cerebral hypoperfusion-induced axonal hypomyelination by regulating gut microbiota-derived metabolism and oligodendrogenesis.","authors":"Shao-Hua Su, Ming Chen, Da-Ding Lu, Yi- Fang Wu, Xiao-Song Huang, Lin Zhang","doi":"10.1016/j.jnutbio.2025.110122","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.110122","url":null,"abstract":"<p><p>Fecal microbiota transplantation (FMT), aimed at rebuilding gut microbiota, has been proposed as a potential therapeutic approach to central nervous system (CNS) diseases. However, the therapeutic effects of FMT against demyelination-related white matter injury (WMI) have not yet been clarified under chronic cerebral hypoperfusion (CCH) condition. We therefore explored the potential roles and mechanisms of FMT on CCH-induced WMI, focusing on myelin integrity, axonal survival, and oligodendrogenesis. FMT restored mitochondrial electron transport chain (ETC) complex I-V activities and promoted the changes of pyruvate metabolism from lactate-generated to acetyl-CoA-generated mode, strengthening mitochondrial ATP production. Furthermore, FMT mitigated CCH-induced demyelination and axonal degeneration, effects mediated in part by oligodendrogenesis-dependent remyelination. Moreover, FMT altered CCH-induced gut microbiota composition by increasing the proportions of some bacterial groups including Verrucomicrobiae, Akkermansiaceae, Verrucomicrobiales, Verrucomicrobiota, Akkermansia, and Akkermansia_muciniphila. These gut microbiota were strongly associated with elevated fecal levels of L-tryptophan, 5-hydroxyindoleacetic acid, and N-a-acetylcitrulline, as well as with increased hippocampal concentrations of L-arginine, L-glutamine, N2-succinyl-L-ornithine, N-acetylornithine, indolepyruvate, indoleacetaldehyde, kynurenic acid, 11, 12-EET, 11, 12-DiHETrE and prostaglandin A2, which were almost involved in tryptophan and arginine related metabolism pathways. This study highlights the beneficial effects of FMT strategy in response to demyelination-mediated WMI under chronic cerebral ischemia condition.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110122"},"PeriodicalIF":4.9,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145113244","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":"From Suboptimal to Supersaturation: Selenium Status After Bariatric Surgery Is Modulated by Supplementation.","authors":"Mr Gabriël Eksteen, Ms Lia Griner, Bart Van der Schueren, Roman Vangoitsenhoven, Ann Mertens, Matthias Lannoo, Dr Ellen Deleus, Tim Vanuytsel, Christophe Matthys","doi":"10.1016/j.jnutbio.2025.110121","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.110121","url":null,"abstract":"<p><p>Metabolic and Bariatric Surgery (MBS) is a proven treatment for obesity but increases risk of nutrient deficiencies. Guidelines recommend vitamin and mineral supplementation after MBS but omits selenium. Adequate selenium status is associated with reduced incidence of chronic diseases, including sarcopenia, yet excess selenium intake is not innocuous. Whilst selenoprotein P is the preferred marker of status, no studies have investigated selenoprotein P after MBS. This cross-sectional study compared Selenoprotein P, plasma selenium and dietary selenium in adults older than 65 years with (BAR) or without previous MBS (CON). Dietary selenium intake was calculated using locally available composition data; Selenoprotein P was categorised as suboptimal, saturated, and supersaturated; and plasma selenium as suboptimal, adequate, and replete. Subgroups were created by selenium supplementation practises (supp vs. none) and linear regression was used to investigate predictors of selenoprotein P. Fifty participants were included per group (BAR 40% male, CON 36%) and BAR participants were two years younger and fewer had diabetes (28% vs 52%). Both selenoprotein P and plasma selenium were higher in BAR-supp compared to BAR-none or CON-none. BAR-supp had a lower prevalence of suboptimal selenoprotein P levels compared to BAR-none (7% vs. 43%) but more participants had supersaturated levels (28% vs 0%). The predictors of selenoprotein P were supplemented selenium, dietary selenium, and total weight loss. Whilst the clinical relevance of Selenoprotein P supersaturated remains uncertain, further studies are needed to investigate the ideal supplement dosage and the impact of surgery type on selenium requirements. Trial registration clinicaltrials.gov ID: NCT05582668 Date of registration: 12 October 2022.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110121"},"PeriodicalIF":4.9,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145113328","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":"Mass spectrometry imaging to evaluate (poly)phenol distribution in animal tissues.","authors":"Marta Berzaghi, Pedro Mena, Daniele Del Rio, Letizia Bresciani","doi":"10.1016/j.jnutbio.2025.110119","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.110119","url":null,"abstract":"<p><strong>Background: </strong>(Poly)phenols are plant-derived compounds with potential benefits for human health. Understanding the absorption and distribution of phenolic compounds within the human body is of great importance for identifying their bioactive form in target organs or tissues, and, consequently, for understanding their biological effects. Mass spectrometry imaging (MSI) is an analytical method that provides a visual in situ representation of the molecular distribution within complex samples and biological tissues. This technique allows to map various molecules in a tissue, providing spatial information that cannot be obtained through traditional mass spectrometry analytical approaches.</p><p><strong>Scope and approach: </strong>This review aims to provide a valuable and informative summary of the published MSI applications for evaluating (poly)phenol absorption and distribution in animal tissues. Following PRISMA guidelines, the search string was launched in two web databases, Web of Science and Scopus.</p><p><strong>Key findings and conclusions: </strong>Of the nine reviewed studies, one applied desorption electrospray ionization (DESI) and the rest matrix-assisted laser desorption ionization (MALDI) to visualize (poly)phenol distribution in mice or rats. MSI represents a viable approach for exploring the absorption and distribution of these bioactive compounds in tissues, useful to enhance the comprehension of their pharmacokinetics, along with their possible site of action and transport mechanisms implicated in their distribution. The findings indicate that the application of MSI to study phenolic compounds in vivo is currently limited, but it is expected to increase as researchers seek to advance their comprehension of the health-promoting attributes of (poly)phenols and their metabolites.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110119"},"PeriodicalIF":4.9,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145102654","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 Selenium deficiency activates the NLRP3 inflammasome to induce gallbladder pyroptosis by regulating glycolysis and histone lactylation through ROS/HIF-1α pathway.","authors":"Zhaoyang An, Haodong Hu, Qian Wang, Yaning Qiu, Jiahong Chu, Yu Xia, Shu Li","doi":"10.1016/j.jnutbio.2025.110118","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.110118","url":null,"abstract":"<p><p>Selenium (Se) is an essential micronutrient, and inadequate intake can disrupt redox balance in digestive organs, promoting inflammation. Enhanced glycolysis leads to lactate accumulation, exacerbating the inflammatory response through inflammation-related pathways. Histone lysine lactylation plays a key role in epigenetic regulation. The effect of Se deficiency on the gallbladder remains unclear. To explore the mechanism of Se deficiency on gallbladder injury and the regulatory role of histone lactylation, we established Se-deficient swine models and in vitro cell models. Histopathological observation of the gallbladder found that Se deficiency led to inflammatory damage to the gallbladder. Metabolomics and proteomics results showed that Se deficiency led to significant enrichment of \"glycolytic flux\", \"oxidative stress\", and \"hypoxia-inducible factor-1 α (HIF-1α) signaling pathway\". Further studies have found that Se deficiency led to oxidative stress in gallbladder tissue, abnormal expression of HIF-1α factor, increased glycolysis levels, excessive lactate production, increased histone lactylation, and pyroptosis. HIF-1α knockdown suppressed Se deficiency-induced glycolysis and reduced lactate accumulation. In vitro studies using N-acetylcysteine (NAC), 2-deoxyglucose (2-DG), Oxamate and A-485 showed that Reactive oxygen species (ROS) regulated increased glycolysis through HIF-1α and increased H3K18 lactylation (H3K18la) levels through substrate-dependent modifications. Furthermore, H3K18la activated NLRP3 inflammasome, triggering pyroptosis and inflammatory cascades. In conclusion, the results of this study showed that dietary Se deficiency promotes glycolysis-dependent histone lactylation via the ROS/HIF-1α pathway, activating NLRP3 inflammasome, leading to pyroptosis and inflammation in gallbladder. These findings provide insights into targeted therapies for Se deficiency-related metabolic disorders and pathological changes in organs.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110118"},"PeriodicalIF":4.9,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145102698","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":"Hydrangenol exerts anti-obesity effects by disturbing adipogenesis via mitotic clonal expansion and gut microbiota dysbiosis.","authors":"Hee-Soo Han, Kyung-Sook Chung, Ye-Rin Kim, Seo-Yun Jang, Sun-Hee Lee, Kyung-Tae Lee","doi":"10.1016/j.jnutbio.2025.110120","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.110120","url":null,"abstract":"<p><p>Obesity is a metabolic disorder influenced by genetic and environmental factors. Developing therapeutic strategies that maintain energy metabolism and gut microbiota balance is essential for addressing obesity. This study investigated the anti-obesity potential of hydrangenol (HG), a bioactive compound found in the leaves of Hydrangea serrata (Thunb.) Ser., in 3T3-L1 preadipocytes as well as high-fat diet (HFD)-induced and db/db obese mice. HG inhibited lipid accumulation in differentiated 3T3-L1 cells by disrupting mitotic clonal expansion through modulation of cell cycle-related proteins (cyclin D1, cyclin E, cyclin B1, CDK2, and p21). It also enhanced AMP-activated protein kinase α (AMPKα) phosphorylation while suppressing Akt and mTOR phosphorylation. In line with these in vitro results, HG also suppressed lipid deposition in obese mice by regulating key adipogenesis-related proteins such as C/EBPα, PPAR-γ, and AMPKα in white adipose and liver tissues, resulting in reduced fat mass. Furthermore, HG lowered plasma cholesterol, low-density lipoprotein, leptin, and insulin levels in HFD-fed mice resulting in the improvement of plasma profiles. 16S rRNA sequencing revealed that HG altered the composition of the gut microbiota, increasing the relative abundance of Bacteroidetes and decreasing Firmicutes and Proteobacteria in obese mice. Overall, these results highlight HG's potential as a promising candidate for reducing lipid accumulation and correcting gut microbiota dysbiosis, offering a strategy for obesity prevention.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110120"},"PeriodicalIF":4.9,"publicationDate":"2025-09-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145102661","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":"Coriander (Coriandrum sativum L. leaves) improves brain and gut pathology in mouse models of brain-first and gut-first Parkinson's disease.","authors":"Hanbyeol Lee, Jin Hee Kim, Yujin Choi, Minji Lee, Hi-Joon Park, Myung Sook Oh","doi":"10.1016/j.jnutbio.2025.110116","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.110116","url":null,"abstract":"<p><p>Recently, an increasing number of studies have focused on the microbiota-gut-brain axis in Parkinson's disease (PD), and a new perspective has emerged regarding the regulation of gut health and the microbiome as potential treatments for PD. We focused on coriander, which is consumed worldwide and exhibits significant anti-inflammatory and antimicrobial activities. In this study, we investigated whether coriander ameliorated PD phenotypes in both brain-first and gut-first PD models. C57BL/6J mice were treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) or Proteus mirabilis (P. mirabilis) for 5 d. In the MPTP-induced model, coriander (30 and 100 mg/kg), including the MPTP injection period, was administered orally for 15 d. In the P. mirabilis-induced model, coriander (100 mg/kg) was administered orally for 21 d, including the period of P. mirabilis administration. The results showed that coriander ameliorated MPTP- and P. mirabilis-induced motor deficits and dopaminergic neuronal death in mice, and suppressed inflammatory responses in both the brain and colon. In addition, coriander improved P. mirabilis-induced α-synuclein pathology in both brain and colon. Coriander reduced the mRNA expression of P. mirabilis and hemolysin A (HpmA) in feces, an endotoxin factor produced by P. mirabilis, in MPTP-induced and P. mirabilis-induced models. These results indicate that coriander has the potential to attenuate PD pathology in the brain and gut in both the brain-first and gut-first PD models. This suggests that coriander is a promising functional food for the prevention and treatment of PD.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110116"},"PeriodicalIF":4.9,"publicationDate":"2025-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145092070","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":"Regulation of endoplasmic reticulum stress and ferroptosis by rutin in a rat model of periodontitis.","authors":"Earl Fu, Chan-Yen Kuo, Martin M Fu, Kuang-Chung Shih","doi":"10.1016/j.jnutbio.2025.110113","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.110113","url":null,"abstract":"<p><p>Periodontitis is a bacteria-induced chronic inflammatory disease affecting tooth-supporting structures, involving endoplasmic reticulum (ER) stress and ferroptosis with a potential link between them. This study investigated the effects of rutin, a plant-derived flavonoid with diverse bioactivities, such as anti-inflammatory and antioxidant properties, on periodontitis in a rat model by modulating ER stress and ferroptosis pathways. Periodontitis was induced in rats using silk ligatures around molars. Rutin (0, 100, or 200 mg/kg) was administered orally for seven consecutive days, starting one day before ligation, with non-ligated rats as controls (8 per group). Using micro-computed tomography (μCT) and histology, the damage in periodontium was evaluated, while the gingival protein expressions for pro-inflammatory cytokines, ER stress, and ferroptosis were analyzed by Western blotting. Through μCT and histological analysis, gingival inflammation and loss of tooth-supporting tissue in rats with periodontitis were confirmed. Rutin reduced these effects dose-dependently. Western blotting showed significantly elevated pro-inflammatory cytokines (tumor necrosis factor-α and interleukin-1β) and ER stress markers (activating transcription factor 6, binding immunoglobulin protein, and C/EBP homologous protein), but reduced ferroptosis markers (solute carrier family 7 member 11 and glutathione peroxidase 4) in rats with periodontitis. Rutin dose-dependently alleviated the alterations in the above cytokines and markers. Parameters of gingival inflammation and soft/hard tissue loss correlated positively with ER stress markers and negatively with ferroptosis markers, though no correlation was found between ER stress and ferroptosis. These findings suggest rutin alleviates periodontitis by independently modulating ER stress and ferroptosis.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110113"},"PeriodicalIF":4.9,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086413","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":"Flavonoid Intake and Kidney Stones: an Exposome-Based Cross-Sectional Study.","authors":"Yuan Gong, Yuanyuan Yang, Lintao Miao, Mingliang Zhong, Qidong Xia, Jie Chang, Shaogang Wang","doi":"10.1016/j.jnutbio.2025.110117","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.110117","url":null,"abstract":"<p><p>The present study aimed to evaluate the relationships between total, subgroup and individual dietary flavonoid intake and the risk of kidney stones. Data from the National Health and Nutrition Examination Survey and the Food and Nutrient Database for Dietary Studies were analyzed. A total of 9033 participants without kidney stones and 985 participants with kidney stones were included. A dose-response relationship curve suggested a J-shaped relationship (p for nonlinearity <0.001) between flavanone intake and kidney stone risk (nadir point: 32.23 mg/d, OR: 0.70, 95%CI: 0.58-0.84). Naringenin (a type of flavanones) was negatively associated with kidney stone risk. Hesperetin was associated with kidney stone risk in a J-shaped manner. These findings suggest that flavanone consumption may be beneficial for individuals with elevated kidney stone risk.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110117"},"PeriodicalIF":4.9,"publicationDate":"2025-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145086429","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}