Journal of Nutritional Biochemistry最新文献

{"title":"Role of vitamin D and omega 3 fatty acids in improving HDL biogenesis among multiple sclerosis patients via orchestrating CHROME/APOA1-AS/ABCA1/APOA1 milieu","authors":"Mai A. Abd-Elmawla ,&nbsp;Heba R. Ghaiad ,&nbsp;Mohammed M. Nooh ,&nbsp;Mai A. Amer ,&nbsp;Lobna Talaat El-Ghoneimy ,&nbsp;Noha A. Mehana","doi":"10.1016/j.jnutbio.2025.110007","DOIUrl":"10.1016/j.jnutbio.2025.110007","url":null,"abstract":"<div><div>Clinical approaches that could correct the disturbed lipid profile may improve neurological disturbances in multiple sclerosis (MS) patients. However, the underlying mechanisms are still not well understood. The study aimed to characterize the performance of vitamin D (Vit.D) and omega 3 fatty acid (ω3) in adjusting the lipid profile of MS patients via modulating CHROME/APOA1-AS/ABCA1/APOA1 along with sphingosine kinase (SPHK)-1/2, and sphingosine 1-phosphate receptors (S1PR)-1/5. 72 MS patients were recruited for this study; 25 received Vit.D, 21 received ω3, and 26 didn’t receive any supplementation. Blood samples were collected and then plasma were separated for further biochemical and molecular investigations. Both vit.D or ω3 improved the lipid profile in the studied groups as well as elevated the expression of the lncRNA CHROME, the concentrations of ABCA1 and ApoA1 along with lowering APOA1-AS relative to MS patients without supplementation. Vit.D supplementation group revealed higher levels of SPHK1 and lower levels of SPHK2, whereas ω3 supplementation reduced both S1PR1 and S1PR5 relative to the MS control group. This study demonstrated the beneficial role of Vit.D and ω3 supplementation in adjusting the lipid profile of MS patients via modulating ABCA1 and ApoA1 and their upstream regulators CHROME and APOA1-AS. The administration of Vit.D upregulated SPHK1 and downregulated SPHK2 gene expression. On the other hand, ω3 supplements downregulated S1PR1 and S1PR5 gene expression in MS patients.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110007"},"PeriodicalIF":4.8,"publicationDate":"2025-06-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144325998","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":"Microbial–purine metabolic crosstalk regulates colitis-related intestinal fibrosis: A multiomics and cohort analysis approach","authors":"Xiaoxuan Mai ,&nbsp;Jinzhen Wu ,&nbsp;Zhenyi Tian ,&nbsp;Le Liu ,&nbsp;Xiaoduan Zhuang ,&nbsp;Zhipeng Liu ,&nbsp;Ruiming Wan ,&nbsp;Bang Li ,&nbsp;Yuting Shi ,&nbsp;Bingsheng Li ,&nbsp;Xinying Wang","doi":"10.1016/j.jnutbio.2025.109984","DOIUrl":"10.1016/j.jnutbio.2025.109984","url":null,"abstract":"<div><div>Intestinal fibrosis (IF) is a severe complication of inflammatory bowel disease (IBD), often requiring surgical interventions. The modulating role of the microbial-metabolic link in IF remains unclear. We aimed to identify disturbances in microbiome–metabolome interactions during IF progression and recognize potential metabolic biomarkers. Compositional and functional signatures, along with murine IF progression, were determined through 16S rRNA sequencing and widely targeted metabolomics. Overall, 109 patients with IBD and 111 healthy controls (HCs) were enrolled and clinically evaluated. Correlations analyses were performed to reveal the relationship between microbial–purine metabolic alterations and disease markers. Gut microbiome analysis identified structural disruptions, including a reduction in uric acid (UA)-decomposed microbes and an increase in hyperuricemia-associated taxa (<em>P</em>&lt;.05), which contributed to impaired purine metabolism (<em>P</em>&lt;.05). Metabolomic profiling further indicated reprogramming of purine metabolism in fibrogenesis, as evidenced by elevated UA levels in fecal, colonic, and serum samples that correlated with inflammatory and fibrotic markers. In IBD patients, compared to HCs, serum UA (342.55±95.69 vs. 294.78±66.58 µmol/L) and UA/creatinine (UA/Cr) levels (5.17±1.57 vs. 4.40±1.28) were greatly increased (<em>P</em>&lt;.001) and positively correlated with the clinical and endoscopic activities, especially in CD patients. Serial measurements demonstrated elevated UA during stenosis formation. UA/Cr may be an independent risk factor (<em>P</em>=.006) for stenosis prognosis. Abnormal purine metabolism may regulate IF, as reflected in purine metabolism-related microbes and metabolites. Elevated serum UA and UA/Cr levels are promising biomarkers for detecting disease activity and predicting stenosis in IBD.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"144 ","pages":"Article 109984"},"PeriodicalIF":4.8,"publicationDate":"2025-06-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144302266","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 Supplement Myo-inositol on Meat Quality, Antioxidant Capacity, and Gene Expression in Procambarus clarkii.","authors":"Changchang Pu, Yuanyi Liu, Ruyi Sun, Bingke Wang, Aimin Wang, Chunnuan Zhang","doi":"10.1016/j.jnutbio.2025.110003","DOIUrl":"https://doi.org/10.1016/j.jnutbio.2025.110003","url":null,"abstract":"<p><p>This study aimed to explore how dietary Myo-inositol (MI) affects the meat quality, antioxidant capacity, and muscle development of Procambarus clarkii (P. clarkii). A total of 360 young P. clarkii were fed six diets containing graded levels of MI (0 (control), 500, 1000, 2000, 3000, and 4000 mg/kg diet) for 6 weeks. After the experiment, the abdominal muscle samples were collected from six groups of P. clarkii. Supplementing MI can increase the abdomen meat content and the content of free MI and phosphatidylinositol (PI) in the muscle tissue of P. clarkii. When an appropriate amount of MI is added to the feed, muscle meat quality will be beneficially improved, mainly reflected in water-holding capacity (WHC), elasticity, meat colour, etc. Compared with the control group, adding 1000 mg/kg of MI to the feed can significantly increase muscle L* value (P < 0.05) and reduce muscle centrifugal loss (P < 0.05). Moreover, when 1000 mg/kg of MI was added to the feed, the total essential amino acid (TEAA) and hydroxyproline (HYP) content of muscles were significantly higher than the control group (P < 0.05). Supplementing MI reduced muscle oxidative metabolite content (ROS, MDA, and LA), and increased antioxidant enzyme activity and related gene expression. These results suggest that dietary MI can activate the Nrf2/Keap1 signalling pathways, increasing muscle antioxidant enzyme activity. In addition, supplementing MI can activate the expression of crayfish GH-IGF axis-related genes. When 1000 mg/kg MI was added, the Mef2a, Mef2b, and IGF-1 genes expression levels were significantly higher than the control group (P < 0.05). In summary, supplementing 1000 mg/kg MI can regulate muscle amino acid metabolism by regulating the Nrf2/Keap1 signaling pathway to promote muscle development and improve meat quality.</p>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":" ","pages":"110003"},"PeriodicalIF":4.8,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293965","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":"1,25(OH)2D3 ameliorates DSS-induced intestinal ferroptosis through the SIRT3–SOD2–mtROS pathway","authors":"Hong-Qian Wang ,&nbsp;Ya-Wen Zhu ,&nbsp;Zi-Yue Dou ,&nbsp;Zhuo Chen ,&nbsp;Cheng-Cheng Tong ,&nbsp;Xue He ,&nbsp;Xiao-Han Ma ,&nbsp;Jing Guan ,&nbsp;De-Xiang Xu ,&nbsp;Xi Chen","doi":"10.1016/j.jnutbio.2025.109999","DOIUrl":"10.1016/j.jnutbio.2025.109999","url":null,"abstract":"<div><div>Ferroptosis has been shown to play a significant role in the pathogenesis of ulcerative colitis (UC). This study investigated the effects of 1,25(OH)₂D₃ supplementation on ferroptosis in dextran sulfate sodium (DSS)-evoked colitis. Intestinal VDR was reduced in UC patients. Accordingly, GPX4 was downregulated and ACSL4 was upregulated in the intestine of UC patients. Animal experiments indicated that vitamin D deficiency exacerbated DSS-induced intestinal ferroptosis in mice. Conversely, pretreatment with 1,25(OH)₂D₃ alleviated DSS-induced ferroptosis in mouse intestine. Similarly, 1,25(OH)₂D₃ supplementation inhibited DSS-induced ferroptosis in HT-29 cells. Furthermore, we found decreased intestinal SIRT3 protein and increased acetylated superoxide dismutase 2 (Ac-SOD2) in UC patients. Pretreatment with 1,25(OH)₂D₃ attenuated DSS-induced downregulation of SIRT3 and acetylation of SOD2 in both mouse intestine and HT-29 cells. Moreover, 1,25(OH)₂D₃ pretreatment inhibited mitochondrial reactive oxygen species (mtROS) in DSS-treated HT-29 cells. Finally, transfection with SIRT3 siRNA antagonized the protective effect of 1,25(OH)₂D₃ on ferroptosis in DSS-treated HT-29 cells. Overall, our results suggest that 1,25(OH)₂D₃ alleviates DSS-induced intestinal ferroptosis via the SIRT3-SOD2-mtROS pathway, further supporting the potential use of 1,25(OH)₂D₃ supplementation in UC treatment.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"144 ","pages":"Article 109999"},"PeriodicalIF":4.8,"publicationDate":"2025-06-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293878","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":"Fucoxanthin ameliorates vascular remodeling via attenuating oxidative stress in hypoxic pulmonary hypertension rats","authors":"Xu Zheng ,&nbsp;Jina Zhao ,&nbsp;Xiaoqin Jia ,&nbsp;Jinjin Pan ,&nbsp;Shuo Xu ,&nbsp;Dingyou Wang ,&nbsp;Junxia Li ,&nbsp;Yuke Ji ,&nbsp;Zhilong Zhu ,&nbsp;Muhammad Hasnain ,&nbsp;Zheng Sui ,&nbsp;Rui Wang ,&nbsp;Yuhui Yuan","doi":"10.1016/j.jnutbio.2025.110002","DOIUrl":"10.1016/j.jnutbio.2025.110002","url":null,"abstract":"<div><div>Hypoxic pulmonary hypertension (HPH) is a fatal cardiopulmonary disease characterized by pulmonary vascular remodeling, primarily resulting from abnormal proliferation of pulmonary artery smooth muscle cells (PASMCs). Fucoxanthin, a natural carotenoid with potent antioxidant activity, was investigated for its therapeutic potential in HPH, given the critical role of oxidative stress in disease pathogenesis. In this study, Sprague–Dawley rats were exposed to intermittent chronic hypoxia for 4 weeks to mimic severe HPH. The results demonstrated that fucoxanthin significantly reduced the elevated right ventricular systolic pressure (RVSP), alleviated right ventricular hypertrophy, and mitigated pulmonary artery remodeling in the HPH rats. Additionally, fucoxanthin enhanced superoxide dismutase (SOD) activity and glutathione (GSH)/glutathione disulfide (GSSG) ratio while decreasing malondialdehyde (MDA) levels in both lung tissues and serum of HPH rats. <em>In vitro,</em> fucoxanthin inhibited cell proliferation and migration, decreased reactive oxygen species (ROS) production in hypoxia-induced PASMCs, and improved cell viability in hypoxia-induced endothelial cells (ECs). Importantly, fucoxanthin reduced hypoxia-inducible factor 1 alpha (HIF-1α) expression in both lung tissues and PASMCs under hypoxia. Notably, fucoxanthin exhibited effects similar to those of 2-methoxyestradiol (2ME2), an inhibitor of HIF-1α, on cell proliferation and ROS production in hypoxia-induced PASMCs. Moreover, fucoxanthin treatment did not significantly alter HIF-1α expression, cell proliferation, or ROS production after 2ME2 blocked HIF-1α. Collectively, fucoxanthin suppressed hypoxia-induced oxidative stress primarily by regulating the HIF-1α-ROS pathway, thereby alleviating pulmonary remodeling in HPH. Our findings represent a promising therapeutic strategy for HPH by improving pulmonary vascular remodeling.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110002"},"PeriodicalIF":4.8,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293880","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 effect of flavan-3-ols on ovariectomy-induced bone loss in mice and the potential mechanisms","authors":"Shanshan Chen ,&nbsp;Jiapeng Huang ,&nbsp;Xuanrui Zhang ,&nbsp;Zhen Hong ,&nbsp;Yanbin Ye ,&nbsp;Xiaoping Lin ,&nbsp;Zheqing Zhang","doi":"10.1016/j.jnutbio.2025.110001","DOIUrl":"10.1016/j.jnutbio.2025.110001","url":null,"abstract":"<div><div>Flavan-3-ols (FLOs) have been reported to confer various health benefits, the majority of which reaching the colon for fermentation by gut microbiota. This study sought to examine the effects of FLOs on bone health and to evaluate the influence of gut microbiota on these effects. Using an ovariectomy-induced bone loss model in mice, the animals were administered either a low or high dose of FLOs, or a combination of FLOs with an antibiotic cocktail (Abs+FLOs). Compared to the control group, serum markers of bone formation, as well as bone quality as determined by micro-CT, were elevated in the groups supplemented with FLOs, particularly when combined with Abs. Furthermore, both FLOs and Abs+FLOs interventions significantly improved the levels of estrogen. However, no additional influence of FLOs on these markers was detected compared to the group supplemented with Abs alone. Analysis of 16S rRNA sequencing data revealed that the abundance of certain operational taxonomic units, such as <em>s__unclassified_Clostridia_UCG_014, s__unclassified_Ruminococcus</em>, and <em>s__unclassified_Lachnospiraceae</em>, was significantly reduced in osteoporotic mice but effectively reversed following the administration of FLOs. Transcriptomic analysis coupled with KEGG enrichment analysis indicated that Adrb3, Gdf10 (BMP3), Fosb, and Cxcl2, along with the PPARα/PGC-1/UCP1 signaling pathway, may potentially mediate the regulation of bone metabolism by flavanols. Collectively, the study uncovers the osteoprotective properties of flavan-3-ols, indicating that these effects may depend on the presence of gut microbiota.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110001"},"PeriodicalIF":4.8,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293882","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":"Dihydromyricetin, the active component of rattan tea alleviates symptoms of systemic sclerosis and atopic dermatitis through modulation of RORγt and IL17A production in T cells","authors":"Debanjan Sarkar ,&nbsp;Anik Pramanik ,&nbsp;Sourav Majumdar ,&nbsp;Dona Das ,&nbsp;Maniprabha Mahato ,&nbsp;Anup Pramanik ,&nbsp;Sankar Bhattacharyya","doi":"10.1016/j.jnutbio.2025.110000","DOIUrl":"10.1016/j.jnutbio.2025.110000","url":null,"abstract":"<div><div>Systemic sclerosis is a chronic inflammatory disease affecting the connective tissue of the human body by inducing fibrosis mainly in skin and lungs. Atopic dermatitis is another chronic inflammatory skin diseases that affects one-fifth of the population in developed countries. Dysregulation of the immune cells are one of the major characteristic features behind establishment of these two diseases. Several medicines are used to treat these diseases, but they have several side effects and high production cost. Low side effect and easy availability has generated renewed interest in studying plant derived medicines. Dihydromyricetin (Ampelopsin), a flavonoid compound extracted from stem and leaves of <em>Ampelopsis grossedentata</em> has shown potent anti-inflammatory property <em>in vitro</em>. In this study, bleomycin induced scleroderma and oxazolone induced dermatitis model were established in male BALB/c mice to check the <em>in vivo</em> efficacy of dihydromyricetin<em>.</em> Immunophenotyping and cytokine production were investigated by flow cytometry; immunofluorescence of skin was studied using confocal microscopy. We observed oral application of dihydromyricetin significantly reduced the inflammatory parameters in both diseases. We also found that dihydromyricetin dose dependently reduced the percentage of IL17A producing T cell population and reduced the total expression of RORγt in diseased T cells. Furthermore, we also found stable and strong binding of dihydromyricetin- RORγt protein complex. Stability of protein-ligand complex was examined by MD simulation study. We suggest that dihydromyricetin alleviates scleroderma and dermatitis symptoms by regulating the RORγt pathway.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"144 ","pages":"Article 110000"},"PeriodicalIF":4.8,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293879","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":"Insufficient iodine intake based on 24-h urinary iodine excretion leads to significant metabolic changes in pregnant women at early stages of pregnancy","authors":"Lijun Fan ,&nbsp;Shiqi Chen ,&nbsp;Ye Bu ,&nbsp;Zhiyong Liu ,&nbsp;Sihan Wang ,&nbsp;Wei Zhang ,&nbsp;Yan He ,&nbsp;Yashu Zhang ,&nbsp;Dianjun Sun","doi":"10.1016/j.jnutbio.2025.109995","DOIUrl":"10.1016/j.jnutbio.2025.109995","url":null,"abstract":"<div><div>The effects of iodine insufficiency during the first and second trimesters on both pregnant women themselves and their offspring exhibit insufficient consistent patterns. In this study, we aimed to address this issue by employing small molecule metabolomics. A total of 98 pregnant women in either the first or second trimester were recruited, with comprehensive data including basic information, 24-h urine samples and blood samples collected, and subsequent evaluation of birth outcomes for their offspring. The 24-h urinary iodine excretion (UIE) was detected and used as the dividing criterion to determine the iodine nutrition status of pregnant women. Serum metabolomics was performed by Ultra High Performance Liquid Chromatography Orbitrap Exploris Mass Spectrometry (UHPLC-OE-MS) platform. Differential metabolites as potential iodine deficiency biomarkers were selected by multivariate statistical analysis methods. Association analysis was used to further analyze the relationship between the potential biomarkers and neonatal birth outcomes. There was no significant difference in maternal thyroid function indicators and neonatal outcomes between the insufficient iodine intake group and the iodine adequate pregnant women. However, the metabolic profile of pregnant women with iodine insufficiency was significantly disturbed compared to these with iodine adequate. A total of 28 different metabolites were screened, which could be used as potential biomarkers of iodine deficiency. After adjusted age and pregnancy trimester, the expression of these biomarkers were also changed significantly. Furthermore, these markers were also related to fatty acid biosynthesis, tyrosine metabolism, tryptophan metabolism, arachidonic acid metabolism, and pentose and glucuronate interconversions. In addition, among these markers, 2-(4-Methyl-5-thiazolyl)ethyl octanoate was found to be associated with neonatal TSH, ACar(12:0), (9S,10E,12Z,15Z)-9-Hydroxy-10,12,15-octadecatrienoic acid showed a correlation with body length; whereas (9S,10E,12Z,15Z)-9-Hydroxy-10,12,15-octadecatrienoic acid was linked to body weight. In conclusion, iodine insufficiency during the first and second trimesters dose not result in overt adverse effects on pregnant women and their offspring. However, at the metabolic level, insufficient iodine intake may disrupt the metabolic profile of pregnant women and impact the development of their offspring.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"144 ","pages":"Article 109995"},"PeriodicalIF":4.8,"publicationDate":"2025-06-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144293881","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":"Perinatal leptin effects on hypothalamic brain-derived neurotrophic factor and energy balance-related gene regulation","authors":"Ana María Rodríguez ,&nbsp;Madhu Asnani-Kishnani ,&nbsp;Zhi Xin Yau-Qiu ,&nbsp;Sebastià Galmés ,&nbsp;Andreu Palou","doi":"10.1016/j.jnutbio.2025.109994","DOIUrl":"10.1016/j.jnutbio.2025.109994","url":null,"abstract":"<div><div>Brain-derived neurotrophic factor (BDNF) and leptin are essential in neurodevelopment and central regulation of feeding and energy balance. We studied the metabolic imprinting effects of physiological leptin supplementation during suckling in the brain of 5-week-old mouse pups. Leptin-treated animals showed lower cumulative food intake and increased energy efficiency, which was related to higher lean mass. Among different brain areas, hypothalamic expression of <em>Bdnf</em> and upstream transcription control-related genes, such as <em>Ppargc1a</em> and <em>Fndc5</em>, was increased by leptin supplementation, especially in females. This was accompanied by higher expression of energy balance key genes (such as <em>Prkaa2</em> and <em>Cpt1c</em>) and insulin/leptin signalling pathways, primarily in females, also with lower levels of total/phosphorylated AMPK, ACC or STAT3, mainly in males. In leptin-treated females, the exon IV <em>Bdnf</em> promoter showed increased methylation at a specific CpG site. Leptin supplementation during suckling can sex-dependently imprint hypothalamic gene expression, regulating the <em>Ppargc1a</em>/<em>Fndc5</em>/<em>Bdnf</em> pathway and related genes involved in energy balance, associated with a leaner phenotype, with a higher positive impact in females.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"144 ","pages":"Article 109994"},"PeriodicalIF":4.8,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258304","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 cadmium-induced Golgi stress via HSPB7/GM130/CX-43 axis in the heart of sheep","authors":"Jingni Li ,&nbsp;Shixuan Lin ,&nbsp;Fan Yang,&nbsp;Xueyan Dai,&nbsp;Chenghong Xin,&nbsp;Zhiwei Xiong,&nbsp;Feiyan Gao,&nbsp;Yun Wang,&nbsp;Jing Chen,&nbsp;Huabin Cao","doi":"10.1016/j.jnutbio.2025.109993","DOIUrl":"10.1016/j.jnutbio.2025.109993","url":null,"abstract":"<div><div>Cadmium (Cd) is a hazardous pollutant and its widespread exposure causes subcellular damage leading to cardiotoxicity. Selenium (Se) possesses the capacity to antagonize Cd toxicity, alleviating the organ damage induced by Cd. However, the relationship between Se mitigation of Cd exposure-induced myocardial damage and the Golgi apparatus remains to be further elucidated. Thus, 48 sheep were divided into four groups and treated with 1 mg Cd kg^-1·BW or/and 0.34 mg Se kg^-1·BW for 50 days. Results showed that Cd exposure caused myocardial myogenic fiber breakage, widened Z-line blurred and swelled of the Golgi apparatus. Cd exposure downregulated the levels of MyoD, MyoG, MyHC, CX-43 and GM130, upregulated the levels of cTnT, FLNC, GOLPH2 and GOLPH3, as well as reduced the number of fluorescent co-localization sites between CX-43 and GM130. Besides, Cd has increased the levels of heat shock proteins (HSPs) and decreased the number of fluorescent colocalization points between HSPB7 and GM130. However, co-treatment with Se ameliorated the above factors alterations associated with Cd exposure. In summary, Se attenuated Cd-induced myocardial injury and Golgi stress in sheep via activation of the HSPB7/GM130/CX-43 axis.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"144 ","pages":"Article 109993"},"PeriodicalIF":4.8,"publicationDate":"2025-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144258305","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}