Journal of Nutritional Biochemistry最新文献_第8页

Kaempferol stimulates dermal papilla cells and upregulates Wnt/β-catenin signaling pathway for androgenetic alopecia treatment 山奈酚刺激真皮乳头细胞和上调Wnt/β-catenin信号通路治疗雄激素性脱发。

IF 4.9 2区医学

Journal of Nutritional Biochemistry Pub Date : 2026-03-01 Epub Date: 2025-12-01 DOI: 10.1016/j.jnutbio.2025.110214

Changjiang Zhao , Lingling Jia , Ruiyu Luo , He Yan , Zihan Li , Hua Jiang , Yufei Li

{"title":"Kaempferol stimulates dermal papilla cells and upregulates Wnt/β-catenin signaling pathway for androgenetic alopecia treatment","authors":"Changjiang Zhao , Lingling Jia , Ruiyu Luo , He Yan , Zihan Li , Hua Jiang , Yufei Li","doi":"10.1016/j.jnutbio.2025.110214","DOIUrl":"10.1016/j.jnutbio.2025.110214","url":null,"abstract":"<div><div>Androgenetic alopecia (AGA) is the most common form of progressive hair loss, marked by a multifaceted pathogenesis and a lack of effective pharmacological treatments to arrest its progression. Flavonoids have drawn considerable research attention for their potential in fostering hair regeneration, yet kaempferol (Kae), a well-researched flavone, remains unexplored as a therapeutic agent for AGA. This study delves into the mechanisms and efficacy of Kae in AGA treatment, employing a blend of <em>in vivo</em> and in vitro experiments, complemented by transcriptome sequencing and molecular docking techniques. In vitro, Kae exhibited no significant toxicity to dermal papilla cells (DPCs); instead, it enhanced DPCs proliferation and migration in a dose-dependent manner, and significantly mitigated dihydrotestosterone (DHT)-induced cellular damage. Transcriptomic analysis and RT-qPCR indicated that Kae modulates the Wnt/β-catenin signaling pathway. Molecular docking studies indicated that Kae has binding potential to β-catenin and Cyclin D1, pivotal proteins within this pathway. Subsequent immunofluorescence experiments and Western blot confirmed Kae’s ability to promote β-catenin nuclear translocation and inhibit DHT-induced downregulation of β-catenin and Cyclin D1. <em>In vivo</em>, oral Kae administration substantially promoted hair regeneration in an AGA mouse model, with efficacy on par with oral finasteride. In conclusion, this study presents robust evidence that Kae effectively stimulates hair growth by bolstering DPCs function and counteracting DHT-induced damage, thus holding promising therapeutic potential for AGA sufferers.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110214"},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145668615","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}

引用次数: 0

Dietary galactose enhances systemic lipid oxidation but decreases intestinal fatty acid oxidation in post-weaning female mice 饲粮半乳糖可增强断奶后雌性小鼠全身脂质氧化，但可降低肠道脂肪酸氧化。

IF 4.9 2区医学

Journal of Nutritional Biochemistry Pub Date : 2026-03-01 Epub Date: 2025-11-23 DOI: 10.1016/j.jnutbio.2025.110193

Ferran S. Fos-Codoner, Jaap Keijer, Melissa Bekkenkamp-Grovenstein, Evert M. van Schothorst

{"title":"Dietary galactose enhances systemic lipid oxidation but decreases intestinal fatty acid oxidation in post-weaning female mice","authors":"Ferran S. Fos-Codoner, Jaap Keijer, Melissa Bekkenkamp-Grovenstein, Evert M. van Schothorst","doi":"10.1016/j.jnutbio.2025.110193","DOIUrl":"10.1016/j.jnutbio.2025.110193","url":null,"abstract":"<div><div>Replacing part of dietary glucose with galactose in the early post-weaning diet of mice, mimicking extended breastfeeding, improves both short- and long-term physiological and metabolic health parameters. As the primary organ for nutrient absorption, the small intestine was hypothesized to play a key role in these effects.</div><div>Young, weaned mice underwent a 3 week dietary intervention comparing isocaloric diets with a monosaccharide fraction of galactose+glucose <em>versus</em> glucose. Physiological parameters were assessed in both sexes, while metabolic analyses, transcriptomics, and immunohistochemistry of the proximal small intestine were conducted in fed female mice.</div><div>Dietary galactose increased whole-body 24 h fatty acid oxidation (FAO), both absolute and relative to carbohydrate oxidation, without changes in body weight or energy expenditure. Contrasting, the small intestine showed lower expression of transcripts involved in FAO, along with reduced enterocytic lipid droplets. Carbohydrate metabolism remained unaffected, while reduced expression of NADPH-dependent and -independent antioxidant enzymes and the pentose phosphate pathway suggested a shift in local metabolism. Despite these intestinal changes, the liver showed no alterations in lipid catabolism, implicating other organs in the observed systemic FAO increase. In addition, <em>Ppargc1a</em>, central regulator of mitochondrial biogenesis was upregulated, which is in line with the known role of galactose in upregulating mitochondrial oxidative phosphorylation.</div><div>In conclusion, replacing half of post-weaning dietary glucose with galactose, mimicking prolonged lactose intake, profoundly affects substrate metabolism at both systemic and intestinal levels. We propose that reduced intestinal FAO redirects fatty acid oxidation to extra-intestinal, extra-hepatic tissues, driving the observed systemic metabolic benefits.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110193"},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145604597","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}

引用次数: 0

Bidirectional regulation of free fatty acid receptors and non-alcoholic fatty liver disease 游离脂肪酸受体与非酒精性脂肪肝的双向调节。

IF 4.9 2区医学

Journal of Nutritional Biochemistry Pub Date : 2026-03-01 Epub Date: 2025-11-10 DOI: 10.1016/j.jnutbio.2025.110180

Yiyu Lin , Yanglong Liu , Jianshen Liu , Jianxing Wu , Kunhua Wei , Jiao Guo , Zhengquan Su

{"title":"Bidirectional regulation of free fatty acid receptors and non-alcoholic fatty liver disease","authors":"Yiyu Lin , Yanglong Liu , Jianshen Liu , Jianxing Wu , Kunhua Wei , Jiao Guo , Zhengquan Su","doi":"10.1016/j.jnutbio.2025.110180","DOIUrl":"10.1016/j.jnutbio.2025.110180","url":null,"abstract":"<div><div>Free fatty acid receptor action is primarily in the area of energy modulation and maintenance of normal metabolism in the body. They have been identified and attributed to specific G protein-coupled receptors (GPCRs). Currently, the main findings include four receptors: FFAR1 to FFAR4. Free fatty acids (FFAs) with different carbon chain lengths respond to different FFAR. Short-chain fatty acids (C2-C6) bind specifically to FFAR2 and FFAR3, whereas medium-chain fatty acids (C6-C12) and long-chain fatty acids (C13-C21) target both FFAR1 and FFAR4. FFARs have been considered as potential target for the treatment of common metabolic diseases such as T2M, cardiovascular diseases and inflammatory bowel diseases. Nonalcoholic fatty liver disease is a common metabolic disorder and is often accompanied by various metabolic and cardiovascular diseases. The expression and modulation of FFARs in the body may be related to the development of nonalcoholic fatty liver disease. This article introduces the source, synthesis and metabolic pathways of fatty acids, and comprehensively summarizes the research on FFARs signal transduction and its physiological functions, the regulation between FFARs and NAFLD, and the prospect of FFARs-based treatment of NAFLD.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110180"},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145505138","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}

引用次数: 0

Dietary supplementation of n - 3 PUFAs ameliorates UV-induced photoaging and skin tumor via GPR120 activation 膳食补充n-3 PUFAs通过激活GPR120改善紫外线诱导的光老化和皮肤肿瘤。

IF 4.9 2区医学

Journal of Nutritional Biochemistry Pub Date : 2026-03-01 Epub Date: 2025-11-14 DOI: 10.1016/j.jnutbio.2025.110186

Shuzhan Shen, Qihang Chang, Yiting Zhao, Xidie Yin, Zhi Cao, Huan Xue, Qingyu Zeng, Xiuli Wang, Peiru Wang

{"title":"Dietary supplementation of n - 3 PUFAs ameliorates UV-induced photoaging and skin tumor via GPR120 activation","authors":"Shuzhan Shen, Qihang Chang, Yiting Zhao, Xidie Yin, Zhi Cao, Huan Xue, Qingyu Zeng, Xiuli Wang, Peiru Wang","doi":"10.1016/j.jnutbio.2025.110186","DOIUrl":"10.1016/j.jnutbio.2025.110186","url":null,"abstract":"<div><div>Chronic ultraviolet (UV) radiation induces cutaneous inflammation and immunosuppression, driving photoaging and skin carcinogenesis. <em>n</em> - 3 polyunsaturated fatty acids (PUFAs) have shown clinical efficacy in mitigating various inflammatory cutaneous diseases and neoplastic diseases via dietary supplementation. However, the precise molecular mechanisms by which <em>n</em> - 3 PUFAs prevent photoaging and carcinogenesis remain incompletely defined. In this study, transcriptomic analysis revealed that <em>n</em> - 3 PUFAs exert antiphotoaging effects by sustaining skin homeostasis through coordinated immunomodulation and anti-inflammatory actions. Multitimepoint sampling in murine models was employed to dynamically characterize stage-specific effects of <em>n</em> - 3 PUFAs during photoaging progression. Mechanistically, <em>n</em> - 3 PUFAs were noted to restore balanced M1/M2 ratios in both early and advanced stage of photoaged murine skin, thereby maintaining microenvironmental homeostasis. Moreover, <em>n</em> - 3 PUFAs were shown to counteract UV-induced immunosuppression by diminishing immunosuppressive cell accumulation. Overall, our findings highlight the crucial role of G protein-coupled receptor 120 (GPR120) as the pivotal mediator: its activation inhibits TAK1/NF-κB signaling and directs M2 macrophage skewing after UV exposure. This study elucidates the mechanism through which <em>n</em> - 3 PUFAs reverse photoaging, and lays the groundwork for enhancing the clinical applications of <em>n</em> - 3 PUFAs.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110186"},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145534750","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}

引用次数: 0

Short-term effect of Ketogenic diet and Low-calorie diet on Ketometabolism and lipid metabolism 生酮饮食和低热量饮食对酮代谢和脂质代谢的短期影响。

IF 4.9 2区医学

Journal of Nutritional Biochemistry Pub Date : 2026-03-01 Epub Date: 2025-11-18 DOI: 10.1016/j.jnutbio.2025.110188

Flora Bahrami , Elija Buetler , Katrin Freiburghaus , Patcharamon Seubnooch , Lia Bally , Jonathan Maurer , Christa E Flück , Reiner Wiest , Mojgan Masoodi

{"title":"Short-term effect of Ketogenic diet and Low-calorie diet on Ketometabolism and lipid metabolism","authors":"Flora Bahrami , Elija Buetler , Katrin Freiburghaus , Patcharamon Seubnooch , Lia Bally , Jonathan Maurer , Christa E Flück , Reiner Wiest , Mojgan Masoodi","doi":"10.1016/j.jnutbio.2025.110188","DOIUrl":"10.1016/j.jnutbio.2025.110188","url":null,"abstract":"<div><div>The ketogenic diet (KD) has shown therapeutic potential for epilepsy, neuroprotective effects, and, more recently, metabolic complications. In this study, we explored the impact of the KD on the promotion of ketometabolism and the improvement of dyslipidemia. To this end, we investigated the outcomes of two different diets, eucaloric KD and low-calorie diet (LCD), on ketogenesis, circulating intact lipids, bile acids, and neuro and pancreatic peptides. Based on our results, the concentration of ketone bodies, namely 3-hydroxybutyric acid, increased significantly by an average of ten and two times for KD and LCD, respectively. Additionally, the concentration of several triglyceride (TAG) species decreased up to 98.3% and 99.1% for KD and LCD, respectively, while these reductions were only significant for LCD. Moreover, our results showed that 3 d of KD led to an increase in the baseline concentration of pancreatic polypeptide 3-36, which suggests that short-term KD has the potential to suppress the appetite. Finally, no significant change in the baseline and kinetic postprandial concentration of bile acid species was observed during the KD. In conclusion, our findings suggest that the ketogenic diet, being less restrictive than the low-calorie diet, has a greater impact on ketometabolism. However, while KD reduces TAG species, this reduction is not statistically significant, unlike the significant decrease observed with LCD.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110188"},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145564174","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}

引用次数: 0

Alpha-linolenic acid regulates white adipose tissue lipolysis independent of background dietary protein α -亚麻酸调节白色脂肪组织的脂肪分解独立于背景膳食蛋白质。

IF 4.9 2区医学

Journal of Nutritional Biochemistry Pub Date : 2026-03-01 Epub Date: 2025-11-13 DOI: 10.1016/j.jnutbio.2025.110185

Siobhan E. Woods , Melissa Gonzalez-Soto , Alexa N. King , Frédéric Capel , David C. Wright , David M. Mutch

{"title":"Alpha-linolenic acid regulates white adipose tissue lipolysis independent of background dietary protein","authors":"Siobhan E. Woods , Melissa Gonzalez-Soto , Alexa N. King , Frédéric Capel , David C. Wright , David M. Mutch","doi":"10.1016/j.jnutbio.2025.110185","DOIUrl":"10.1016/j.jnutbio.2025.110185","url":null,"abstract":"<div><div>White adipose tissue (WAT) is an endocrine organ essential for maintaining whole-body energy balance by regulating fatty acid uptake, storage, and release. Emerging evidence indicates that omega-3 fatty acids have a role in modulating WAT lipid metabolism. While most studies have focused on marine-derived omega-3s, considerably less is known about alpha-linolenic acid (ALA). Previous research suggests that ALA may prevent or restore impaired lipolysis in dysfunctional WAT. The primary objective of this study was to examine the effects of ALA on WAT lipolytic activity and whether this varied with background dietary protein. Male C57BL/6N mice (<em>n</em>=16/group) were fed moderate-fat diets containing either 1% (low-ALA) or 3% (high-ALA) energy from ALA (provided by flaxseed oil), and either skim milk protein or a soy protein isolate for 8 weeks. Mice fed high-ALA diets showed increased body weight gain and WAT depot weights, reduced serum triglycerides, and increased serum glycerol levels. The higher serum glycerol levels in high-ALA fed mice were reflected in higher glycerol release from cultured adipose tissue explants stimulated with a β-adrenergic agonist. Markers of WAT lipolysis, including ATGL and phosphorylated HSL, were either lower or unchanged in mice fed high-ALA diets. Background dietary protein (from either dairy or soy) had little-to-no-effect on study endpoints. Our data suggests that increased dietary ALA intake improves circulating TAG levels while reducing markers of lipolysis in WAT depots. The increase in glycerol observed with high-ALA intake may point to a potential regulation of WAT glycerogenesis and/or aquaporin expression that warrants future investigation.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110185"},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145530736","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}

引用次数: 0

P-coumaric-acid ameliorates acute kidney injury induced by ischemia-reperfusion injury via suppressing ferroptosis 对香豆酸通过抑制铁下垂改善缺血再灌注急性肾损伤。

IF 4.9 2区医学

Journal of Nutritional Biochemistry Pub Date : 2026-03-01 Epub Date: 2025-11-07 DOI: 10.1016/j.jnutbio.2025.110175

Yuhang Gong , Jiang Zhu , Zijing Yuan , Jianheng Chen , Jie Song

{"title":"P-coumaric-acid ameliorates acute kidney injury induced by ischemia-reperfusion injury via suppressing ferroptosis","authors":"Yuhang Gong , Jiang Zhu , Zijing Yuan , Jianheng Chen , Jie Song","doi":"10.1016/j.jnutbio.2025.110175","DOIUrl":"10.1016/j.jnutbio.2025.110175","url":null,"abstract":"<div><div>AKI resulting from IRI has hindered the development of therapeutic drugs due to unclear pathogenesis. Natural herbal monomers, grounded in the concept of food and medicine sharing the same origin, may provide a novel direction for the development of AKI treatments. p-CA, which is abundantly found in vegetables, fruits, and grains, exhibits anti-apoptotic and antioxidant properties, mechanisms that are closely associated with the pathological processes of AKI. Therefore, p-CA could be developed as an effective therapeutic agent for the treatment of AKI. This study aims to elucidate the molecular mechanisms through which p-CA mitigates renal injury in AKI. Kidney injury was evaluated using HE and Masson staining. The expression of iron death-related proteins was assessed using ELISA, qPCR, iron assay, IF, and WB. p-CA inhibits renal damage induced by ischemia-reperfusion injury, regulates iron ion homeostasis in the kidneys, and concurrently suppresses the pathological process of ferroptosis. Additionally, p-CA improves renal injury induced by IRI <em>in vivo</em> and significantly inhibits ferroptosis. Furthermore, p-CA demonstrates notable protective effects against cell damage induced by H/R and Erastin in vitro. Mechanistically, this study reveals that p-CA significantly upregulates the expression of ferroptosis-related proteins, including SLC7A11 and GPX4, ultimately leading to effective alleviation of AKI. p-CA demonstrates significant efficacy in ameliorating kidney injury and inhibiting ferroptosis. The findings from this study are expected to provide experimental evidence for the development of novel therapeutics for AKI.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110175"},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145482571","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}

引用次数: 0

Maternal vitamin D deficiency during pregnancy impaired offspring’s spatial learning and memory ability: Insights into the role of the CaMKK2/AMPK/FoxO3a pathway 孕妇孕期维生素D缺乏会损害后代的空间学习和记忆能力：CaMKK2/AMPK/FoxO3a通路的作用

IF 4.9 2区医学

Journal of Nutritional Biochemistry Pub Date : 2026-03-01 Epub Date: 2025-11-24 DOI: 10.1016/j.jnutbio.2025.110196

Xiaoxia Sun , Yu Qiao , Yu Han , Yufei Hou , Jiongnan Wang , Shangyun Lu , Jia Wang , Fubin Qiu

{"title":"Maternal vitamin D deficiency during pregnancy impaired offspring’s spatial learning and memory ability: Insights into the role of the CaMKK2/AMPK/FoxO3a pathway","authors":"Xiaoxia Sun , Yu Qiao , Yu Han , Yufei Hou , Jiongnan Wang , Shangyun Lu , Jia Wang , Fubin Qiu","doi":"10.1016/j.jnutbio.2025.110196","DOIUrl":"10.1016/j.jnutbio.2025.110196","url":null,"abstract":"<div><div>Vitamin D deficiency (VDD) is a pressing global health concern, with pregnant women being identified as a high-risk population for VDD. Our previous study demonstrated that maternal VDD diet impaired placental development. Here, we aimed to investigate the effects of maternal VDD diet during pregnancy on offspring’s spatial learning and memory ability. Our results showed that maternal VDD diet resulted in a decreased vitamin D levels in dams and their offspring, reduced offspring’s body length and body weight, delayed offspring’s nerve reflex behavior and impaired offspring’s spatial learning and memory ability in Y maze and Morris water maze tests. Moreover, maternal VDD diet caused offspring’s neuronal damage and loss, decreased the expressions of neurotrophic factors. While, maternal vitamin D supplementation during pregnancy has positive improvement on the above indexes, and with the most obvious in first trimester supplement group. Moreover, proteomic analysis of the offspring’s hippocampal tissues was conducted to explore relative molecular mechanisms. Results showed that maternal VDD diet overactivated CaMKK2/AMPK/FoxO3a signaling pathway. While, CaMKK2 inhibitor STO-609 attenuated VDD-induced neuronal apoptosis and necrosis in vitro. Consistantly, maternal vitamin D supplementation during pregnancy also inhibited the overactivation of CaMKK2/AMPK/FoxO3a pathway. In conclusion, the present study provided novel insights into the mechanisms of maternal VDD on offspring’s spatial learning and memory ability.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110196"},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145634773","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}

引用次数: 0

Copper-induced duodenal injury: Unveiling the dual role of cuproptosis and ferroptosis via the FDX1/GPX4 axis 铜诱导的十二指肠损伤：通过FDX1/GPX4轴揭示铜下垂和铁下垂的双重作用

IF 4.9 2区医学

Journal of Nutritional Biochemistry Pub Date : 2026-03-01 Epub Date: 2025-11-10 DOI: 10.1016/j.jnutbio.2025.110181

Tao Zhang , Xueyan Dai , Huating Wang , Yang Hu , Xiaona Gao , Xueting Shu , Huabin Cao , Guoliang Hu , Chenghong Xing , Fan Yang

{"title":"Copper-induced duodenal injury: Unveiling the dual role of cuproptosis and ferroptosis via the FDX1/GPX4 axis","authors":"Tao Zhang , Xueyan Dai , Huating Wang , Yang Hu , Xiaona Gao , Xueting Shu , Huabin Cao , Guoliang Hu , Chenghong Xing , Fan Yang","doi":"10.1016/j.jnutbio.2025.110181","DOIUrl":"10.1016/j.jnutbio.2025.110181","url":null,"abstract":"<div><div>Copper (Cu) is an essential trace element for humans but also a common environmental pollutant. Excessive intake can lead to poisoning, yet the mechanisms by which it causes duodenal injury remain unclear. To investigate the involvement of cuproptosis and ferroptosis in this process, we conducted an experiment using 72 one-day-old Peking ducks, randomly assigned to four groups according to dietary Cu levels: control, 100 mg/kg Cu, 200 mg/kg Cu, and 400 mg/kg Cu. Our findings demonstrate that excessive Cu exposure markedly reduced body weight, caused pathological damage to the duodenum, and triggered oxidative stress. Mechanistically, Cu accumulation in tissues suppressed the expression of ATP7A, PDHB, and FDX1, while upregulating DLAT, Lip-DLAT and HSP70, thereby promoting cuproptosis. Subsequently, cuproptosis acts through the FDX1/GPX4 axis to elevate the expression of TfR1 and increase intracellular iron/ferrous ion levels, while reducing the expression of GPX4, SLC7A11, Cyt C, ISCU, FTH-1, and NAF1. These collective alterations ultimately induce ferroptosis. These changes exhibit a dose-dependent relationship with Cu. In summary, our study suggests that excessive Cu disrupts copper homeostasis, initiates cuproptosis, and perturbs iron metabolism through FDX1- and GPX4-mediated regulation, thereby triggering ferroptosis. These results provide new mechanistic insights into Cu-induced cytotoxicity.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110181"},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145505156","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}

引用次数: 0

Protective effects of pyrroloquinoline quinone in CNS disorders 吡咯喹啉醌对中枢神经系统疾病的保护作用。

IF 4.9 2区医学

Journal of Nutritional Biochemistry Pub Date : 2026-03-01 Epub Date: 2025-11-12 DOI: 10.1016/j.jnutbio.2025.110178

Sara Aboulhassane , Vishal Sangha , Reina Bendayan

{"title":"Protective effects of pyrroloquinoline quinone in CNS disorders","authors":"Sara Aboulhassane , Vishal Sangha , Reina Bendayan","doi":"10.1016/j.jnutbio.2025.110178","DOIUrl":"10.1016/j.jnutbio.2025.110178","url":null,"abstract":"<div><div>Pyrroloquinoline quinone (PQQ) is an enzyme belonging to the family of quinone cofactors (or quinoproteins) naturally found in soil and food. PQQ was initially discovered as an essential cofactor for bacterial dehydrogenases and has since been reported to be involved in several biological processes important for mammalian growth and development. Animal studies have demonstrated that insufficient dietary intake of PQQ can lead to notable deficits, including impaired growth and compromised reproductive outcomes. In more recent years, PQQ has been recognized for its neuroprotective effects in several <em>in vitro</em> and <em>in vivo</em> models of brain injury and disease, rendering it an attractive compound to be incorporated into treatment strategies for various neurological disorders. More specifically, PQQ has been reported to enhance mitochondrial function and mitigate inflammatory and oxidative stress responses in the central nervous system (CNS) through the activation of several signaling pathways. Additionally, PQQ has emerged as a promising compound that could be incorporated in treatment strategies for cerebral folate deficiency, a pediatric neurological condition characterized by suboptimal folate levels in the cerebrospinal fluid, leading to developmental delays, epilepsy, and other neurological symptoms. This review will address the biochemical properties, mechanism of action, and physiological roles of PQQ with a specific focus on its antioxidant and anti-inflammatory effects as well as its role in enhancing mitochondrial function. The therapeutic implications of these findings will be discussed, emphasizing PQQ’s potential as a novel pharmacological approach for the management of neurological disorders, including its emerging role in cerebral folate deficiency.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"149 ","pages":"Article 110178"},"PeriodicalIF":4.9,"publicationDate":"2026-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145523686","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}

引用次数: 0