Journal of Nutritional Biochemistry最新文献

{"title":"Type 3 resistant starch from Canna edulis improves Parkinson’s symptoms, including behavioral function and nerve damage, in Parkinson’s model rats by regulating the gut–brain axis","authors":"Nan Zhang,&nbsp;Fangyuan Zhao,&nbsp;Tingting Miao,&nbsp;Nan Wang,&nbsp;Jiahui Wu,&nbsp;Shuting Tan,&nbsp;Xiang Wang,&nbsp;Xier Lihou,&nbsp;Yan Li,&nbsp;Yang Li,&nbsp;Feng Ou,&nbsp;Maochun Xiao,&nbsp;Aji Li,&nbsp;Rongting Min,&nbsp;Shiyao Su,&nbsp;Xueyong Wang","doi":"10.1016/j.jnutbio.2025.110191","DOIUrl":"10.1016/j.jnutbio.2025.110191","url":null,"abstract":"<div><div>Intestinal microorganisms affect the pathogenesis of Parkinson’s disease (PD) and, therefore, are a new research focus of PD treatment. Type 3 resistant starch from <em>Canna edulis</em> (Ce-RS3) regulates gut microbes and has prebiotic properties. The effects include decreased blood lipids, weight, and inflammation, as well as increased glycolipid metabolism. There are few reports on the use of prebiotics alone in the treatment of Parkinson's. In this study, based on the gut–brain axis, the pharmacological effects and related mechanisms of Ce-RS3 on PD were studied by analyzing intestinal bacteria and brain transcriptomics. Ce-RS3 improved motor function in PD model rats over a defined period and repaired PD-induced inflammation-related organ and neural damage. In addition, Ce-RS3 increased the number of short-chain fatty acid-producing, and other beneficial, bacteria. Transcriptomics showed that Ce-RS3 decreased inflammatory gene expression, upregulated the expression of the protein homeostasis-related gene <em>Hspb1</em> and downregulated the expression levels of the protein aggregation-related genes <em>Hdac6</em> and <em>Ubd</em>. Therefore, we hypothesized that Ce-RS3 plays a role in the treatment of PD by regulating the α-synuclein-related pathway through the brain–gut axis and protecting the neural tissues. This study provides a new intervention plan for the prevention and treatment of PD.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110191"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145668641","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":"Curcumin alleviates murine ulcerative colitis by modulating Tfh-B cell crosstalk via the CD40/CD40L costimulatory pathway","authors":"Ji Yu ,&nbsp;Yazhen Liu ,&nbsp;Jiaqi Huang ,&nbsp;Xiyan Zhu ,&nbsp;Duanyong Liu ,&nbsp;Haimei Zhao ,&nbsp;Bailing Deng ,&nbsp;Youbao Zhong","doi":"10.1016/j.jnutbio.2025.110256","DOIUrl":"10.1016/j.jnutbio.2025.110256","url":null,"abstract":"<div><div>Ulcerative colitis (UC) progression is closely associated with dysregulated T follicular helper (Tfh)-B cell crosstalk, a process are centrally mediated through the CD40/CD40L costimulatory pathway. This study aimed to investigate whether curcumin (Cur) alleviates UC by regulating Tfh-B cell crosstalk via modulation of this pathway. Mice with dextran sulfate sodium (DSS)-induced UC were administered were treated with Cur for 14 consecutive days. Tfh and B cell subsets were analyzed using flow cytometry, while CD40/CD40L gene and protein expression were assessed via qRT-PCR and WB. Cellular spatial interactions were examined through immunofluorescence. Additionally, molecular docking, molecular dynamics simulations and surface plasmon resonance (SPR) were performed to evaluate Cur's binding to the CD40/CD40L complex. Cur treatment significantly reduced the disease activity index, restored colon length, ameliorated histological damage, and suppressed proinflammatory cytokines (<em>e.g.</em>, IL-6, IL-21) as well as IgG levels. Mechanistically, Cur downregulated significantly CD40L⁺ Tfh cells and CD40⁺ B cells, and inhibited significantly key GC transcription factor Bcl-6 and plasma cell differentiation regulator Blimp-1. Molecular simulations confirmed that Cur stably binds to the CD40/CD40L interface through van der Waals forces and electrostatic complementarity, effectively blocking their interaction. The evidence from kinetic and competitive SPR assays demonstrates that Cur not only exhibits strong binding affinity by directly targeting CD40L, but also concentration-dependently blocks its interaction with CD40, resulting in significant functional inhibition of the CD40/CD40L signaling axis. Collectively, these findings demonstrate that Cur ameliorates UC by inhibiting the CD40/CD40L complex, which disrupts pathological Tfh-B cell crosstalk and ultimately restores gut immune homeostasis.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110256"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145889540","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 disodium fumarate relieves high-concentrate diet-induced hepatic injury by inhibiting endoplasmic reticulum stress, mitochondrial dysfunction and autophagy via epigenetic modifications in lactating hu sheep","authors":"Nana Ma,&nbsp;Wan Xie,&nbsp;Huimin Shi,&nbsp;Shendong Zhou,&nbsp;Hongzhu Zhang,&nbsp;Guangjun Chang,&nbsp;Xiangzhen Shen","doi":"10.1016/j.jnutbio.2025.110254","DOIUrl":"10.1016/j.jnutbio.2025.110254","url":null,"abstract":"<div><div>A high-concentrate diet fed to ruminants induced the release of LPS from the rumen to the liver. Dietary disodium fumarate (DF) fed to ruminants helps restore rumen homeostasis by improving the pH of the rumen fluid. However, the effects of dietary disodium fumarate on hepatic injury induced by high-concentrate diet have not been thoroughly explored. Eighteen lactating Hu sheep with rumen fistula were randomly divided into three groups: the low-concentrate diet group (LC, forage:concentrate=7:3, <em>n</em>=6), the high-concentrate diet group (HC, forage:concentrate=3:7, <em>n</em>=6) and the high-concentrate diet with DF supplementation group (FHC, 10g DF per sheep daily, <em>n</em>=6). After 8 weeks, the rumen fluid, portal vein and hepatic blood and liver tissue were collected for analysis. A high-concentrate diet decreased the pH of the rumen fluid and increased the LPS concentration in portal vein blood, resulting in morphological damage and an inflammatory response. GRP78-regulated unfolded protein response receptors and CHOP were upregulated, indicating ER stress; The imbalance between fusion and fission, mitophagy and PGAM5 upregulation indicated the mitochondrial damage in the liver of the HC group. Dietary DF supplementation relieved these hepatic injuries, accompanied by reduced autophagy. The level of methylation and chromatin compaction of ER stress- and autophagy-related genes were also increased by DF supplementation. These epigenetic modifications were negatively correlated with the mRNA expression of the target genes. Therefore, DF supplementation alleviated the inflammatory response, ER stress, and mitochondrial damage, not only by reducing LPS release but also through epigenetic modifications in the livers of Hu sheep fed a high-concentrate diet.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110254"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145900715","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":"Lycopene protects against myocardial ischemia-reperfusion injury by inhibiting FABP3-mediated pyroptosis in cardiac microvascular endothelial cells","authors":"Yuetong Sha ,&nbsp;Yawen Xie ,&nbsp;Xue Guan ,&nbsp;Xinran Wang ,&nbsp;Qianhui Zhang ,&nbsp;Yonggang Cao ,&nbsp;Pilong Shi ,&nbsp;Hongli Sun","doi":"10.1016/j.jnutbio.2026.110270","DOIUrl":"10.1016/j.jnutbio.2026.110270","url":null,"abstract":"<div><div>Cardiac microvascular damage exhibits a significant association with myocardial ischemia/reperfusion injury (MI/RI) development, which correlates with mitochondrial dysfunction. Lycopene has demonstrated pharmacological efficacy against cardiovascular diseases. Nevertheless, the potential roles and underlying mechanisms through which lycopene influences MI/RI remain incompletely understood. This study aimed to investigate the effect of lycopene on cardiac microvascular endothelial cells (CMECs) function in a rat model of MI/RI. This investigation sought to elucidate lycopene’s role in MI/RI and its mechanistic foundation. A rat MI/RI model was employed, and multiple experimental approaches were conducted, encompassing quantitative real-time polymerase chain reaction, western blot analysis, immunofluorescence microscopy, enzyme-linked immunosorbent assay, molecular docking, and molecular dynamics simulations. <em>In vitro</em> studies involved the establishment of a hypoxia-reoxygenation model using CMECs to evaluate lycopene’s contribution to pyroptosis suppression and mitochondrial dysfunction prevention. Lycopene was found to enhance mitochondrial function through inhibition of the YTHDF1/E2F8/FABP3 axis in CMECs, suppress cGAS-STING signaling pathway activation, reduce cellular inflammatory responses, and inhibit cellular pyroptosis. These effects ultimately resulted in improved CMECs function, enhanced microvascular integrity, and increased perfusion and oxygen delivery to cardiomyocytes.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110270"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145994425","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 inulin mediates the molecular mechanism of intestinal metabolites to alleviate high salt diet-induced chronic kidney disease in mice","authors":"Qinglin Qu,&nbsp;Huajing Gao,&nbsp;Xue Gao,&nbsp;Peihua Li,&nbsp;Yanquan Mou,&nbsp;Xiangrui Kong,&nbsp;Xintong Tan","doi":"10.1016/j.jnutbio.2026.110269","DOIUrl":"10.1016/j.jnutbio.2026.110269","url":null,"abstract":"<div><div>It is recognized that excessive dietary salt intake is a critical factor contributing to chronic kidney disease (CKD). A high-salt diet (HSD) disrupts the balance of the gut microbiota, but the molecular mechanisms linking gut dysbiosis to target organ damage remain unclear. This study identified dietary prebiotic inulin (INU) as a potent regulator of the gut-short-chain fatty acid-kidney axis, capable of counteracting HSD-induced CKD. Sequencing analysis showed that INU selectively enriched <em>Bifidobacterium</em> and <em>Faecalibaculum</em> while downregulating <em>Desulfovibrio</em>. This microbiome shift restored intestinal tight junction proteins and reduced serum lipopolysaccharide (LPS) levels, thereby inhibiting TLR4/NF-κB-mediated renal inflammation. Notably, the effects of direct SCFA supplementation align with the renal protective effects of INU, confirming the critical role of the gut-kidney axis. Our study reveals INU as a dietary strategy that combats HSD-induced CKD via SCFAs produced by the microbiota, offering new insights into the gut-SCFAs-kidney axis as a therapeutic target.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110269"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145994409","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 eicosapentaenoic and docosahexaenoic acids reduce oxylipins that provide early mediators of colonic inflammation induced by chemotherapy","authors":"Sarah Ruth Parsons ,&nbsp;Irma Magaly Rivas-Serna ,&nbsp;Peter Odion Isesele ,&nbsp;Md Monirujjaman ,&nbsp;Abha Dunichand-Hoedl ,&nbsp;Aducio Leonel Thiesen ,&nbsp;Michael Thomas Clandinin ,&nbsp;Vera Christine Mazurak","doi":"10.1016/j.jnutbio.2025.110192","DOIUrl":"10.1016/j.jnutbio.2025.110192","url":null,"abstract":"<div><div>Combination chemotherapy, irinotecan+5-fluorouracil, treats advanced colorectal cancer but causes intestinal toxicity mediated by cytokines and oxylipins. The objective of this study is to determine the effect of dietary eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA) on cytokines and the balance of oxylipins in colon tissue after chemotherapy. Ward colon tumors were implanted into female Fischer 344 rats (13–14 weeks old, n=56) and grew for 2 weeks before initiating chemotherapy (day 0). Subsequently, rats were maintained on the control diet (n=32) or switched to the EPA+DHA diet (n=24), an isocaloric diet that differed mainly in EPA and DHA content. Rats were euthanized on day 0 (baseline), 2, 4 and 8. The reference (no tumor, n=8) and baseline D0 (with tumor, n=8) groups did not receive chemotherapy. Cytokines, phospholipid fatty acids, and oxylipins in colon tissue were compared between the diets and over days post-chemotherapy. Feeding EPA+DHA resulted in a 9- and 2-fold increase in colon phospholipid by day 8 mirrored by a 10- and 2-fold increase in total oxylipins derived from EPA and DHA, respectively. Incorporation of EPA and DHA by day 2 prevented an increase in pro-inflammatory arachidonic acid (AA)-derived oxylipins after chemotherapy, including prostaglandin (PG) D₂, PGE₂, 6-keto-PGF_1α, thromboxane B₂, and 5-hydroxyeicosatetraenoic acid. Displacement of AA by EPA and DHA in colonic membrane attenuates early inflammatory lipid oxylipins. Dietary EPA+DHA may mitigate intestinal perturbations in colorectal cancer patients receiving irinotecan+5-fluorouracil.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"150 ","pages":"Article 110192"},"PeriodicalIF":4.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145604641","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":"Ketogenic diet attenuates high fat diet induced obesity in rats: insights into hepatic and intestinal tissues","authors":"Nada F. Abo El-Magd ,&nbsp;Nehal M. Ramadan ,&nbsp;Yomna F. Hassan ,&nbsp;Amr M. Mahmoud ,&nbsp;Maha M. Azzam ,&nbsp;Salma M. Eraky","doi":"10.1016/j.jnutbio.2025.110237","DOIUrl":"10.1016/j.jnutbio.2025.110237","url":null,"abstract":"<div><div>The rising global prevalence of obesity and its impact on health and economy make finding available safe treatment an urgent need. Ketogenic diet represents trendy dietary intervention, while underlying molecular mechanisms remains unclear. Twenty-four male Sprague-Dawley rats were randomized into three groups: Control (maintained on conventional chow diet for 24 weeks), HFD (fed High-fat diet (HFD) for 24 weeks), keto (fed HFD for 12 weeks, then ketogenic diet for additional 12 weeks). Effect of ketogenic diet on serum metabolomics using Ultra Performance Liquid Chromatography coupled with Liquid Chromatography on both positive and negative modes; hepatic tissue using histopathological examination, enzyme-linked immunosorbent assay (ELISA), Real time Polymerase Chain Reaction, proteome array detection; intestinal tissue using histopathological examination, ELISA and adipose tissue using histopathological examination were evaluated. The ketogenic diet reduced rat weight, food intake, epididymal fat mass, and blood glucose level compared to HFD group. Furthermore, it resulted in a decrease in serum methionine, linolenic acid, Lyso Phosphatidylcholine (PC) (15.0:0.0), Lyso PC (18.0:0.0) with hepatic repression of fibroblast growth factor 21 (FGF21), and type II cell surface protein/ Dipeptidyl peptidase 4, Intercellular Adhesion Molecule 1, Insulin growth factor-1, Lipocalin-2, Serpin E1, tissue inhibitor of matrix metalloproteinase-1, receptor for advanced glycation end products and induction of Farnesoid X receptor (FXR), hepatocyte growth factor (HGF) which leads to hepatic antioxidant effects and histopathological amelioration. In addition, the ketogenic diet caused intestinal induction of melanocortin-4 receptors/ glucagon-like peptide 1 pathway, which causes intestinal antioxidant effects and histopathological amelioration. Thus, ketogenic diet stated potential anti-obesity effect that mitigates HFD-induced organ damage through the modulation of key metabolic and signaling networks.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"150 ","pages":"Article 110237"},"PeriodicalIF":4.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145763186","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":"Jujuboside A ameliorates glomerular podocytes lipotoxicity in diabetic mice by YY1-mediated promotion of intracellular cholesterol transport and efflux","authors":"Ying Liu ,&nbsp;Dandan Pan ,&nbsp;Pinyan Zhang ,&nbsp;Yuting Shao ,&nbsp;Yinhua Kong ,&nbsp;Zhenzhou Jiang ,&nbsp;Wenjing Zhu ,&nbsp;Houwen Wang ,&nbsp;Xinghan Liu ,&nbsp;Sitong Qian ,&nbsp;Tao Wang ,&nbsp;Xia Zhu ,&nbsp;Tingting Yang ,&nbsp;Qian Lu","doi":"10.1016/j.jnutbio.2025.110231","DOIUrl":"10.1016/j.jnutbio.2025.110231","url":null,"abstract":"<div><div>Glomerular podocytes injury represents a critical pathological hallmark of diabetic kidney disease (DKD), in which lipotoxicity plays a central pathogenic role. Our previous investigations in type 2 diabetes mellitus (T2DM) have demonstrated that Jujuboside A (Ju A), a triterpene saponin isolated from Semen <em>Ziziphi Spinosae</em> (SZS), exerted dual therapeutic effects in T2DM by ameliorating hepatic steatosis and renal dysfunction. However, the role of podocytes lipid metabolism in Ju A-mediated protection against DKD remain undefined prior to the present study. In this work, we reported that Ju A significantly attenuated glomerular podocytes injury and lipotoxicity in DKD, while concurrently improving renal function and preserving glomerular morphology. Mechanistically, Yin Yang 1 (YY1)-mediated alleviation of lipotoxicity contributed to the protective effect of Ju A against glomerular podocytes injury, primarily by promoting intracellular cholesterol transport and efflux. In conclusion, our findings demonstrated that Ju A mitigated lipid overload in glomerular podocytes by modulating cholesterol homeostasis via YY1, which not only intercepted the pathological progression of DKD but also provided a potential therapeutic target (YY1) and candidate agent (Ju A) for DKD intervention.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"150 ","pages":"Article 110231"},"PeriodicalIF":4.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145763162","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":"Lnc-Gm26626 in visceral adipose tissues participates in energy metabolism via IDH3α-associated tricarboxylic acid cycle activity","authors":"Haoneng Tang ,&nbsp;Fen Xiao ,&nbsp;Yaru Chen ,&nbsp;Chenyi Tang ,&nbsp;Yue Guo ,&nbsp;Huixuan Wu ,&nbsp;Yinghui Zhou ,&nbsp;Houde Zhou","doi":"10.1016/j.jnutbio.2025.110243","DOIUrl":"10.1016/j.jnutbio.2025.110243","url":null,"abstract":"<div><div>The identification of novel long noncoding RNAs (lncRNAs) is involved in visceral adipose tissue development under fasting and refeeding conditions may be unravel the mechanisms of diet induced obesity. In this study, adult mice were subjected to fasting and refeeding intervention and mesenteric adipose tissue was extracted for transcriptome sequencing. Lnc-Gm26626 was identified and its role on tricarboxylic acid cycle (TCA) and isocitrate dehydrogenase 3α (IDH3α) expression was investigated using adenovirus-mediated gene interference. <em>In vivo</em> experiments were further performed to clarify whether lnc-Gm26626 affected the plasticity of adipose tissues. A total of 3,570 differentially expressed lncRNAs and 5,032 differentially expressed mRNAs were identified, lnc-Gm26626 was regulated by external nutritional stimulation and was observed to translocate from the nucleus to the cytoplasm under high glucose conditions. The knockdown of lnc-Gm26626 could inhibit the expression of IDH3α in vitro; AAV-mediated lnc-Gm26626 knockdown increased the fat content of mesenteric adipose tissues and alleviated the fluctuations in glucose and lipid metabolism during fasting and refeeding. Collectively, we identified lnc-Gm26626 as a novel regulator of energy metabolism that participate in the response to energy restriction by regulating IDH3α expression in the TCA cycle, thereby affecting visceral adipose tissue plasticity in male mice.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"150 ","pages":"Article 110243"},"PeriodicalIF":4.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145819694","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":"Bovine milk fat and cancer risk: A double-edged sword?","authors":"Laura Elaine Strittmatter ,&nbsp;Alban Piotrowsky ,&nbsp;Luigi Marongiu ,&nbsp;Sascha Venturelli ,&nbsp;Christian Leischner","doi":"10.1016/j.jnutbio.2025.110233","DOIUrl":"10.1016/j.jnutbio.2025.110233","url":null,"abstract":"<div><div>Among the many macro- and micronutrients contained in cow's milk, one of the most important is the lipid fraction. While the nutritional and physiological benefits of milk consumption after the first years of life are the subject of some debate, there also appear to be conflicting views on the health aspects of the milk lipids, including their involvement in cancer.</div><div>Positive <em>in vitro</em> and/or <em>in vivo</em> data on growth-inhibiting or cytotoxic effects are available for lipid components of milk such as sphingomyelins and their degradation products or various hydroxy fatty acids. Isomers of linoleic acid and branched-chain fatty acids have also been shown to have anticarcinogenic potential in animal models by inducing apoptosis.</div><div>On the other hand, there is evidence of an association between increased cancer mortality and the consumption of high-fat milk, which contradicts the tumor-protecting effects observed <em>in vitro</em> and <em>in vivo</em>. Consumption of high-fat dairy products appears to be associated with an increased risk of developing types of cancer compared to low-fat dairy or other topical soy-based alternatives.</div><div>There are ambiguous results for an anticarcinogenic effect of various lipid constituents of cow's milk as well as for an association between general milk fat consumption and the occurrence especially of breast, colorectal, and prostate tumors.</div><div>Whether the effects observed in epidemiological studies can be attributed to milk lipids or whether the promising preclinical data on their anti-cancer efficacy can be transferred to humans remains unclear at present, therefore this review summarizes the latest findings.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"150 ","pages":"Article 110233"},"PeriodicalIF":4.9,"publicationDate":"2026-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145751892","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}