Journal of Nutritional Biochemistry最新文献

{"title":"Correlation of serum trace elements with clinical features and gut microbiota in patients with Crohn's disease.","authors":"Yuanyuan Wang, Yumei Lin, Jiaxing Feng, Liqun Lin, Lupeng Liu, Jingling Su, Chenxi Xie, Huaxiu Shi","doi":"10.1016/j.jnutbio.2025.109917","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109917","url":null,"abstract":"<p><strong>Introduction: </strong>Changes of several trace elements have been reported to contribute to the pathogenesis of Crohn's disease (CD), which is associated with gut microbiota imbalance. This study aimed to investigate changes in trace elements in Chinese CD patients, and explore the correlation of trace element status with clinical features and gut microbiota.</p><p><strong>Methods: </strong>Eighty CD patients and forty-five healthy volunteers were enrolled between July 2022 and November 2022. Serum zinc, copper, magnesium and selenium were measured by inductively coupled plasma mass spectrometry. The nutritional status was assessed based on body mass index and albumin and disease severity was determined according to the Crohn's disease activity index and C-reactive protein. Fecal gut microbiota was analyzed using 16SrRNA gene sequencing.</p><p><strong>Results: </strong>Compared with healthy controls, serum copper increased, but serum selenium reduced in Chinese CD patients. The serum levels of selenium and magnesium were positively related to nutritional status, and the serum levels of selenium and copper were associated with disease severity. Selenium deficiency in CD patients was closely related to the diversity and abundance of gut microbiota.</p><p><strong>Discussion: </strong>The serum levels of several trace elements change in the CD patients and are associated with nutritional status and disease severity. Selenium deficiency in CD patients is associated with the diversity of gut microbiota, suggesting an interaction between trace elements and gut microbiota.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109917"},"PeriodicalIF":4.8,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143795219","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":"Ketone Bodies in Renal Function and Diabetic Kidney Disease.","authors":"Hamza Mechchate","doi":"10.1016/j.jnutbio.2025.109915","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109915","url":null,"abstract":"<p><p>Diabetes, as a leading cause of chronic kidney disease (CKD) and diabetic kidney disease (DKD), underscores a significant concern, especially due to its association with health decline and mortality. In this context, the roles of ketone bodies, especially beta-hydroxybutyrate are increasingly recognized for their impact in renal physiology and the pathology of DKD. Moving beyond their conventional perception as metabolic by products, ketone bodies have been found to play a crucial role in renal health, particularly under the stresses of diabetic conditions. Serving as alternative energy sources during periods of glucose scarcity, they also function as important signaling molecules. These ketones significantly influence oxidative stress, nutrient-sensing pathways, and mitochondrial function within the kidneys. The adaptability of renal cells to utilize ketone bodies in diabetes highlights a dynamic metabolic interplay, essential for understanding renal health. The exploration of ketone body metabolism modulation, particularly through interventions like SGLT2 inhibitors and ketogenic diets, opens new avenues in managing DKD. Such insights pave the way for rethinking the role of ketone bodies in renal pathology and diabetes, pointing to novel research directions and therapeutic potentials.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109915"},"PeriodicalIF":4.8,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143788550","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 Impact of Folic Acid Deficiency on Ischemic Stroke: Role of Inflammation and Long Noncoding RNA H19.","authors":"Meng Wang, Linran Shi, Zonghang Tong, Yinyue Liu, Yuxuan Bai, Xueli Yang, Yanhong Wang, Zhongying Gong, Qiang Zhang, Xumei Zhang","doi":"10.1016/j.jnutbio.2025.109916","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109916","url":null,"abstract":"<p><p>It has been validated that folic acid deficiency (FD) is associated with an increased risk of stroke and a worse prognosis. However, the specific mechanisms by which FD exerts its detrimental effects on ischemic stroke (IS) have not been fully understood. The results of this case-control study indicated that patients with IS had a decreased serum folate level, along with up-regulated long non-coding RNA H19 (lncRNA H19) and enhanced inflammatory responses. Meanwhile, it was corroborated that the serum folate level was negatively correlated with H19 expression and the systemic immune-inflammation index (SII). Similarly, FD was demonstrated to exacerbate neurological injury in the middle cerebral artery occlusion/reperfusion (MCAO/R) rats by up-regulating the expression of inflammatory cytokines and H19 in both peripheral blood and brain tissue. Notably, the alterations in the expression of these factors in peripheral blood were consistent with those observed in brain tissue. Additionally, in a co-culture of N2a neurons and BV2 microglia, FD promoted the transition of BV2 cells towards a pro-inflammatory state by up-regulating the expression of H19, which aggravated neuronal injury. Moreover, blocking H19 in BV2 cells mitigated inflammation and partially reversed the injury in N2a cells exacerbated by FD after the treatment with oxygen-glucose deprivation and reperfusion (OGD/R). These findings provide a more in-depth insight into the regulatory role of H19-mediated systemic inflammatory responses in the context of FD, suggesting the potential clinical utility of folic acid in managing ischemic brain injury.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109916"},"PeriodicalIF":4.8,"publicationDate":"2025-04-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143788554","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":"Linoleic Acid Modulates Vascular Reactivity, Alters Cyclooxygenase-2-Derived Products, and Promotes Eutrophic Remodeling in Small Mesenteric Arteries of Normotensive Rats: Vascular Modulation and Remodeling Induced by Linoleic Acid in Normotensive Rats.","authors":"Dieli Oliveira Nunes, Vinicius Bermond Marques, Camila Cruz Pereira Almenara, Wena Marcarini Dantas, Eduardo Hertel Ribeiro, Ivanita Stefanon, Alessandra Simão Padilha","doi":"10.1016/j.jnutbio.2025.109913","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109913","url":null,"abstract":"<p><p>Linoleic acid (LA) is a polyunsaturated fatty acid with essential roles in cardiovascular regulation. Despite its known vascular effects, its impact on mesenteric resistance arteries (MRA) in normotensive models remains unclear. This study aimed to determine whether LA induces functional and structural changes in MRA of normotensive rats by modulating endothelial mechanisms. We hypothesized that LA treatment reduces vasoconstrictor reactivity and promotes vascular remodeling via enhanced nitric oxide (NO) bioavailability. Male Wistar rats were treated with LA (15 mg/kg) or vehicle for 15 days. LA did not alter blood pressure, mechanical parameters, or collagen and elastin levels in the MRA, but it increased both external and internal diameters of the vessels, reducing the wall-to-lumen ratio. LA decreased the contractile response to phenylephrine, without affecting responses to acetylcholine or sodium nitroprusside. L-NAME (100 µM) enhanced vasoconstriction to a greater extent in the LA-treated group, associated with increased nitric oxide (NO) bioavailability, independent of inducible NO synthase (iNOS) and phosphatidylinositol 3- kinase (PI3K). The NADPH oxidase pathway had a lesser impact on vasoconstriction in the LA group, although the superoxide anion scavenger tiron (1 mM) and the production of reactive oxygen species showed similar results. Inhibition of ciclooxigenase (COX) and cytochrome-P450 (CYP450) attenuated vascular reactivity in the LA group, with greater involvement of COX-2-derived products. While SC 19220 (EP1 receptor antagonist, 10 µM) reduced vasoconstrictor responses to phenylephrine only in MRA from the LA-treated group, SQ 29.548 (TP receptor antagonist, 1 µM) reduced responses only in controls. In conclusion, LA reduces vasoconstriction, increases NO bioavailability and decreases NADPH oxidase participation associated with alterations in CYP450 and COX-2-derived products.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109913"},"PeriodicalIF":4.8,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143788552","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":"Medium-chain triglyceride attenuates obesity by activating brown adipose tissue via upregulating the AMPK signaling pathway.","authors":"Min Jia, Hao Yue, Xiuxiu Wang, Aizhen Zong, Tongcheng Xu, Yong-Jiang Xu, Yuanfa Liu","doi":"10.1016/j.jnutbio.2025.109914","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109914","url":null,"abstract":"<p><p>Medium-chain triacylglycerol (MCT) is a healthy lipid mainly composed of medium-chain fatty acids (MCFA), which has been proven to have physiological activities in improving metabolic disorders, reducing blood cholesterol, and controlling weight. Brown adipose tissue (BAT) has been regarded as a potential organ to fight obesity due to the function of thermogenesis and energy dissipation. Previous reports found that a diet rich in MCT contributed to the activation of BAT. However, the potential mechanism between MCT and BAT remains unknown. In the current study, MCFA was applied on C3H/10T1/2 cells differentiated brown adipocytes, and MCT was applied on high-fat diet (HFD) induced obese mice. The results showed that MCFA and MCT induced browning of adipocytes and activation of BAT, significantly increased the enrichment of mitochondria, and significantly reduced intracellular lipid accumulation and body weights in vivo and in vitro. Mechanically, MCT significantly increased the level of UCP1, AMPK, and the downstream signaling factors of Pgc1α and Ulk1, further significantly elevated the brown differentiation factor of Pparγ. Moreover, The AMPK inhibitor dorsomorphin partially impaired the beneficial effects caused by MCT. In conclusion, this study proved that AMPK is the potential target of MCT to induce BAT activation and provided theoretical evidence for the application of MCT in the future.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109914"},"PeriodicalIF":4.8,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143780280","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":"Changes in lipid metabolism in visceral rather than the subcutaneous adipose tissue depot attenuate metabolic disturbances in obesity-resistant mice fed a high-fat diet.","authors":"Miloš Vratarić, Ana Teofilović, Danijela Vojnović Milutinović, Nataša Veličković, Ljubica Vučićević, Goran Đmura, Ana Djordjevic","doi":"10.1016/j.jnutbio.2025.109912","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109912","url":null,"abstract":"<p><p>Obesity is characterized by an enlargement of white adipose tissue caused by caloric excess. The depot-specific adaptation of white adipose tissue in individuals resistant to obesity despite a high-calorie diet is crucial for understanding the pathogenesis of obesity and related metabolic disorders. Our aim was to characterize the metabolic and morphological state of obesity resistance and to investigate depot-specific changes in signaling pathways in epididymal visceral (eVAT) and inguinal subcutaneous (iSAT) white adipose tissue of C57BL/6J male mice on a high-fat diet (60 kcal% fats). After 14 weeks, the mice were categorized as obese (at least 30% higher body mass compared to the control group) or obesity-resistant (weight gain below 30%). Biochemical and morphological parameters, as well as histology, and signaling pathways involved in lipid metabolism, inflammation, and insulin sensitivity were investigated in eVAT and iSAT. The results showed unaltered body, total VAT and iSAT mass in obesity-resistant mice despite increased caloric intake. Leptin levels and glucose homeostasis were improved in these animals compared to the obese mice. In both eVAT and iSAT of the obesity-resistant mice, adipocyte size and lipolytic capacity were retained at control levels, while compared to the obese mice, preserved capacity for adipogenesis, improved local insulin sensitivity and the absence of inflammation were observed only in the eVAT. In conclusion, metabolic adaptation of eVAT rather than iSAT may have a substantial impact on the maintenance of the obesity-resistant phenotype with fewer metabolic complications, which could contribute to the improvement of existing obesity therapies.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109912"},"PeriodicalIF":4.8,"publicationDate":"2025-03-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143772717","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":"Modeling how iso-caloric macronutrient substitutions are longitudinally associated with plasma kynurenines in colorectal cancer survivors up to 12 months posttreatment.","authors":"Daniëlle D B Holthuijsen, Eline H van Roekel, Martijn J L Bours, Per M Ueland, Stéphanie O Breukink, Maryska L G Janssen-Heijnen, Joop L Konsten, Eric T P Keulen, Adrian McCann, Stefanie Brezina, Biljana Gigic, Dieuwertje E Kok, Cornelia M Ulrich, Matty P Weijenberg, Simone J P M Eussen","doi":"10.1016/j.jnutbio.2025.109910","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109910","url":null,"abstract":"<p><p>Dietary intake of several macronutrients is associated with plasma kynurenines after colorectal cancer (CRC), and kynurenines have been linked to health-related outcomes. It is unknown how macronutrient substitution affects plasma kynurenines, which may be relevant for developing guidelines to improve post-CRC quality of life through dietary changes. Using iso-caloric substitution models, we investigated how substituting one macronutrient with another is longitudinally associated with plasma tryptophan, kynurenines, and kynurenine ratios in CRC survivors. Measurements were performed at 6-weeks, 6-months, and 12-months posttreatment in 247 stage I-III CRC survivors. Macronutrient intake was measured by seven-day dietary records and plasma kynurenines by LC/MS-MS. For analysis, we applied linear mixed models with false discovery rate (FDR) to adjust for multiple testing. After FDR adjustment, substituting 100 kcal/day of total carbohydrates with 100 kcal/day of total protein was associated with higher plasma concentrations of kynurenic acid (KA), xanthurenic acid (XA), and a higher kynurenic acid-to-quinolinic acid (KA/QA) ratio. Substituting 100 kcal/day of total carbohydrates with 100 kcal/day of total fat was associated with higher tryptophan concentrations, higher KA/QA ratio, and a lower kynurenine-to-tryptophan ratio (KTR) and hydroxykynurenine ratio (HKr). Substituting 100 kcal/day of total fat with 100 kcal/day of total protein was associated with higher XA concentrations. Altogether, iso-caloric macronutrient substitutions, particularly substituting carbohydrates with protein or fat, were longitudinally associated with higher concentrations of potentially favourable kynurenines and ratios (i.e., KA, XA, and KA/QA ratio) and lower ratios with pro-inflammatory or neurotoxic properties (i.e., KTR and HKr) in CRC survivors up to 12-months posttreatment.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109910"},"PeriodicalIF":4.8,"publicationDate":"2025-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143753167","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":"Sulforaphanin ameliorates the damage of the Cyprinus carpio liver induced by Aeromonas hydrophila via activating AMPK pathway.","authors":"Jiaxiang Zhu, Bingke Wang, Jianshuang Ma, Changchang Pu, Lu Wang, Feng Yang, Yong Deng, Chunnuan Zhang","doi":"10.1016/j.jnutbio.2025.109911","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109911","url":null,"abstract":"<p><p>This study aims to explore how the sulforaphane (SFN) exerts a mitigating effect on the liver injury of Cyprinus carpio (C. carpio) caused by Aeromonas hydrophila (A. hydrophila). A total of 450 C. carpio. (40.2 ± 2.8 g) were randomly assigned to 5 groups, each consisting of 3 replicates. The control group was not infected with A. hydrophila and was fed with the ordinary commercial feed. The other different groups were attacked by A. hydrophila and fed four sulforaphane-graded diets (0, 10, 15 and 20 mg/kg) for 8 weeks. The findings indicated that supplementation SFN (15 and 20 mg/kg) could recover or even significantly reduce the levels of tumor necrosis factor-α (TNF-α) ,interleukin-1β (IL-1β) and IL-6 and increased the level of IL-10 in the liver by repressing the NF-κB signaling pathway compared to the only A. hydrophila-infection group (P < 0.05). Also, SFN supplementation increased the immunoglobulin M (IgM) level, complement 3 (C3) and C4 concentrations in comparison with the only A. hydrophila-infection group in the liver of C. carpio to enhance the immune function (P < 0.05). After that, transcriptome through KEGG enrichment analysis suggested that differentially expressed genes (DEGs) were associated with immunological diseases, as well as fat digestion and absorption pathways. Notably, these pathways include antigen processing and presentation, as well as the AMP-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor (PPAR) signaling pathways. In conclusion, it was determined that C. carpio fed with suitable amount (15 mg/kg) of SFN improved lipid deposition caused by A. hydrophila via regulating the lipid metabolism pathway.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109911"},"PeriodicalIF":4.8,"publicationDate":"2025-03-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143743050","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":"Zinc amino acid chelate and the Aryl Hydrocarbon Receptor (AHR) cooperate in improving the barrier function of a Caco-2 cell intestinal epithelium.","authors":"Xiuchuan Hu, Rui Wang, Peter Kille, Wolfgang Maret, Christer Hogstrand","doi":"10.1016/j.jnutbio.2025.109909","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109909","url":null,"abstract":"<p><p>Zinc and several physiologically relevant ligands of the Aryl Hydrocarbon Receptor (AHR) are nutrients that promote intestinal barrier function. We have identified that AHR activation upregulates the expression of zinc importers in the intestinal epithelium to increase intracellular zinc concentrations, which leads to improved epithelial barrier function. Here, we investigated if an amino acid chelate of zinc, in cooperation with AHR activation, can improve the barrier function of a differentiated Caco-2 cell epithelium. Functional assays of the Caco-2 cell epithelium demonstrate that both ZnSO₄ and a lysine and glutamic acid chelate of Zn, in combination with the physiological AHR agonist 6-formylindolo[3,2-b]carbazole (FICZ), increase expression of tight junction proteins at the mRNA and protein levels. FICZ increases uptake of zinc into the epithelium in the presence of ZnSO₄ or the amino acid Zn chelate in the medium to equal extents. We conclude that the lysine and glutamic acid chelate of Zn is as efficacious as ZnSO₄ in reducing permeability of the Caco-2 cell epithelium in the presence of FICZ. The results suggest that dietary supplementation with bioavailable forms of zinc together with nutritional AHR agonists may be beneficial in improving gut barrier function and help prevent inflammatory bowel disease (IBD).</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109909"},"PeriodicalIF":4.8,"publicationDate":"2025-03-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143743100","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":"Selenium alleviates high-fat diet induced hepatocyte lipid accumulation via exosome miR-22/FGFR1 pathway in grass carp.","authors":"Chi Wang, Xiaotian Zhang, Guohao Liu, Cheng Zhang, Pengju Li, Pan He, Sha Liu, Hong Ji, Haibo Yu","doi":"10.1016/j.jnutbio.2025.109907","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.109907","url":null,"abstract":"<p><p>The current study aims to investigate whether exosomal miRNAs are involved in lipid reduction by selenium (Se) in the liver of grass carp, through miRNA sequencing, transfection of miRNA mimic (miR-22m) or inhibitor (miR-22i), isolation of hepatocyte-derived exosomes and treatment, and detection of lipid metabolism-related genes and proteins. The miRNAs sequencing and bioinformatics revealed that miR-22 was most abundantly expressed in the differentially expressed miRNAs after selenium treatment, and was enriched in lipid metabolism-related pathways. Moreover, Se significantly up-regulated the miR-22 levels and reduced the lipid content in liver or hepatocytes of grass carp. Furthermore, the miR-22m significantly increased levels of miR-22 and reduced lipid content in grass carp hepatocytes, which were consistent with the Se-treatment. However, the miR-22i reversed these trends. Besides, the miR-22 suppressed the FGFR1-PI3K-AKT-mTOR signaling pathway and its downstream genes related to lipid synthesis. More importantly, the Se-treated hepatocyte-exosomes which were enriched in the miR-22 significantly reduced the triglycerides content in the oleic acid-treated hepatocytes. In summary, Se alleviated high fat-induced lipid accumulation in grass carp liver by up-regulating the expression of miR-22 which negatively regulates FGFR1 and its downstream regulatory genes. Moreover, exosomes participate in the lipid reduction by Se, which may be through carrying miR-22.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"109907"},"PeriodicalIF":4.8,"publicationDate":"2025-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143730553","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}