Journal of Nutritional Biochemistry最新文献

{"title":"Hepatic lipidomics reveals lipid metabolism reprogramming response to different branched-chain amino acids interventions in nonalcoholic fatty liver disease of laying hens","authors":"Huafeng Jian ,&nbsp;Fengcheng Miao ,&nbsp;Yi Zheng ,&nbsp;Zhiyu Li ,&nbsp;Yao Shen ,&nbsp;Xiaoqian Long ,&nbsp;Bing Dai ,&nbsp;Hua Yang ,&nbsp;Xiaoting Zou ,&nbsp;Jiangang Ma","doi":"10.1016/j.jnutbio.2025.110161","DOIUrl":"10.1016/j.jnutbio.2025.110161","url":null,"abstract":"<div><div>Dietary restrictions of protein or branched-chain amino acids (BCAA) reprogram lipid metabolism and ameliorate metabolic health. However, dietary high protein (enriched in BCAA) or BCAA supplementation is effective for the therapy of nonalcoholic fatty liver disease (NAFLD), yet their metabolic effects on hepatic lipidomic changes and how the response to different BCAA interventions have not been systemically characterized. Here, we comprehensively analyzed the hepatic lipid landscape following different BCAA interventions and identified over 1400 unique lipid species. Strikingly, we find that High Leu intervention upregulates the synthesis of diacylglycerols (DGs) and monoacylglycerols (MGs), and preferentially downregulates glycerophospholipid metabolism and autophagy, but fails to activate the mitogen-activated protein kinase (MAPK) pathway. High Ile and High LeuIle interventions activate glycerophospholipid metabolism and induce the inhibition of MAPK and autophagy signaling pathways, whereas they are toxic and adverse to metabolic health and contribute to insulin resistance. Intriguingly, we find High BCAA feeding strongly reprograms the hepatic lipidome by activating the MAPK and autophagy signaling pathways and downregulating glycerophospholipid metabolism. By integrating multiomics approaches, we uncovered the cross-talk between amino acid metabolism, tryptophan metabolites, and lipidome remodeling in response to High BCAA intervention. Our results highlight the differential hepatic lipidome alterations in response to distinct dietary BCAA interventions and suggest that modest BCAA supplementation may serve as a new approach for treating and preventing metabolic dysfunction-associated fatty liver disease (MASLD) in humans and fatty liver hemorrhagic syndrome (FLHS) in laying hens.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"148 ","pages":"Article 110161"},"PeriodicalIF":4.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145401059","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":"UPP1 as a potential target for astilbin in ameliorating high-fat diet-induced bone loss via MAPK signaling: a study incorporating gut microbiota and metabolomics","authors":"Hui Su ,&nbsp;Luyao Liu ,&nbsp;Zechen Yan ,&nbsp;Jun Dong ,&nbsp;Xianze Chen ,&nbsp;Lin Wang ,&nbsp;Guangxin Huang ,&nbsp;WenXuan Guo ,&nbsp;Rujie Zhuang ,&nbsp;Yu Pan","doi":"10.1016/j.jnutbio.2025.110140","DOIUrl":"10.1016/j.jnutbio.2025.110140","url":null,"abstract":"&lt;div&gt;&lt;div&gt;This study aims to investigate the therapeutic effects and underlying mechanisms of astilbin on high-fat diet (HFD)-induced bone loss, focusing on its regulation of the UPP1-Mitogen-Activated Protein Kinase (MAPK) axis, metabolic reprogramming, and gut microbiota modulation. Male C57BL/6 mice were fed an HFD for 10 weeks to induce obesity and bone loss, followed by astilbin intervention at different doses (25, 50, 100 mg/kg/d) for 8 weeks. Body weight, serum biochemical parameters, bone microstructure (via micro-CT), and bone metabolism markers were assessed. Transcriptomic, 16S rRNA sequencing, and serum metabolomics analyses were performed to explore the molecular mechanisms. &lt;em&gt;In vitro&lt;/em&gt; experiments using bone marrow-derived mesenchymal stem cells (BMSCs) were conducted to evaluate osteogenic and adipogenic differentiation under palmitic acid and astilbin treatment. Astilbin significantly reduced HFD-induced weight gain, dyslipidemia, and bone loss, as evidenced by improved bone mineral density and trabecular bone structure. It upregulated osteogenic markers (RUNX2, alkaline phosphatase) while downregulating adipogenic markers (PPAR-γ) and inflammatory signals (p38MAPK). Transcriptomic analysis revealed that astilbin restored UPP1 expression, which was downregulated in HFD mice, and modulated the MAPK signaling pathway. Metabolomic analysis showed that astilbin downregulated proinflammatory lipids (&lt;em&gt;e.g.&lt;/em&gt;, prostaglandin F2α) and upregulated anti-inflammatory metabolites (&lt;em&gt;e.g.&lt;/em&gt;, sphingolipids and 4-hydroxyindole). Gut microbiota analysis demonstrated that astilbin restored microbial diversity, reduced the Firmicutes/Bacteroidetes ratio, and suppressed proinflammatory genera while promoting beneficial bacteria. &lt;em&gt;In vitro&lt;/em&gt;, astilbin enhanced osteogenic differentiation and inhibited adipogenic differentiation in bone marrow mesenchymal stem cells by regulating the UPP1-MAPK axis and reducing oxidative stress. Astilbin ameliorates HFD-induced bone loss by targeting the UPP1-MAPK axis, modulating lipid metabolism, reducing inflammation, and restoring gut microbiota homeostasis. These findings provide a comprehensive understanding of the multi-target mechanisms of astilbin in metabolic bone diseases and highlight its potential as a therapeutic agent for osteoporosis. The present study demonstrates significant novelty and innovation by elucidating astilbin’s multi-target therapeutic mechanism in HFD-induced bone loss, integrating for the first time its regulation of the UPP1-MAPK signaling axis with metabolic reprogramming and gut microbiota modulation, which has not been previously reported. Unlike existing literature focusing on isolated pathways, this work reveals astilbin’s unique capacity to simultaneously restore UPP1 expression, downregulate proinflammatory MAPK signaling, reshape gut microbiota composition (reducing Firmicutes/Bacteroidetes ratio), and modulate osteogenic-adipogenic differentiation through ","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"148 ","pages":"Article 110140"},"PeriodicalIF":4.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145274828","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":"Salivary amylase activity: A potential modulator of glucose homeostasis, insulin secretion, and appetite regulation","authors":"Gita Erta,&nbsp;Gita Gersone,&nbsp;Antra Jurka,&nbsp;Pēteris Tretjakovs","doi":"10.1016/j.jnutbio.2025.110154","DOIUrl":"10.1016/j.jnutbio.2025.110154","url":null,"abstract":"<div><div>This review examines the potential mechanisms by which SAA may influence glucose homeostasis and insulin sensitivity, emphasizing that current evidence is largely correlational and requires further investigation to establish causality. Salivary α-amylase (SAA), a key enzyme in the breakdown of dietary starch, has emerged as a potential regulator of glucose homeostasis, insulin secretion, and appetite control. Beyond its primary role in carbohydrate digestion, growing evidence highlights the influence of SAA on metabolic processes through its impact on early glucose release and its interaction with hormonal signaling pathways. This review examines the mechanisms by which SAA may affect insulin secretion and appetite regulation, focusing on its involvement in in incretin and other gut hormone-mediated pathways. Despite challenges posed by interindividual variability in SAA activity, its potential utility as a biomarker for metabolic health remains promising. Future research should prioritize uncovering the mechanistic links between SAA activity and metabolic outcomes, as well as establishing standardized protocols for its evaluation in both clinical and research contexts.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"148 ","pages":"Article 110154"},"PeriodicalIF":4.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145355049","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":"Clostridium sporogenes and its tryptophan metabolite indole -3- propionic acid repair antibiotic-induced muscle atrophy in mice","authors":"Xin Liu ,&nbsp;Yong Yang ,&nbsp;Xiaoyu Qiu ,&nbsp;Jing Wang ,&nbsp;Qi Wang ,&nbsp;Feiyun Yang ,&nbsp;Zuohua Liu ,&nbsp;Renli Qi","doi":"10.1016/j.jnutbio.2025.110167","DOIUrl":"10.1016/j.jnutbio.2025.110167","url":null,"abstract":"<div><div>Antibiotic-induced dysbiosis of the gut microbiota disrupts essential nutrient metabolism and bioactive compound production, contributing to systemic health deterioration including skeletal muscle atrophy. This study assessed the reparative effects of <em>Clostridium sporogenes</em> (CS) and its metabolite indole-3-propionic acid (IPA) on antibiotic-induced muscle atrophy in mice. A 14-day antibiotic treatment resulted in approximately a 90% reduction of gut microbiota in the mice, leading to an 11.92% decrease in grip strength and muscle atrophy characterized by a 31.22% reduction in myofiber diameter. After an 18-day intervention, both CS and IPA treatments effectively reversed these impairments, achieving over 60% grip strength recovery, near-normal muscle mass weight, and morphology. Notably, CS demonstrated superior myofiber recovery, with a diameter recovery rate of 31.74%, approximately double that of IPA-treated mice. Mechanistically, both CS and IPA enriched short-chain fatty acid (SCFA)-producing gut microbes such as <em>Lachnospiraceae</em> and <em>Lactobacillaceae</em>, positively reconstructing the microbiota and improving metabolic profiles. Specifically, the treatments restored IPA homeostasis, activated amino acid metabolic pathways including tryptophan and glutamate, and reduced toxic metabolites like chlorobenzene. Additionally, the expression of myogenic factors (<em>Myf5, Pax3, Pax7</em>) and atrophy-related genes (<em>Atrogin-1, MuRF-1</em>) returned to baseline levels in treated mice. These findings highlight the therapeutic potential of CS and IPA as nutritional interventions to mitigate antibiotic-associated muscle loss through microbial restoration, modulation of key metabolic pathways, and preservation of protein homeostasis.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"148 ","pages":"Article 110167"},"PeriodicalIF":4.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145445215","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":"High-fat diet exacerbates atopic dermatitis through alterations in the gut microbiome","authors":"Keito Tabata ,&nbsp;Nobutomo Ikarashi ,&nbsp;Ryotaro Yoshida ,&nbsp;Yui Shinozaki ,&nbsp;Yoshihiro Kato ,&nbsp;Risako Kon ,&nbsp;Yusuke Iwasaki ,&nbsp;Koki Yokoyama ,&nbsp;Rinka Saito ,&nbsp;Hiroyasu Sakai ,&nbsp;Tomoo Hosoe","doi":"10.1016/j.jnutbio.2025.110164","DOIUrl":"10.1016/j.jnutbio.2025.110164","url":null,"abstract":"<div><div>Atopic dermatitis (AD) is a chronic, relapsing skin disorder characterized by pruritic eczema. In addition to genetic predispositions, environmental factors such as diet are thought to contribute to the exacerbation of AD. The aim of this study was to provide scientific evidence on how environmental factors, particularly a high-fat diet (HFD), influence the pathogenesis of AD. AD was induced in NC/Nga mice fed an HFD through the application of 2,4-dinitrochlorobenzene. In the AD-HFD group, the expression levels of inflammatory markers (<em>Tnfa, Il1b, Ptgs2</em>, and <em>Nos2</em>) and AD-related factors (<em>Il4, Ccl17</em>, and <em>Tslp</em>) in the skin were significantly elevated compared with those in the AD group (mice fed a normal diet). Alteration of gut microbiota was observed in the AD-HFD group, characterized by a reduction in the abundances of <em>Bacteroides acidifaciens</em> and <em>Parabacteroides distasonis</em>, bacteria involved in short-chain fatty acid (SCFA) production. Moreover, the levels of acetate, propionate, and butyrate in the cecal contents were significantly decreased in the AD-HFD group. Fecal microbiota transplantation experiments revealed that alterations in the gut microbiota were associated with the exacerbation of AD symptoms. Furthermore, the administration of acetate alleviated the increase in the expression of skin inflammation markers and AD-related factors and the overall exacerbation of AD-like symptoms induced by the HFD. HFD intake exacerbates AD-like symptoms, and this exacerbation is linked to alteration of gut microbiota and a decrease in SCFA levels. These results suggest that acetate and acetate-producing bacteria may serve as potential tools for the prevention and treatment of AD.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"148 ","pages":"Article 110164"},"PeriodicalIF":4.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145452223","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":"Short-term exposure to lauric acid promotes adipose tissue lipolysis and reduces leptin expression via a PPARγ-dependent mechanism","authors":"Jesús Fernández-Felipe ,&nbsp;Laura Romero-Muñoz ,&nbsp;Victoria Cano ,&nbsp;Enrique Sánchez-Hita ,&nbsp;Lidia Morales ,&nbsp;Mariano Ruiz-Gayo ,&nbsp;Adrián Plaza ,&nbsp;Beatriz Merino","doi":"10.1016/j.jnutbio.2025.110163","DOIUrl":"10.1016/j.jnutbio.2025.110163","url":null,"abstract":"<div><div>Coconut oil has gained popularity for its potential health benefits, particularly regarding energy metabolism. One of its key components, lauric acid (LA), has been reported to reduce body fat and improve insulin sensitivity, making it beneficial for individuals with obesity and type 2 diabetes. However, its full metabolic effects remain unclear, and further research is needed.</div><div>This study investigated how LA influences fat cells (adipocytes) metabolism. Mice fed a diet containing 40% coconut oil showed elevated blood levels of glycerol and free fatty acids (FAs), indicating enhanced lipolysis. Gene expression analysis showed upregulation of pathways involved in FA uptake and metabolism. Concurrently, leptin expression in white adipose tissue (WAT), and circulating leptin levels, were reduced. Protein analysis revealed increased activation of lipid turnover regulators, including hormone-sensitive lipase (HSL) and perilipin 1 (PLIN1). In vitro, rat adipocytes treated with LA showed enhanced activity of metabolic processes that support fat oxidation, such as citrate synthase and carnitine palmitoyltransferase, along with a higher rate of oxygen consumption. Leptin production was likewise reduced by LA in vitro. The reduction in leptin levels and increased lipolysis appear to be partly mediated by the modulation of peroxisome proliferator-activated receptor gamma (PPARγ), a key regulator of lipid metabolism. While these effects support fat mobilization, the concurrent reduction in leptin expression may influence energy homeostasis, potentially counteracting the metabolic benefits of LA. These findings underscore the complex role of lauric acid in adipose tissue metabolism and raise questions about potential trade-offs.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"148 ","pages":"Article 110163"},"PeriodicalIF":4.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145422269","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":"Vitamin D3 and vitamin A synergistically prevent visuospatial memory impairment in mice model of the dopaminergic system disorder","authors":"Sirajo M. Umar ,&nbsp;Yusuf Usman ,&nbsp;Vivian Atuadu ,&nbsp;Kabir Shehu ,&nbsp;John C. Oyem ,&nbsp;Ibrahim M. Badamasi","doi":"10.1016/j.jnutbio.2025.110145","DOIUrl":"10.1016/j.jnutbio.2025.110145","url":null,"abstract":"<div><div>Motor, visual, and cognitive decline are early signs of dopaminergic system dysfunction (DSD), yet the mechanisms underlying associated visuospatial memory impairment are poorly understood. This study evaluated visuospatial memory in DSD and the neuroprotective effects of vitamins D3 and A. Animals were grouped as NS (control), -D2 (15 mg/kg Haloperidol), -D2+VD (Haloperidol + 800 IU vitamin D3), -D2+VA (Haloperidol + 1000 IU vitamin A), -D2+(VD+VA) (Haloperidol + vitamins D3 and A), and -D2+D2 (Haloperidol + 10 mg/kg Bromocriptine). Visuospatial memory was assessed using the visual water box and Y-maze tests. Brain regions and retina were analyzed for histology, immunohistochemistry, oxidative stress, and ELISA for TNF-α, IL-6, IL-4, IL-13, and dopamine. DSD induced significant visuospatial memory deficits, decreased SOD, IL-4, and IL-13, and increased TNF-α, IL-6, LDH, MDA, reactive astrocytes, degenerating neurons, and extracellular fibrils. Vitamin D alone was moderately effective, while combined vitamin D and A treatment more effectively regulated IL-6, IL-13, MDA, and reactive astrocytes in the prefrontal cortex and hippocampus. Other parameters were similarly improved by single or combined treatment. Dopaminergic system dysfunctions are linked to visuospatial memory impairment due to increased cytotoxicity, pro-inflammatory cytokines, oxidative stress, neural alterations, and reactive astrocyte expression, leading to reduced dopamine concentration in the PFC, HPC, visual cortex, and retina. Administration of vitamin A and D is more potent in providing a defensive mechanism by downregulating oxidative stress, reactive astrocytes, and their associated proinflammatory cytokines. All of which contribute to the regulation of dopamine levels.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"148 ","pages":"Article 110145"},"PeriodicalIF":4.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145301510","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":"Stigmasterol mitigates cholesterol gallstone formation by modulating bile acid metabolism and gut microbiota in mice fed a lithogenic diet","authors":"Dazhang Deng ,&nbsp;Yutong Xie ,&nbsp;Ya Wang ,&nbsp;Shan Wang ,&nbsp;Zhixin Li ,&nbsp;Tingyi Mo ,&nbsp;Honghui Guo","doi":"10.1016/j.jnutbio.2025.110147","DOIUrl":"10.1016/j.jnutbio.2025.110147","url":null,"abstract":"<div><div>Stigmasterol (STG) has demonstrated cholesterol-lowering properties; however, its influence on the bile acid (BA) metabolic profile and its potential in preventing cholesterol gallstone formation remain unclear. This study explores the inhibitory effects of STG on cholesterol gallstone development under a lithogenic diet (LD). Female C57BL/6 mice were fed either an LD or an LD supplemented with STG (L-STG) for 16 weeks. Ultra-performance liquid chromatography-tandem mass spectrometry (UPLC-MS/MS) was employed to quantify BAs in colon contents, serum, and gallbladder bile, while 16S rRNA gene sequencing analyzed gut microbiota composition. The results demonstrated that STG supplementation significantly reduced the cholesterol saturation index in mouse bile compared to the LD group, thereby inhibiting cholesterol crystal formation and mitigating gallbladder and liver damage. In the L-STG group, BA hydrophobicity was decreased, and secondary BA levels were markedly reduced, particularly the hepatotoxic deoxycholic acid. Additionally, STG enhanced gut microbiota α-diversity, reversed LD-induced alterations in microbial relative abundance, and especially curbed the abnormal expansion of BA–metabolizing bacteria. These findings suggest that STG can attenuate the overproduction of secondary BAs, thereby alleviating liver injury and facilitating BA excretion. Ultimately, this leads to reduced biliary cholesterol saturation and inhibition of gallstone formation.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"148 ","pages":"Article 110147"},"PeriodicalIF":4.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145313159","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":"Vitamin A acts as a potent suppressor of selenoprotein P with potential relevance for multivitamin supplementation","authors":"Sophia Karmeli ,&nbsp;Thilo Samson Chillon ,&nbsp;Rajas Sane ,&nbsp;Maria Schwarz ,&nbsp;Uwe Gröber ,&nbsp;Julian Hackler ,&nbsp;Anna P. Kipp ,&nbsp;Lutz Schomburg","doi":"10.1016/j.jnutbio.2025.110142","DOIUrl":"10.1016/j.jnutbio.2025.110142","url":null,"abstract":"<div><div>Multivitamin supplementation is a widely used strategy to prevent disease, slow the ageing process, improve quality of life and extend life span, although recent clinical findings do not support these claims. Since selenium (Se) deficiency is associated with morbidity and mortality risk, we tested the hypothesis that certain vitamins interfere with the regular biosynthesis of the Se transporter selenoprotein P (SELENOP).</div><div>Human liver cancer cells (HepG2) were treated with different concentrations of folic acid, nicotinamide, nicotinic acid, pyridoxal phosphate, thiamine, vitamin A, vitamin C, vitamin D2, vitamin D3, vitamin E, vitamin K and vitamin B12. Secreted SELENOP was quantified by ELISA and characterized by Western blot analysis. SELENOP transcript levels and promoter activity were determined, and resveratrol as a negative and thyroid hormone as a positive modulator were included for comparison.</div><div>The concentration of extracellular SELENOP decreased twofold in response to micromolar concentrations of vitamin A. The SELENOP transcript concentration decreased to 70% after incubation with 1 µM vitamin A, and a moderate concomitant decrease in SELENOP core promoter activity was observed. Co-incubation experiments of vitamin A with the active thyroid hormone T3 revealed dose-dependent effects and suggested competitive activities of these two modifiers of SELENOP expression in opposite directions.</div><div>We conclude that vitamin A is able to suppress hepatic SELENOP biosynthesis and secretion, which may confer health risks in self-administered or clinically indicated supplementation with retinoids, especially in individuals with marginal Se intake and status.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"148 ","pages":"Article 110142"},"PeriodicalIF":4.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145313132","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":"Supplementation with refined Brazil nut oil (Bertholletia excelsa) during pregnancy and lactation improves physical, biochemical and hepatic parameters in rat offspring","authors":"Ana Paula de Mendonça Falcone ,&nbsp;Larissa Maria Gomes Dutra ,&nbsp;Maria Elizângela Ferreira Alves ,&nbsp;Thales Daniel Oliveira de Lima e Silva ,&nbsp;Januse Míllia Dantas de Araújo ,&nbsp;Diogo Leonardo Santos Silva ,&nbsp;Glaucia Veríssimo Faheina Martins ,&nbsp;Juliano Carlo Rufino Freita ,&nbsp;Vanessa Bordin Viera ,&nbsp;Juliana Késsia Barbosa Soares","doi":"10.1016/j.jnutbio.2025.110150","DOIUrl":"10.1016/j.jnutbio.2025.110150","url":null,"abstract":"<div><div>This study evaluated the impact of maternal consumption of crude and refined Brazil nut oil on the physical, biochemical, and hepatic parameters of offspring in both male and female rats. Three maternal groups were formed: control (CG), crude oil (CO), and refined oil (RO), treated with 3,000 mg/kg of oil during gestation and lactation. The offspring were divided into male and female groups. Crude Brazil nut oil consumption resulted in increased body weight, total and mesenteric fat, as well as elevated coronary and cardiovascular risk indices. Conversely, the refined oil consumption reduced retroperitoneal fat and lowered the same risk indices. Both oils affected plasma triglycerides and cholesterol levels, with refined oil showing better results in lipid profiles, particularly by increasing HDL. The CO-F group exhibited higher blood glucose, while the RO-F group had lower glucose levels compared to CO-F. Changes in hepatic enzymes were observed, along with higher deposition of saturated fatty acids (SFA) and a reduction in mono and polyunsaturated fatty acids (MUFA and PUFA) in the liver of the offspring treated with crude oil. Lipid peroxidation was lower in the oil-treated groups compared to the control group. The effects were similar between male and female offspring. It was concluded that refined oil provided superior benefits compared to crude oil, improving biochemical parameters and hepatic health in the offspring.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"148 ","pages":"Article 110150"},"PeriodicalIF":4.9,"publicationDate":"2026-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145318404","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}