Journal of Nutritional Biochemistry最新文献

{"title":"The interaction of ascorbic acid with hemoglobin: Relevance to hemin release and lipid peroxidation","authors":"Shi-Ya Peng,&nbsp;Naihao Lu,&nbsp;Rong Tian","doi":"10.1016/j.jnutbio.2025.110246","DOIUrl":"10.1016/j.jnutbio.2025.110246","url":null,"abstract":"<div><div>The interactions between L-ascorbic acid (<em>i.e.</em>, Vitamin C, VC) and bovine hemoglobin (Hb) were comprehensively analyzed using fluorescence, circular dichroism, UV−vis absorption spectra and molecular docking method, to elucidate the structural mechanisms through which VC altered Hb redox states and stabilities. VC interacted with the central cavities of Hb to form Hb-VC complex via static quenching mechanism involving nonradiative energy transfer, with van der Waals forces and hydrogen bonds playing predominant roles in the binding processes. VC was surrounded by residues such as α1-Thr137, α1-Ser138, α1-Tyr140 and α1-Arg141 residues. After that, the binding of VC would narrow the crevices near the heme domain of Hb, which converted ferric (met-) Hb to ferrous (oxy-) Hb and deoxy-Hb state and suppressed hemin liberation (level of free hemin was 4.35 µM (Hb alone) and 2.77 µM (Hb-VC complex)). Moreover, VC significantly inhibited Hb-catalyzed lipid peroxidation in liposome and washed muscle, which was probably due to the conversion to oxy-Hb state and reduced dissociation of hemin (not free iron). In accordance with its effects on Hb redox states and stability, VC effectively maintained the red color of hemeprotein during the storage. Altogether, the attenuation of free hemin release from Hb molecule represents a new mechanism towards the anti-oxidant capacity of VC in Hb-containing foods.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110246"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145846686","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 zinc deficiency regulates the ROS/TLR4/NF-κB pathway to induce pancreatic inflammation and cell death in mice","authors":"Ziyi Li,&nbsp;Yao Xue,&nbsp;Kan Li,&nbsp;Man Qian,&nbsp;Fuhan Wang,&nbsp;Ji-long Luo,&nbsp;Xue-jiao Gao","doi":"10.1016/j.jnutbio.2026.110262","DOIUrl":"10.1016/j.jnutbio.2026.110262","url":null,"abstract":"<div><div>Zinc (Zn) deficiency disrupts redox homeostasis in the body. The pancreas is a vital digestive and endocrine organ of the body, and its normal functional operation cannot proceed without the involvement of Zn. In this study, we established in vivo mouse models, including the normal Zn group (CG, 34 mg Zn/kg), Zn-deficient group (LZn, 2 mg Zn/kg), and Zn-supplemented group (HZn, 100 mg Zn/kg), as well as an in vitro Zn-deficient model of Mouse INsulinoma 6 (MIN6) cells. We systematically investigated the effects of Zn deficiency on pancreatic oxidative stress, inflammation, and cell death. The results showed that Zn deficiency significantly decreased the activities of α-amylase and lipase in the pancreas, and led to pancreatic histological damage. Through flow cytometry and detection of antioxidant enzyme activities, it was found that Zn deficiency induces excessive accumulation of reactive oxygen species (ROS) and malondialdehyde (MDA) in the pancreas, and inhibits antioxidant enzyme activities. Using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and Western blot, it was observed that Zn deficiency activates the TLR4/NF-κB pathway and significantly increases the expression of the NLRP3 inflammasome and inflammatory factors. Furthermore, Zn deficiency significantly upregulates the expression of apoptosis-related factors (Bax, Caspase-3, Caspase-7, Caspase-9) and necroptosis-related factors (RIPK1, RIPK3, MLKL). Treatment with the antioxidant N-acetylcysteine (NAC) reduces the level of ROS and inhibits the activation of the TLR4/NF-κB pathway, thereby alleviating Zn deficiency-induced inflammation and cell death. Taken together, Zn deficiency induces pancreatic inflammation and cell death by regulating the ROS/TLR4/NF-κB pathway.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110262"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145948793","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":"Complex interactions between stress, nutrition, gut microbiota, and infectious diseases and their impact on health in global conflicts: A narrative review","authors":"Pavlo Petakh ,&nbsp;Iryna Halabitska ,&nbsp;Halyna Petrecka ,&nbsp;Wolfgang Huber ,&nbsp;Oleksandr Kamyshnyi","doi":"10.1016/j.jnutbio.2026.110267","DOIUrl":"10.1016/j.jnutbio.2026.110267","url":null,"abstract":"<div><div>Following the global recovery from the COVID-19 pandemic, wars and conflicts have escalated to levels unseen since the Cold War. It is well known that conflict is accompanied not only by significant losses among both military personnel and civilians but also by rising levels of stress and stress-related disorders within the general population. Stress is bidirectionally connected with the state of the gut microbiota through the gut–brain axis. Dietary factors and eating behaviours also play crucial roles in shaping gut microbiota composition. On the one hand, conflict negatively affects food availability and dietary patterns, leading to reduced meal frequency and potentially diminishing microbiota diversity. On the other hand, stress-induced alterations in eating behaviour, such as bulimia or anorexia, can further impair gut microbiota composition. Additionally, individuals in conflict zones face heightened risks of infectious diseases due to disrupted vaccination schedules, poor sanitation, and limited access to clean drinking water. Stress-related immune changes may increase susceptibility to infections and raise the likelihood of adverse outcomes. Moreover, the frequent use of antibiotics to treat infections during conflicts contributes to reduced gut microbiota diversity.</div><div>This review narratively examines the complex interactions among stress, immune responses, dietary patterns, infectious diseases, and gut microbiota in conflict-affected areas, and provides new perspectives on the role of artificial intelligence in modelling such comorbid pathologies.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110267"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145994268","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":"Natural products as modulators of ferroptosis: Therapeutic implications and molecular mechanisms in disease treatment","authors":"Weifang Tong ,&nbsp;Xupeng Mu ,&nbsp;Haitao Xu ,&nbsp;Xunzhe Yin","doi":"10.1016/j.jnutbio.2026.110259","DOIUrl":"10.1016/j.jnutbio.2026.110259","url":null,"abstract":"<div><div>Ferroptosis is a regulated form of cell death characterized by iron-dependent lipid peroxide accumulation and is implicated in the pathogenesis of various diseases, including cancer, neurodegenerative disorders, diabetes, and cardiovascular diseases. Natural products, with their unique chemical scaffolds and multitarget pharmacological effects, have recently been recognized as potent modulators of ferroptosis, offering promising drug-like properties. This review comprehensively summarizes the molecular mechanisms underlying ferroptosis, encompassing iron metabolism, lipid peroxidation, and the SLC7A11-GSH-GPX4 antioxidant axis, and systematically categorizes natural products such as terpenoids, flavonoids, alkaloids, saponins, and polyphenols based on their structural classes and mechanisms of action. These compounds modulate ferroptosis through various pathways, including iron chelation, ROS regulation, and key protein interactions, demonstrating efficacy in both experimental and preliminary clinical settings across a spectrum of diseases. In oncology, natural compounds can sensitize tumors to chemotherapy and overcome drug resistance by activating ferroptotic cell death. Conversely, their antiferroptotic actions protect against tissue injury in nononcological diseases such as neurodegenerative conditions, metabolic disorders, and organ injury. Nevertheless, their application remains limited by restricted availability, compositional complexity, and unstable pharmacokinetic features. Advances in nano-delivery systems and synthetic biology are highlighted as promising strategies to overcome these barriers. Overall, natural products represent a valuable resource for developing novel ferroptosis-targeting therapies, with significant implications for future drug discovery and therapeutic innovation in a wide range of human diseases.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110259"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145906281","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 naringenin alleviates experimental autoimmune encephalomyelitis in mice partially via estrogen receptor-mediated pathway","authors":"Chaolei Jin ,&nbsp;Qiaozhen Zhu ,&nbsp;Tong Wang ,&nbsp;Zejin Liu ,&nbsp;Hang Wu ,&nbsp;Xinli Niu ,&nbsp;Junpeng Wang","doi":"10.1016/j.jnutbio.2026.110266","DOIUrl":"10.1016/j.jnutbio.2026.110266","url":null,"abstract":"<div><div>Multiple sclerosis (MS) is a T-cell-mediated autoimmune disease of the central nervous system (CNS) characterized by inflammation, demyelination, axonal injury, and loss of oligodendrocytes. Disease severity is influenced by sex hormones, particularly estrogens, which protects against MS and its animal model, experimental autoimmune encephalomyelitis (EAE). However, its clinical use is limited by risks such as thrombosis and reproductive tumors. Naringenin, a citrus-derived flavonoid, exhibits anti-inflammatory and neuroprotective properties and has been reported to possess phytoestrogenic activity. In this study, we investigated whether dietary naringenin alleviates autoimmune neuroinflammation in a mouse model of MS with estrogen deficiency induced by ovariectomy. Using a combination of network pharmacology, molecular docking, and <em>in vivo</em> experiments, we examined the effects of naringenin on EAE progression, immune cell responses, cytokine profiles, and estrogen receptor (ESR) signaling. Network pharmacology identified common targets of naringenin, estrogen, and MS, and molecular docking showed stable binding to ESR1. In ovariectomized EAE mice, naringenin attenuated EAE progression via dampening antigen-specific T cell responses, decreasing TNF-α, IL-6, and IL-1β, IFN-γ and IL-17A and increasing anti-inflammatory cytokines IL-10 and TGF-β. Furthermore, naringenin raised serum estradiol and CNS ESRα expression, and its benefits were partially reduced by the ESR antagonist ICI182,780, suggesting ESR signaling contributes to, but does not fully explain, naringenin’s immunomodulatory actions. Overall, these findings demonstrate that dietary naringenin ameliorates autoimmune neuroinflammation in an estrogen-deficient EAE model through mechanisms partially dependent on estrogen receptor signaling, supporting its potential as a dietary or adjunctive strategy for MS.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110266"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145994392","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":"Schisandrin B alleviates sulfolane-induced liver injury via the APOA1/ROS/NF-κB signaling pathway","authors":"Yuechen Xing ,&nbsp;Bo Zhang ,&nbsp;Shuo Jin ,&nbsp;Youtong Guo,&nbsp;Yueru Chen,&nbsp;Lili Chen,&nbsp;Yue Wang","doi":"10.1016/j.jnutbio.2025.110255","DOIUrl":"10.1016/j.jnutbio.2025.110255","url":null,"abstract":"<div><div>Sulfolane is a widely used industrial solvent and emerging groundwater contaminant. Sulfolane has hepatotoxicity, but the molecular mechanisms remain poorly understood. Schisandrin B (Sch B), a bioactive lignan isolated from <em>Schisandra chinensis</em>, has been shown to exert hepatoprotective effects. To elucidate the mechanisms underlying sulfolane-induced liver injury and to determine whether Sch B protects against this toxicity by modulating the APOA1/ROS/NF-κB signaling axis. Male C57BL/6 J mice were administered sulfolane (0, 10, 30 or 300 mg/kg) by oral gavage for 28 d, with or without Sch B (8 mg/kg). Liver injury was assessed using histopathology, serum biochemistry, hepatic lipid deposition, ROS levels, and inflammatory marker expression. Bioinformatic analyses integrating “sulfur compound” and “liver injury” datasets were used to identify candidate pathways. The protective effects of Sch B were investigated through APOA1 gene knockdown, APOA1 overexpression, treatment with the antioxidant NAC, and molecular docking experiments of Sch B with APOA1. Sulfolane caused dose-dependent steatosis, oxidative stress and inflammation in mouse liver and AML12 cells. sulfolane suppressed APOA1, increased ROS and activated NF-κB and downstream cytokines. Sch B restored APOA1 expression, reduced ROS accumulation and NF-κB–dependent cytokine production, and markedly improved biochemical and histological indices of liver injury <em>in vivo</em> and <em>in vitro</em>. Sulfolane-induced hepatotoxicity is mediated by suppression of APOA1 and subsequent activation of the NF-κB signaling pathway in a ROS-dependent manner. Schisandrin B protects the liver against this injury by modulating the APOA1/ROS/NF-κB axis.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110255"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145878572","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":"Myeloid monoamine oxidase A protects against glucose intolerance, insulin resistance and weight gain in high-fat diet-fed mice by preventing the hyperactivation of macrophages","authors":"Seonwook Kim ,&nbsp;Matthew R. Eber ,&nbsp;Alessandro G. Salerno ,&nbsp;Elena Boudyguina ,&nbsp;Reto Asmis","doi":"10.1016/j.jnutbio.2025.110257","DOIUrl":"10.1016/j.jnutbio.2025.110257","url":null,"abstract":"<div><div>The aim of this study was to determine the role of myeloid monoamine oxidase A (Mao A) in diet-induced obesity (DIO). Ten-week-old male and female LysMCre^tg/tg (CTL) and LysMCre^tg/tgMaoA^fl/fl (Mao A_Myeloid^−/−) mice were fed a high-fat diet for 20 week. Male but not female mice with myeloid Mao A deficiency showed increased weight gain, increased visceral adipose tissue (AT) weight as well as elevated fasting blood glucose and leptin levels. However, both male and female Mao A_Myeloid^−/- mice showed increased insulin resistance of the AT and glucose intolerance. Mao A mRNA levels were reduced by 90% and 94% in bone marrow-derived macrophages (BMDM) from male and female Mao A_Myeloid^−/- mice, respectively, but neither Mao A mRNA expression nor protein levels or Mao A activity in AT were altered by myeloid Mao A deficiency. Targeted gene profiling of M_TNFα+IFNγ and M_IL-4-polarized BMDM from Mao A KO mice and 129S1 strain-matched control mice revealed that Mao A deficiency amplifies the expression of polarization state-specific marker genes in BMDM from male mice but affects only a few selected marker genes in female polarized BMDM. Myeloid Mao A protects male but not female mice from AT inflammation, AT expansion and DIO, possibly by suppressing the polarization of monocyte-derived macrophages recruited into the AT. However, myeloid Mao A deficiency promoted insulin resistance in AT and glucose intolerance in both male and female mice suggesting that macrophage Mao A in other tissues contributes to the maintenance of glucose tolerance and homeostasis.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110257"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145900796","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 a high-fat diet leads to neuroinflammation and impairs memory and cholinergic signaling in the hippocampal CA3 region of male mice","authors":"Suleyma Oliveira Costa ,&nbsp;Iracema Monteiro Silva ,&nbsp;Wenicios Ferreira Chaves ,&nbsp;Andrea Maculano Esteves ,&nbsp;Beatriz Franco ,&nbsp;Leticia Martins Ignácio-Souza ,&nbsp;Marciane Milanski ,&nbsp;Michael Glenn Ross ,&nbsp;Mina Desai ,&nbsp;Marcio Alberto Torsoni ,&nbsp;Adriana Souza Torsoni","doi":"10.1016/j.jnutbio.2026.110274","DOIUrl":"10.1016/j.jnutbio.2026.110274","url":null,"abstract":"<div><div>Consumption of a high-fat diet (HFD) can lead to cognitive dysfunction and neuroinflammation in the hippocampus, particularly the CA3 region, which is vital for associative memory. Cholinergic input from the basal forebrain to the hippocampus is critical for regulating excitability, plasticity, and overall cognitive function in this area. Neuroinflammation may disrupt the expression of the α7 nicotinic acetylcholine receptor (α7nAChR), essential for the anti-inflammatory cholinergic pathway. We sought to assess the effects of brief HFD exposure on hippocampal cholinergic function and neurobehavior. Adult Swiss male mice were fed either a standard chow diet (Control; CTR) or a 60% HFD for 3 d. The Open Field (OF) and Novel Object Recognition (NOR) tests were used to evaluate anxiety-like behavior and memory performance, respectively. Following testing, the CA3 region of the hippocampus was analyzed using Western Blotting, PCR, and immunofluorescence techniques. Additionally, HFD-fed mice treated intracerebroventricularly with the α7nAChR-selective agonist PNU-282987 and α7nAChR knockout (<em>Chrna7</em>^-/-) mice were evaluated to elucidate the role of cholinergic signaling in cognition. Results showed that HFD-fed mice performed worse on the NOR test compared to CTR mice and exhibited reduced α7nAChR expression and increased acetylcholinesterase (AChE) levels, along with signs of neuroinflammation in the CA3 area. Treatment with PNU-282987 for 3 d mitigated memory impairments and neuroinflammation. In contrast, <em>Chrna7</em>^-/- mice fed a HFD displayed poorer performance on the NOR test. Our findings suggest that short-term HFD intake is linked to cholinergic impairment and inflammation in the CA3 region, indicating that targeted agonist therapy may help alleviate HFD-induced memory deficits. These results highlight the critical role of α7nAChR activation in memory regulation during neuroinflammatory episodes.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110274"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146018868","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 phospholipids alleviate high fat diet-induced intestinal lipid deposition through ATF4-PPARα-MTTP/SAR1B pathway in yellow catfish","authors":"Hua Zheng ,&nbsp;Xiao-Ying Tan ,&nbsp;Biao Wang ,&nbsp;Chong-Chao Zhong ,&nbsp;Xiao-Lei Wei ,&nbsp;Chang-Chun Song ,&nbsp;Zhi Luo","doi":"10.1016/j.jnutbio.2026.110261","DOIUrl":"10.1016/j.jnutbio.2026.110261","url":null,"abstract":"<div><div>Phospholipids serve as an efficient emulsifier and transport carrier for lipids. However, the regulatory mechanism by which phospholipids ameliorate lipid metabolic disorders induced by high-fat diet (HFD) remains unclear. The study aimed to investigate the effects and regulatory mechanisms of dietary phospholipids and HFD on intestinal lipid metabolism. We found that dietary phospholipids alleviated HFD-induced intestinal lipid deposition by inhibiting sterol regulatory element binding proteins 1 (SREBP1)-dependent lipogenesis and promoting peroxisome proliferator-activated receptor α (PPARα)-dependent lipolysis. Dietary phospholipids alleviated HFD-induced impairment in chylomicrons (CMs) synthesis and secretion by promoting microsomal triglyceride transfer protein (MTTP), apolipoprotein B and secretion-associated, Ras-related GTPase 1b (SAR1B) mRNA and protein expression. Moreover, dietary phospholipids alleviated the reduction in phosphatidylcholine synthesis induced by HFD <em>via</em> promoting cytidine triphosphate: phosphocholine cytidylyltransferase (CCTα) protein expression and mitigated HFD-induced ER stress by inhibiting glucose-regulated protein 78 (GRP78), protein kinase R like endoplasmic reticulum kinase (PERK) and activating transcription factor 4 (ATF4) mRNA and protein expression. Mechanistically, phosphatidylcholine promoted CCTα protein expression to alleviate the obstruction of CMs synthesis and secretion caused by fatty acid (palmitic acid and oleic acid). Moreover, phosphatidylcholine enhanced the transcription of <em>mttp</em> and <em>sar1b</em> genes by PPARα through reducing the interaction between ATF4 and PPARα, thereby promoting the CMs assembly and secretion to alleviate fatty acid-induced lipid deposition in primary intestinal cells of yellow catfish. Overall, this study reveals that phospholipids alleviate HFD-induced intestinal lipid accumulation through the ATF4-PPARα-MTTP/SAR1B pathway, and provides strong basis for phospholipids in the prevention of obesity-related metabolic diseases.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110261"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145933847","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":"Discovery of myristic acid, from chick early amniotic fluid for the treatment of acute gastric ulcers by targeting pyruvate carboxylase to improve TCA cycle","authors":"Fan Chen ,&nbsp;Ke-jia Wu ,&nbsp;Ziru Zhou ,&nbsp;Jiajun Yin ,&nbsp;Xuezheng Gao ,&nbsp;Yanfa Dai ,&nbsp;Lin Shao ,&nbsp;YaNan Zhu ,&nbsp;Zhenhe Zhou ,&nbsp;Ning Sun","doi":"10.1016/j.jnutbio.2026.110264","DOIUrl":"10.1016/j.jnutbio.2026.110264","url":null,"abstract":"<div><div>Gastric ulcer (GU) is a common digestive disease. We recently identified early chicken embryo amniotic fluid (ceAF) as a potent antioxidant, which exerts effects via its active components. This study demonstrates the potential of ceAF and one of its active components, myristic acid (MA), as GU protectants. UPLC-MS and GC-MS identified the key components and fatty acid contents in ceAF. In absolute ethanol-induced acute gastric ulcer (AGU) mice, ceAF and MA treatment significantly reduced ulcer area, while improving histopathology and inflammatory factor infiltration. Further, proteomics was used to elucidate the molecular mechanism by which MA ameliorates AGU: the gastroprotective potential of MA is mediated by targeting pyruvate carboxylase (PCX) to improve the Tricarboxylic acid cycle (TCA cycle). Our findings indicate that ceAF and MA show potential as candidate substances for GU prevention in preclinical studies, providing a new direction for the development of functional foods.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"151 ","pages":"Article 110264"},"PeriodicalIF":4.9,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145985015","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}