Journal of physiology and biochemistry最新文献

{"title":"Cold-induced serum amyloid A3 amplifies cAMP-PKA signaling to drive adaptive thermogenesis in brown adipocytes.","authors":"Pei-Chi Chan, Hung-Che Chien, Pei-Ru Lin, Yu-Feng Tian, Po-Shiuan Hsieh","doi":"10.1007/s13105-026-01235-6","DOIUrl":"10.1007/s13105-026-01235-6","url":null,"abstract":"<p><p>Serum amyloid A3 (SAA3) is typically associated with inflammation, but its role in brown adipose tissue (BAT) thermogenesis remains elusive. Here, we identify SAA3 as a cold-inducible, locally acting amplifier of BAT thermogenesis. Using lentiviral modulation and BAT-specific knockout mice, we demonstrate that SAA3 is essential for cold tolerance and energy expenditure. Mechanistically, secreted SAA3 augments thermogenic signaling via a GPR3-dependent cAMP/PKA axis, driving robust UCP1 induction. Notably, this activation triggers transcriptional upregulation of endogenous Saa3 and Gpr3, establishing an autocrine/paracrine amplification loop that accelerates thermogenic output. Consequently, SAA3 loss blunts thermogenic responses in vivo and in vitro. These findings establish SAA3 as a BAT-derived regulator linking cold exposure to energy dissipation via a GPR3-mediated mechanism, highlighting its therapeutic potential for metabolic diseases.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13619661/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149075109","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Nucleotide metabolic reprogramming: a \"double-edged sword\" in obesity-related inflammation-from metabolic adaptation to pathological imbalance.","authors":"Zijing Li, Yushang Liu, Xinye Ouyang, Wenjuan Wu, Maoyuan Wang","doi":"10.1007/s13105-026-01238-3","DOIUrl":"10.1007/s13105-026-01238-3","url":null,"abstract":"<p><p>Obesity has become a serious global public health challenge, characterized by chronic, sterile, low-grade inflammation with excessive NLRP3 inflammasome activation; however, the mechanism underlying the reduced activation threshold remains unclear. A recent study by Liu et al. demonstrated that obesity induces the phosphorylation and inactivation of SAMHD1, leading to a massive accumulation of cytosolic dNTPs. This causes excess dNTPs to enter mitochondria via the PNC1/2 transporters, bypassing the classical CMPK2 salvage synthesis pathway and triggering uncontrolled mtDNA synthesis and oxidative damage, ultimately resulting in the excessive activation of NLRP3 and an inflammatory response. Based on this finding, this paper presents a \"double-edged sword\" model of nucleotide metabolic reprogramming in obesity-related inflammation. Early reversible inactivation of SAMHD1 may represent a metabolic adaptive response that confers functional benefits to macrophages; however, once metabolic stress persists and causes nucleotide metabolic reprogramming to exceed a yet-to-be-defined threshold, an inflammatory positive feedback loop may be established. In terms of clinical translation, targeting PNC1/2 could specifically inhibit NLRP3 activation, which may provide new upstream intervention strategies for various aseptic inflammatory conditions such as gout; however, this approach also carries potential risks of mitochondrial toxicity and impaired anti-infective immunity. Future efforts should focus on macrophage-specific delivery, precision interventions tailored to disease stages, and precise anti-inflammatory strategies based on biomarkers such as circulating dNTPs, p-SAMHD1, and ox-mtDNA, thereby advancing the clinical translation of metabolism-related inflammation within safe parameters.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13616003/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149061983","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Macroalbuminuria as a marker of cardiac damage in patients with type 2 diabetes: insights from multimodality cardiac imaging and biomarkers.","authors":"Xabier Irazusta Olloquiegui, Saioa Echeverria Andueza, Marina Pascual Izco, Gonzalo Luis Alonso Salinas, Loreto Fernández Lorente, Susana Ravassa Albéniz, Sergio M Solis-Barquero, Verónica Aramendía-Vidaurreta, José María Mora-Gutiérrez, Josune Orbe, Maria A Fernández-Seara, Nuria García-Fernández","doi":"10.1007/s13105-026-01236-5","DOIUrl":"10.1007/s13105-026-01236-5","url":null,"abstract":"<p><strong>Background and aims: </strong>Albuminuria reflects renal and cardiovascular damage in type 2 diabetes (T2D), but its association is not fully understood. We evaluated the association of macroalbuminuria with cardiac structure and function.</p><p><strong>Methods: </strong>Cross-sectional study of 49 adults with T2D and stage 3 chronic kidney disease (CKD), stratified by macroalbuminuria, and 20 controls. Cardiac assessment included cardiac magnetic resonance (MRI), transthoracic echocardiography (TTE) and nine serum biomarkers, including soluble suppression of tumorigenicity 2 (sST2), a biomarker of myocardial stress and fibrosis.</p><p><strong>Results: </strong>Patients with T2D exhibited higher circulating levels of TIMP-1, MMP-10, neutrophil gelatinase-associated lipocalin (NGAL), NT-proBNP and hs-TnT than controls (p < 0.05). Among patients with T2D, macroalbuminuria was associated with an additional increase in TIMP-1 (p < 0.05). Patients with T2D had higher T1 values in MRI scans, particularly those with macroalbuminuria (1051 ms [IQR: 1035-1074] vs. 1009 ms [IQR: 989-1020] in controls, p < 0.001). Although sST2 levels were higher in patients with T2D than in controls and tended to be higher in those with macroalbuminuria, these differences did not reach statistical significance. Nevertheless, higher T1 values were associated with higher sST2 levels, particularly in patients with macroalbuminuria (p for interaction < 0.01). Among patients with macroalbuminuria, high sST2 levels were associated with higher T1 values (1071 ms [IQR: 1052-1087] vs. 1029 ms [IQR: 1013-1043], p < 0.05).</p><p><strong>Conclusions: </strong>In T2D and stage 3 CKD, macroalbuminuria identifies a subgroup with more cardiac structural and functional abnormalities, particularly with elevated sST2. Prospective validation is needed.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-09-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13593709/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"149016365","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A combination of aerobic and resistance training induces white adipose tissue browning.","authors":"Caroline de Carvalho Picoli, Gustavo Renan Gilio, Felipe Henriques, Kaltinaitis B N H Santos, Magno Alves Lopes, Solange Marta Franzói de Moraes, Luzmarina Hernandes, Miguel Luiz Batista, Sidney Barnabé Peres","doi":"10.1007/s13105-026-01234-7","DOIUrl":"10.1007/s13105-026-01234-7","url":null,"abstract":"<p><p>Combined training (CT) has been widely recommended as a strategy to improve metabolic health and is often prescribed in the context of obesity and its comorbidities. The present study aimed to evaluate the effects of CT on the induction of brown-like adipocytes and white adipose tissue (WAT) remodeling. Sixty male Swiss mice were randomly assigned to two experimental groups: sedentary (SED; n = 30) and combined training (CT; n = 30). Animals underwent incremental and load tests at the beginning of each week to adjust training intensity. The total CT training period lasted 8 weeks, with sessions performed five days a week. After euthanasia, WAT from the inguinal and retroperitoneal (iWAT and rpWAT) were harvested. Performance in the CT group was improved after 8 weeks, as indicated by an increase in V_{peak_k} and the load lifted. The expression of vascular endothelial growth factor (VEGF), cluster of differentiation 31 (CD31), and uncoupling protein 1 (UCP1) was higher in the CT group than in the SED group. CT also increased the abundance of multilocular adipocytes and the expression of genes associated with brown and beige adipocyte phenotypes in iWAT and rpWAT. Together, these findings indicate that CT induces browning in iWAT and rpWAT in lean mice, supporting its potential relevance as a strategy for promoting WAT remodeling in the context of metabolic health.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13585781/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148990403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zileuton protects pancreatic stellate cells from oxidative stress and ferroptosis by modulating the Nrf2 pathway and mitochondrial activity.","authors":"Matías Estarás, Cándido Ortiz-Placín, Salomé Martínez-Morcillo, Remigio Martínez, Miguel Fernández-Bermejo, Pablo Solís-Muñoz, José María Mateos, Juan Iovanna, Patricia Santofimia-Castaño, Antonio Gonzalez","doi":"10.1007/s13105-026-01224-9","DOIUrl":"10.1007/s13105-026-01224-9","url":null,"abstract":"<p><p>Lipoxygenases exhibit a leading role in cancer development and growth. Additionally, pancreatic stellate cells (PSCs) are pivotal in the formation of fibrotic tissue in pancreatic tumors. In this work, we have studied the effects of the 5-lipoxygenase (5-LOX) inhibitor, zileuton, on rat PSCs. Cell viability was analyzed by employing crystal violet. Reactive oxygen species (ROS) generation, reduced (GSH) and oxidized (GSSG) levels of glutathione and protein and lipid oxidation were analyzed by fluorescence and colorimetric methods respectively. The phosphorylation of nuclear factor erythroid 2-related factor (Nrf2) and the expression of superoxide dismutase (SOD) was studied by western blotting. The effect of zileuton on erastin-induced ferroptosis was assessed by colorimetric methods. Mitochondrial metabolic activity was studied employing Alamar Blue^®. Mitochondrial membrane potential was monitored by fluorescence techniques. The results show that the 5-LOX inhibitor protected PSCs against oxidation evoked by hydrogen peroxide, which induced an increase in CM-H₂DCFDA-derived fluorescence, a decrease in the reduced/oxidized glutathione ratio and increases in the detection of lipid and protein oxidation. In the presence of zileuton, increases in the phosphorylation of nuclear factor erythroid 2-related factor and in the expression of the antioxidant enzymes catalase, glutamate-cysteine ligase,,heme oxygenase-1, NAD(P)H quinone oxidoreductase 1, and superoxide dismutases 1 and 2 were observed. Additionally, zileuton diminished erastin-evoked ferroptosis. Finally, a drop in the reduction of resazurin by mitochondria and a slowing of the Krebs cycle flow rate were observed, whereas no detectable changes in mitochondrial membrane potential were noted in the presence of zileuton. We conclude that the inhibition of 5-LOX by zileuton places cells in a state of antioxidant readiness coupled with a protected metabolic deceleration.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13582277/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148983000","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic administration of a calafate (Berberis microphylla) polyphenol-rich extract modulates gut microbiota and metabolic homeostasis associated with thermogenic activation in high-fat diet-fed mice.","authors":"Lissette Duarte, Vanessa Villanueva, Robert Barroux, Juan Francisco Orellana, Denisse Uribe, Javier J Quezada, Luisa Amanda Ramirez, Karla Vasquez, Carlos Poblete-Aro, Martin Gotteland, Fabien Magne, Rodrigo Valenzuela, Diego F Garcia-Diaz","doi":"10.1007/s13105-026-01232-9","DOIUrl":"10.1007/s13105-026-01232-9","url":null,"abstract":"<p><p>Obesity is characterized by a pathological increase in white adipose tissue (WAT). In addition to WAT, humans and animals have brown (BAT) and beige adipose tissue, specialized in thermogenesis. Increasing thermogenesis could help treat obesity. Polyphenols, such as those found in Calafate (Berberis microphylla), promote thermogenesis, but their effectiveness depends on gut microbiota (GM) composition. This study aimed to evaluate the impact of a Calafate extract on GM composition and thermogenic activity of brown and beige adipose tissue in mice fed a high-fat diet (HFD). Forty 8-week-old C57BL/6J mice were subdivided into 4 groups: control diet (C), control/Calafate diet (CC), high-fat diet (HF) and high-fat/Calafate diet (HFC). CC and HFC groups received daily 50 mg total polyphenols/kg body weight of Calafate extract in the drink for 4 months. Before euthanasia, mice underwent an energy expenditure (EE) measurement. RT-PCR was used to evaluate transcripts of thermogenic markers in ATs. Short-chain fatty acids (SCFAs) and GM composition were analyzed in cecal contents. Calafate extract administration reduced weight gain and increased EE, regardless of diet. It also enhanced the expression of thermogenic markers in BAT and inguinal WAT. While no significant changes in GM α-diversity were found, Calafate extract administration influenced GM composition. Additionally, correlations were observed between thermogenic markers and the abundance of specific gut bacteria. In conclusion, Calafate extract prevents excessive weight gain in HFD-fed male mice, potentially via a thermogenic transcriptional response associated with an enriched abundance of SCFA-producing bacteria.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-09-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148982941","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeting lncRNA-regulated macrophage polarization: a novel therapeutic strategy for pancreatic ductal adenocarcinoma.","authors":"Hongshi Sun, Jia Wang, Zhongbo Xie, Zhichao Yang, Tiantian Yang","doi":"10.1007/s13105-026-01230-x","DOIUrl":"10.1007/s13105-026-01230-x","url":null,"abstract":"<p><p>Pancreatic ductal adenocarcinoma (PDAC), which is the most common type of pancreatic cancer (PC), carries a poor prognosis with a 5-year survival rate of less than 12%. Suboptimal therapeutic responses are primarily attributed to the immunosuppressive features of the tumor microenvironment (TME). In the PDAC TME, tumor-associated macrophages (TAMs) constitute the dominant immune cell population. Polarization of TAMs toward the M2 phenotype promotes tumor progression, immune escape, therapeutic resistance, and disease advancement. Recent studies have demonstrated that long non-coding RNAs (lncRNAs) regulate M2-TAM polarization and PDAC progression via transcriptional, epigenetic, and post-transcriptional mechanisms. This review summarizes key lncRNAs involved in TAM polarization in PDAC, highlighting their roles in inducing the M2 phenotype and promoting PDAC progression through epigenetic modifications, ceRNA networks, and signal transduction pathways. Based on these regulatory mechanisms, potential therapeutic strategies targeting lncRNAs, such as siRNA-mediated knockdown, CRISPR-based editing, antisense oligonucleotides, downstream-targeting strategies, and nanoparticle delivery systems, may provide more precise control over lncRNA activity to repolarize TAMs and reverse immunosuppression in the TME. Furthermore, advances in developing clinical prognostic models that incorporate lncRNAs linked to M2-TAMs offer potential for refined patient outcome prediction and the identification of tailored PDAC treatment options.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-09-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148930160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hyperpolarized NMR study of the impact of alzheimer's disease on diabetes using a novel rat model.","authors":"Usman Rehman, Keshav Datta, Shie-Chau Liu, Jae Mo Park, Renuka Sriram, Donghyun Hong, Qian Chen, Hidetoshi Mori, Vu Trinh, Robert Berman, Ralph Hurd, Daniel Spielman, Thomas Jue","doi":"10.1007/s13105-026-01231-w","DOIUrl":"10.1007/s13105-026-01231-w","url":null,"abstract":"<p><p>Most researchers have long focused on linkage between type 2 diabetes (T2D) and the increased risk of Alzheimer's disease (AD) but have often overlooked whether AD modulates T2D. Investigating the reciprocal interaction between two complex diseases provides perspectives on the mechanistic linkage. The endeavor, however, confronts challenges without a robust rodent model that develops T2D and AD as the animal ages. Cross breeding a T2D rat with a hemizygous TgF344AD +/- rat that contains the mutant human amyloid precursor protein (APPsw) and the presenilin 1 (PS1ΔE9) genes has produced a new T2D-AD +/- rat model. The T2D-AD +/- rat expresses both the T2D and AD phenotypes as the animal ages. As AD progresses, the time to T2D onset decreases, and the diabetes severity increases. Hyperpolarized NMR experiments using dynamic nuclear polarization (DNP) show that T2D and T2D-AD rats share a common metabolic impairment in the brain pyruvate dehydrogenase (PDH) activity as reflected in the NMR determined decline in the bicarbonate/lactate (bic/lac) ratio. The bic/lac ratio decreases in both T2D and T2D-AD brain. AD exacerbates the decline of the bic/lac ratio.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148920275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction: METTL3 suppresses pyroptosis in obstructive sleep apnea-associated hypertension via YTHDF2-mediated SOX4 mRNA degradation.","authors":"Wenjun Zhu, Yanyan Hou, Can Yang, Yaping Tian, Linna Cao, Wenjun Li, Liang Xie, Lirong He","doi":"10.1007/s13105-026-01227-6","DOIUrl":"https://doi.org/10.1007/s13105-026-01227-6","url":null,"abstract":"","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148906162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decoding dysbiosis: the role of gut microbiota in MASLD progression and emerging therapeutic interventions.","authors":"Dinesh Mohan Swamikkannu, Santhosha Dasarapu, Kanishk Dinesh Mohan, Allimalarkodi Shanmugam","doi":"10.1007/s13105-026-01199-7","DOIUrl":"10.1007/s13105-026-01199-7","url":null,"abstract":"<p><p>Metabolic dysfunction-associated steatotic liver disease (MASLD), affects a substantial proportion of the global population and is closely associated with metabolic disorders. The gut microbiota, comprising a diverse community of microorganisms within the gastrointestinal tract, plays a crucial role in maintaining host health. Dysbiosis, defined as an imbalance in this microbial ecosystem, has been increasingly implicated in the development and progression of liver diseases, including MASLD. This review examines the role of the gut microbiota in MASLD pathogenesis and highlights its potential as a therapeutic target. The gut-liver axis facilitates bidirectional communication between the intestine and the liver, thereby influencing metabolic regulation. In MASLD, dysbiosis characterized by reduced microbial diversity and an increased abundance of Gram-negative bacteria leads to altered bile acid metabolism, increased intestinal permeability, enhanced endotoxin translocation, and hepatic inflammation. Additionally, it disrupts short-chain fatty acid production and interferes with the endocannabinoid system and choline metabolism, collectively driving disease progression. Emerging non-invasive diagnostic approaches, including gut microbiome profiling, show promise for early detection. Although specific pharmacological treatments remain limited, microbiota-targeted strategies such as probiotics, prebiotics, and synbiotics aim to restore microbial balance. Furthermore, emerging modalities within microbiome-based therapies, including mesenchymal stromal cell therapy and bacteriophage therapy, offer potential for targeted modulation of the gut microbiota and liver repair. The gut microbiota-liver axis plays a central role in the pathogenesis of MASLD. Growing insights into this relationship have driven the development of microbiome-based diagnostic and therapeutic approaches. Non-invasive diagnostic tools, particularly gut microbiome profiling, show promise for early detection. Therapeutically, microbiota-targeted strategies including probiotics, prebiotics, synbiotics, and emerging modalities such as cellular and bacteriophage-based therapies offer potential to restore microbial balance and improve liver function. Nevertheless, robust clinical studies are essential to validate their efficacy, safety, and applicability in personalized MASLD management.</p>","PeriodicalId":16779,"journal":{"name":"Journal of physiology and biochemistry","volume":"82 1","pages":""},"PeriodicalIF":5.1,"publicationDate":"2026-09-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148897439","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}