Journal of Nutritional Biochemistry最新文献

{"title":"Gut microbiota-related glutathione metabolism is key mechanism for sulforaphane ameliorating ulcerative colitis","authors":"Yanan Lv ,&nbsp;Jian He ,&nbsp;Jing Peng ,&nbsp;Hao Li ,&nbsp;Yayuan Yang ,&nbsp;Zeyi Liang ,&nbsp;Wenxiang Shen ,&nbsp;Ghasem Hosseini Salekdeh ,&nbsp;Xuezhi Ding","doi":"10.1016/j.jnutbio.2025.110042","DOIUrl":"10.1016/j.jnutbio.2025.110042","url":null,"abstract":"<div><div>Gut barrier dysfunction is associated with dysbiosis of the gut microbiota and its metabolites, which is closely linked to the pathogenesis of ulcerative colitis (UC). Recent studies have demonstrated that Sulforaphane (SFN) exerts beneficial effects on UC. However, the role of the gut microbiota and microbial metabolism in the anti-UC mechanisms of SFN remains inadequately understood. In this study, we observed that SFN administration significantly improved the pathological phenotype, restored gut barrier integrity, and reduced colon inflammation in dextran sulfate sodium (DSS)-induced colitis mice. Gut microbiota analysis illustrated that SFN administration rebalances the alterations in gut microbiota composition, including genera such as <em>Turicibacter, Lactobacillus</em> and <em>Bacteroides</em>, in DSS-induced mice. Furthermore, untargeted metabolomics analysis indicated that the levels of microbial arachidonic acid metabolism, as well as the metabolism of alanine, aspartate, and glutamate, and glutathione metabolism in the gastrointestinal tract, were significantly altered in DSS-induced mice. Interestingly, SFN treatment significantly restore the alterations in glutathione metabolism and the levels of associated metabolites. Additionally, we observed that the MAPK/NF-κB signaling pathway, regulated by glutathione metabolism, was inhibited in the colon of DSS-induced mice following SFN treatment. Collectively, these results suggest that SFN can alleviate DSS-induced colitis in mice by restoring dysregulated gut microbiota and glutathione metabolism, thereby modulating the MAPK/NF-κB signaling pathway, enhancing intestinal barrier function and reducing colonic inflammation. Importantly, our findings elucidate a novel mechanism by which SFN improves gut barrier function, highlighting its potential to advance the development of SFN-derived therapeutics for the clinical management of colitis.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"146 ","pages":"Article 110042"},"PeriodicalIF":4.9,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144718048","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":"Lactoferrin attenuates renal fibrosis and uremic sarcopenia in a mouse model of adenine-induced chronic kidney disease","authors":"Yukina Iwamoto ,&nbsp;Seiko Yamakoshi ,&nbsp;Akiyo Sekimoto ,&nbsp;Koji Hosomi ,&nbsp;Takashi Toyama ,&nbsp;Yoshiro Saito ,&nbsp;Jun Kunisawa ,&nbsp;Nobuyuki Takahashi ,&nbsp;Eikan Mishima ,&nbsp;Emiko Sato","doi":"10.1016/j.jnutbio.2025.110039","DOIUrl":"10.1016/j.jnutbio.2025.110039","url":null,"abstract":"<div><div>The prevalence of chronic kidney disease (CKD) continues to rise, highlighting the urgent need for effective therapeutic interventions to address its various complications including sarcopenia. Lactoferrin, a multifunctional iron-binding glycoprotein found in mammalian breast milk, exhibits various biological activities and holds potential for treating CKD and its complications. This study investigated the effects of lactoferrin on CKD progression, its complications, and underlying mechanisms. A mouse model of adenine-induced renal failure was used as a CKD model. Lactoferrin was administered during the same period as adenine administration to assess its preventative effect on the progression of CKD. In another experiment, lactoferrin was administered after the adenine administration period to examine its effect on already advanced CKD. Effects of lactoferrin on renal function, renal pathology, and muscle atrophy were evaluated. Additionally, mechanistic insights were explored through mRNA and protein expression profiling, gut microbiota characterization, and metabolomic analysis. Lactoferrin administration improved reduction of renal function, and mitigated renal atrophy, and tubulointerstitial damage, and ameliorated skeletal muscle atrophy in CKD mice. In the skeletal muscle, CKD induced aberrant activation of mTOR1, impaired autophagy, and disrupted branched-chain amino acid metabolism. This abnormal activation of the proteolysis pathways was ameliorated by lactoferrin. Furthermore, lactoferrin attenuated dysbiosis-induced production of microbiota-derived uremic toxins, thereby reducing the indoxyl sulfate accumulation in blood and muscle. These effects contributed to decreased renal damage and delayed sarcopenia progression. Collectively, these findings suggest that lactoferrin may serve as a promising preventive and therapeutic agent for CKD-associated sarcopenia via the gut-kidney-skeletal muscle axis.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"146 ","pages":"Article 110039"},"PeriodicalIF":4.9,"publicationDate":"2025-07-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144718049","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 cannabidiol oil mitigates metabolic dysfunction in mice with high-fat diet-induced obesity","authors":"Alejandro Bravo Iniguez ,&nbsp;Qi Sun ,&nbsp;Qiyu Tian ,&nbsp;Min Du ,&nbsp;Mei-Jun Zhu","doi":"10.1016/j.jnutbio.2025.110040","DOIUrl":"10.1016/j.jnutbio.2025.110040","url":null,"abstract":"<div><div>Metabolic syndrome (MetS) is a widespread health concern driven largely by lifestyle behaviors such as dietary choices and physical inactivity. Excessive caloric intake promotes adiposity and dysregulation of metabolic signaling in adipose tissue. This study employed a mouse model of diet-induced obesity to evaluate the ability of cannabidiol (CBD), a cannabis-derived phytochemical, to mitigate metabolic dysfunction. Five-week-old mice received a standard diet or a high-fat diet (HF) with or without CBD (25 mg/kg bw) for 9 weeks. CBD supplementation reduced weight gain and lowered serum glucose concentration in HF mice. These improvements were accompanied by reduced white adipose tissue mass and smaller adipocyte size. Additionally, CBD treatment recovered protein levels of key metabolic regulators, including peroxisome proliferator-activated receptor-γ coactivator 1 alpha and Sirtuin 1, in both inguinal and epididymal adipose tissues. Consistently, CBD supplementation upregulated the mRNA expression of <em>Prdm16</em> and promoted uncoupling protein 1 at both mRNA and protein levels, showing the browning of adipose tissues. Upstream, CBD supplementation increased transient receptor potential vanilloid 1 (TRPV1) in HF mice at both the mRNA and protein levels, which possibly helped orchestrate the observed improvements. In summary, dietary CBD mitigates weight gain and improves the metabolic health of HF-challenged mice, potentially through the promotion of white adipose tissue browning.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"146 ","pages":"Article 110040"},"PeriodicalIF":4.9,"publicationDate":"2025-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144718046","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":"Antioxidant management to protect male offspring from the progression of MASLD programmed by maternal obesity in mice","authors":"Jialing Zhang ,&nbsp;Jiayu Wang ,&nbsp;Da Xu ,&nbsp;Fang Wu ,&nbsp;Yonghao Gui","doi":"10.1016/j.jnutbio.2025.110038","DOIUrl":"10.1016/j.jnutbio.2025.110038","url":null,"abstract":"<div><div>Background: Maternal obesity is a significant risk factor for liver dysfunction and metabolic dysfunction-associated steatotic liver disease (MASLD) in offspring, with oxidative stress playing a critical role in developmental programming. Understanding oxidative stress-mediated metabolic reprogramming during intrauterine overnutrition is crucial for developing MASLD preventive strategies. Methods: Female mice were fed a Western diet to induce obesity before mating. Biochemical detection and histopathological staining were employed to assess changes in lipid metabolism and liver fibrosis. Oxidative stress indices were measured using ELISA, while metabolic profiling was conducted through liquid chromatography-tandem mass spectrometry (LC-MS) analysis. Protein expression was evaluated by western blot. Results: Male offspring from obese dams (OffOb) exhibited increased activities of ALT, AST, GGT, and ALP, along with evident hepatic steatosis and fibrosis. These male offspring also showed impaired antioxidant defenses in liver. Administration of the antioxidant N-acetylcysteine during pregnancy (OffObnac) enhanced some antioxidant enzymes/substances and reversed these abnormal changes in the male offspring's liver. Notably, antioxidant treatment significantly mitigated the IL-6 increase induced by maternal obesity. According to KEGG analyses, the differential metabolites between OffOb and OffCon, as well as between OffObnac and OffOb, were primarily enriched in the forkhead box O (FoxO) signaling pathway. Protein expression results indicated that antioxidant treatment inhibited the phosphorylation activation of JAK2, STAT3, and FoxO6 in the liver of male offspring from obese mothers. Conclusions: Antioxidant management effectively alleviated oxidative stress conditions, blocked the IL-6-STAT3-FoxO6 axis, and had a robust impact on mitigating MASLD following intrauterine overnutrition-induced hepatic impairments in a mouse model.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110038"},"PeriodicalIF":4.9,"publicationDate":"2025-07-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144682711","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":"Genistein maintains intestinal homeostasis in colitis mice via activating GPR30-Nrf2 signaling pathway","authors":"Ji Cao ,&nbsp;Donglin Shi ,&nbsp;Yong Cui ,&nbsp;Haiyan Zhu ,&nbsp;Haiping Liang ,&nbsp;Qing Wei ,&nbsp;Jianzhen Huang","doi":"10.1016/j.jnutbio.2025.110036","DOIUrl":"10.1016/j.jnutbio.2025.110036","url":null,"abstract":"<div><div>Genistein (GEN) is a natural polyphenolic compound widely present in leguminous plants, which has many biological functions such as anti-inflammatory and antioxidant activities, and has attracted attention in the treatment of inflammatory bowel disease (IBD). However, the molecular mechanism underlying the beneficial effects of GEN in IBD remains unclear. Here, we demonstrated that GEN enhanced the relative abundance of beneficial bacteria (e.g., <em>Akkermansia muciniphila</em>) and increased microbiota-derived short-chain fatty acids (SCFAs) levels in colitis mice. Further, the antibiotic cocktails (ABX) and fecal microbiota transplantation (FMT) experiments confirmed that gut microbiota at least partially mediated the anti-colitis effect of GEN. Interestingly, we found that GEN could also activate G protein-coupled receptor 30 (GPR30) and its downstream transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) in intestinal epithelial cells (IECs). The activation of the GPR30-Nrf2 signaling led to reduced reactive oxygen species (ROS) production, which consequently inhibited NLRP3 inflammasome activation and improved intestinal epithelial barrier dysfunction. In addition, studies using GPR30 knockout mice confirmed that GPR30 is crucial for inhibiting NLRP3 inflammasome activation and alleviating colitis. Collectively, our study unveils that GEN is an effective anti-inflammatory agent and suggests that both the gut microbiota and the GPR30-Nrf2 signaling pathway represent potential therapeutic targets for treating IBD.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110036"},"PeriodicalIF":4.9,"publicationDate":"2025-07-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144675056","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":"Tetrahydrocurcumin ameliorates metabolic disorders associated with obesity by regulating gut microbiota homeostasis","authors":"Shuyang Zhang ,&nbsp;Liping Chen ,&nbsp;Yongzhong Wang","doi":"10.1016/j.jnutbio.2025.110034","DOIUrl":"10.1016/j.jnutbio.2025.110034","url":null,"abstract":"<div><div>Obesity, a global health crisis, demands novel therapeutic strategies. Tetrahydrocurcumin (THC), a natural compound, shows promise in mitigating obesity by regulating gut microbiota and lipid metabolism. Using in vitro (Hepa1-6 cells) and in vivo (<em>C. elegans</em> and HFD C57BL/6 J mice) models, we evaluated THC’s effects on lipid accumulation, oxidative stress, and key metabolic markers. In glucose-induced obese <em>C. elegans</em>, THC reduced lipid deposition and enhanced antioxidant capacity. In HFD mice, THC improved hepatic function (reduced AST/ALT), decreased liver fat content, and lowered oxidative stress. Mechanistically, THC downregulated Stearoyl-CoA desaturase-1 (SCD1) and Diacylglycerol O acyltransferase 1 (DGAT1) expression (Western blot/RT-qPCR), pivotal regulators of lipid metabolism. Fecal 16S rRNA sequencing revealed THC-modulated gut microbiota, including reduced <em>Firmicutes/Bacteroidetes</em> ratio and <em>Desulfobacterota</em> abundance, alongside elevated short-chain fatty acids (SCFAs). In vitro, THC suppressed lipid accumulation in Hepa1-6 cells. Collectively, THC alleviates obesity by targeting lipid metabolism, oxidative stress, and gut microbial homeostasis, highlighting its therapeutic potential.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"146 ","pages":"Article 110034"},"PeriodicalIF":4.9,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144667821","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":"Baicalein reduces cardiac inflammatory infiltration in EAM mice by blocking the CCL2-CCR2 signaling axis through its binding with TNF-α and CCR2","authors":"Huimin Tong ,&nbsp;Shuang Wang ,&nbsp;Meng Liu ,&nbsp;Tiantian Wang ,&nbsp;Xihui Jia ,&nbsp;Yuanyuan Li ,&nbsp;Dongyu Yu ,&nbsp;Ling Li","doi":"10.1016/j.jnutbio.2025.110029","DOIUrl":"10.1016/j.jnutbio.2025.110029","url":null,"abstract":"<div><div>Myocarditis refers to localized or diffuse inflammatory lesions of the myocardium. Experimental autoimmune myocarditis (EAM) in mice is commonly utilized as an animal model for studying the pathogenesis of myocarditis. Baicalein (BAI), the main active component extracted from <em>Scutellaria baicalensis</em> root, has been proven to possess diverse effects such as anti-inflammatory, anti-tumor, and antioxidant activities. However, further investigation is warranted to elucidate the mechanism of action underlying BAI's efficacy in EAM. The aim of this study is to the potential of BAI in combination with TNF-α to downregulate the TNF-α/TNFR1-AP-1 signaling pathway. Furthermore, we will explore whether BAI exhibits an inhibitory effect on the CCL2/CCR2-ROCK1 signaling pathway. In this study, we employed the EAM animal model to investigate the inhibitory effect of BAI on macrophage and Th1 cell chemotaxis towards cardiac tissue in EAM mice. Techniques such as HE staining, immunofluorescence, and other methods were utilized for assessment. Additionally, computer-simulated molecular docking, Streptavidin pull-down, and co-immunoprecipitation experiments were conducted to explore the potential binding of BAI with TNF-α and CCR2. Furthermore, real-time quantitative polymerase chain reaction (qPCR), western blotting, and flow cytometry were employed to elucidate the impact of BAI on the TNF-α/TNFR1-CCL2/CCR2 signaling pathway. BAI suppressed the expression of chemokine CCL2 in EAM mouse myocardial tissue and attenuated the infiltration of macrophages and Th1 cells. In vitro, BAI exhibited binding affinity to TNF-α, leading to downregulation of the TNF-α/TNFR1-AP-1 signaling pathway and subsequent inhibition of CCL2 secretion by macrophages and vascular endothelial cells. Additionally, BAI demonstrated binding capability to CCR2, resulting in downregulation of the CCL2/CCR2-ROCK1 pathway and consequent inhibition of chemotactic migration of macrophages and Th1 cells. This study demonstrates that BAI can downregulate the secretion of CCL2 and the CCL2/CCR2-ROCK1 signaling pathway by binding with TNF-α and CCR2, thereby inhibiting the migration of macrophages and Th1 cells to the lesion site, thus alleviating the inflammation severity in EAM.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110029"},"PeriodicalIF":4.9,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626549","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":"Neuroregulatory effect of royal jelly","authors":"Feng Zhu ,&nbsp;Ruili Yang ,&nbsp;Biao He,&nbsp;Yi Xu,&nbsp;Hui-Li Wang","doi":"10.1016/j.jnutbio.2025.110028","DOIUrl":"10.1016/j.jnutbio.2025.110028","url":null,"abstract":"<div><div>Royal jelly (RJ), a nutrient-rich secretion fed exclusively to queen honeybees, exhibits diverse biological activities. Due to limited insights into its effects on central nervous system (CNS)-related functions and pathologies, this review attempts to recapitalize the recent advances of neuroregulatory function of RJ in mammals and humans. Another central aim of this review is to summarize the known mechanisms underlying the neuroregulatory effect of RJ. RJ components were first discussed concerning their link to neuroprotection, with a focus on the queen bee acid (QBA, 10-HDA, trans-10‑hydroxy-2-decenoic acid), MRJPs (major royal jelly proteins), and microbiota. The neuroregulatory implications of RJ are then categorized into three domains: fundamental CNS functions, including learning and memory, <em>in vitro</em> neuronal cell activity and social behavior; neurological disorders such as Alzheimer's disease (AD), Parkinson’s disease (PD), anxiety and depression; neurotoxic events. In terms of mechanistic insights, RJ modulates neuroinflammation, a pivotal driver of neurological disorders, and acts as an HDAC (histone deacetylase) inhibitor among other epigenetic regulators, influencing gene expression in the CNS. Emerging evidence also implicates the microbiota-gut-brain (MGB) axis, where RJ alters gut microbiota composition, subsequently impacting brain function. Finally, we outline critical research directions, including clinical significance, comparisons with other honeybee products, epigenetic mechanisms, and RJ’s untapped role in reshaping social behaviors. This review aims to consolidate our knowledge on the neuroregulatory effects of RJ, underscoring its therapeutic potential for neurological conditions in both nutritional and pharmaceutical contexts.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110028"},"PeriodicalIF":4.9,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626551","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":"Multi-omics analyses revealed the distinct effects of calorie restriction diets with different fat-to-energy ratios on body weight and glycolipid metabolism in rats","authors":"Jiedong Chen,&nbsp;Yijie Wang,&nbsp;Ke Sun,&nbsp;Yiqi Lin,&nbsp;Fuchuan Guo","doi":"10.1016/j.jnutbio.2025.110026","DOIUrl":"10.1016/j.jnutbio.2025.110026","url":null,"abstract":"<div><div>To explore the distinct effects of different fat-to-energy ratio calorie restriction (CR) diets on health, 50 male Wistar rats were randomly assigned to five groups: two ad libitum groups were fed with either normal (ND–AL) or high–fat (HF–AL) diets, and three CR groups were fed with respective low-(10% [cal] fat, LF–CR), medium-(35% [cal] fat, MF–CR) and high-(45% [cal] fat, HF–CR) fat-to-energy ratio diets for 10 weeks after obesity modeling. Among the three CR groups, HF-CR had the most pronounced weight loss effect, but it also exacerbated glycolipid metabolism disorders. In the HF-CR group, an increase in gut microbiota associated with glucose metabolism disorder (e.g., <em>Collinsella</em> and <em>Enterorhabdus</em>) was observed compared to the LF-CR group. Additionally, there was a significant decrease in the expression levels of genes involved in hepatic gluconeogenesis, glycogen synthesis, and insulin signaling in the MF-CR and HF-CR groups when compared to the LF-CR group. Further analysis indicated that <em>Enterorhabdus</em> may potentially regulate the gene expression of the glucokinase regulator (GCKR) by modulating choline metabolism, thereby impacting glucose metabolism. Our study emphasizes the importance of maintaining an appropriate fat-to-energy ratio in CR diets to promote healthy weight loss by balancing dietary fat, gut microbiota, and glucose metabolism.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110026"},"PeriodicalIF":4.9,"publicationDate":"2025-07-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144626550","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":"Effect of the early introduction of trophic donor human breast milk on the preservation of postoperative gut functions in a fasting animal model","authors":"Ayse Tuzlaci ,&nbsp;Fetiye Kolayli ,&nbsp;Bahar Muezzinoglu ,&nbsp;Bekir Haluk Güvenç","doi":"10.1016/j.jnutbio.2025.110030","DOIUrl":"10.1016/j.jnutbio.2025.110030","url":null,"abstract":"<div><div>Dietary restrictions, such as avoiding oral intake until postoperative ileus resolves, can result in negative nitrogen balance, weakened immune function, and impaired digestive system performance. This study investigates the efficacy of donor human breast milk (HM) in early trophic enteral feeding and its impact on gut functions during prolonged postoperative fasting in an animal model. Male Wistar rats were deprived of food for 48 hours with free water access. After a complete ileal transection and an end-to-end intestinal anastomosis, the rats were divided into three groups: prolonged fasting (PF), early trophic feeding with HM, and feeding with commercial formula (CF). Each group was further divided into 48- and 72-h postoperative subgroups. The study measured the number of colony-forming units in mesenteric lymph nodes, serum alkaline phosphatase (ALP) levels, and histopathological data between groups. At postoperative 48 and 72 hours, the mean apoptotic index of HM group was significantly lower than in PF group (<em>P</em>&lt;.001). A significant decrease was observed in apoptosis in HM group over time (<em>P</em>=.047), while the CF (<em>P</em>=.327) and PF (<em>P</em>=.959) groups did not show significant changes. HM significantly prevented villus atrophy (<em>P</em>&lt;.01), and bacterial translocation to mesenteric lymph nodes (<em>P</em>&lt;.05) compared to CF and PF. Serum ALP levels, an indicator of intestinal mucosal regeneration, was significantly highest in the HM group at 72 hours compared to other groups (<em>P</em>=.03). These findings suggest that HM not only maintains the structural and functional gut integrity but also promotes earlier and more effective recovery of the intestinal health.</div></div>","PeriodicalId":16618,"journal":{"name":"Journal of Nutritional Biochemistry","volume":"145 ","pages":"Article 110030"},"PeriodicalIF":4.9,"publicationDate":"2025-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144618558","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}