Mitochondrial dysfunction and impaired neurogenesis are central to mitochondrial DNA polymerase (POLG)-related disorders, yet therapeutic options remain limited. Here, patient-derived induced pluripotent stem cell (iPSC)-based cortical organoids are used to model POLG-associated neurodegeneration and assess the therapeutic potential of metformin. Single-cell RNA-seq reveals distinct vulnerabilities in dopaminergic, glutamatergic, and GABAergic neuronal subtypes, with dopaminergic neurons exhibiting the most severe loss and mitochondrial transcriptomic deficits. Metformin treatment (250µm, 2months) significantly restores neuronal identity, subtype-specific gene expression, and mitochondrial function. Functional assays demonstrate improved mitochondrial membrane potential (TMRE), increased mitochondrial mass (MTG, MTDR), and reduced oxidative stress (MitoSOX, BAX/cleaved caspase 3). Notably, mitochondrial DNA (mtDNA)copy number and the expression of mitochondrial replisome proteins (POLG, POLG2) are upregulated, indicating enhanced mitochondrial genome maintenance. Calcium measurement confirms improved neuronal excitability. Untargeted metabolomics further reveals metformin-induced metabolic reprogramming, including enrichment of the tricarboxylic acid (TCA) cycle, amino acid metabolism, and redox-related pathways. Together, these findings demonstrate that metformin enhances mitochondrial integrity and neural function across multiple neuronal subtypes and offer mechanistic insights into its potential as a treatment for POLG-related disorders.

Despite feeding on a high-lignocellulose bamboo diet, the giant panda (Ailuropoda melanoleuca) retains a typical gut microbiome of Carnivora. We conducted shotgun metagenomic sequencing and functional validation of the giant panda's gut microbiome to elucidate its physiological roles and explore its functional adaptation to the species' specialized diet. Our results revealed that Streptococcus alactolyticus significantly increased in the guts of subadult, adult, and elderly individuals versus that in cubs. The gut microbiome of these non-cub giant pandas was significantly enriched in pathways and modules associated with tryptophan biosynthesis. Whole-genome sequencing and in vitro fermentation of S. alactolyticus demonstrated its ability to biosynthesize tryptophan. Gavage of S. alactolyticus in mice led to the enrichment of aromatic amino acid metabolism pathways in gut microbiome, accompanied by significantly elevated levels of 5-hydroxyindole acetic acid and kynurenine in fecal and/or serum samples (p < 0.05). Transcriptome sequencing of colons from mice revealed that most significant upregulated Gene Ontology (GO) terms mainly were related to spindle checkpoint signaling and chromosome segregation, while most significant downregulated GO terms mainly involved synaptic functional regulation. These findings suggest that S. alactolyticus enriched in the non-cub giant panda gut can regulate tryptophan, influencing host gut physiology via tryptophan metabolites.

d-serine administration prevents kidney damage in murine models of acute kidney injury, and risperidone inhibits the activity of d-amino acid oxidase, which regulate plasma d-amino acid levels. This pilot randomized controlled trial investigated the effects of risperidone on glucose, amino acid metabolism, and kidney function in healthy adults. Healthy adults with a homeostasis model assessment of insulin resistance (HOMA-IR) of ≥ 1.6 and estimated glomerular filtration rate (eGFR) of ≥ 60 mL/min/1.73m2 were randomly assigned to the risperidone and control groups. The risperidone group received 0.5 mg/day risperidone for 4 days. The primary outcome was mean change in HOMA-IR on day 5, and the secondary outcomes were changes in d-amino acid levels, eGFR, and urinary albumin. Seven participants were randomized to the risperidone and control groups. The changes in HOMA-IR, eGFR, and urinary albumin on day 5 were not significantly different between the two groups (all p > 0.05). Mean changes in plasma d-serine level and urinary d-serine/creatinine ratio were significantly higher in the risperidone group than in the control group (0.2 vs. −0.3 nmol/mL, p = 0.03 and 38.2 vs. −25.8 nmol/mL, p = 0.01, respectively). Short-term risperidone affects d-serine metabolism without instigating acute adverse effects on kidney or glucose homeostasis in healthy individuals.Clinical Trial Registry number: This study was registered with the Japan Registry for Clinical Trials (jRCTs041210165).

Surgical castration, a common practice in animal husbandry, raises animal welfare concerns and adversely affects growth performance. Active immunization against gonadotropin-releasing hormone (GnRH) provides a non-surgical alternative. Both methods ultimately suppress sex hormone production, but their comparative effects on the gut microbiota, a crucial regulator of host health and metabolism, remain unclear. Here, 60 Sprague Dawley (SD) rats were randomly allocated into three groups—control (n = 20; 10 female and 10 male), surgical castration (n = 20; 10 female and 10 male), and GnRH immunocastration groups (n = 20; 10 female and 10 male)—at 4–5 weeks of age to comparatively investigate the impacts of surgical versus GnRH immunocastration on the gut microbiota. Our study demonstrated GnRH immunocastration significantly reduced gonadal weight, effectively suppressing gonadal development to a level comparable to surgical castration. However, the two methods induced distinct, sex-dependent shifts in the gut microbiota. Surgical castration reduced the gut microbial community diversity, whereas the community structure of GnRH immunocastrated rats more closely resembled that of the control group, indicating a milder impact on the microbial diversity and composition. Notably, GnRH immunocastration resulted in higher microbial alpha diversity than surgical castration in both female and male SD rats. Specific bacterial genera, such as Clostridia_UCG014, Lactobacillus, and Lachnospiraceae_UCG006, were similarly altered in both surgical castration and GnRH immunocastration female SD rats, while Intestinimonas and Erysipelatoclostridiaceae_UCG004 were concurrently changed in male SD rats. Conversely, Eubacterium_nodatum_group exhibited opposite responses, increasing with GnRH immunocastration but decreasing with surgical castration in male SD rats. Functional prediction revealed fundamental sex differences in microbial metabolic pathways. In females, nitrogen metabolism, glyoxylate/dicarboxylate metabolism, and mismatch repair were changed, while the pathways involved in siderophore biosynthesis, the citrate cycle (TCA cycle), genetic information processing, and amino acid metabolism were changed in male SD rats. In conclusion, GnRH immunocastration appears to be a less disruptive intervention, better preserving microbial diversity and inducing a unique functional profile. These findings highlighted the importance of considering the castration method’s impact on the gut microbial ecosystem in animal production and provided insights for developing humane and effective approaches to animal population control.

Temozolomide (TMZ) is a frontline chemotherapeutic agent for glioblastoma multiforme (GBM); however, approximately half of patients develop resistance to therapy. This study investigates the role of altered cellular bioenergetics and metabolism in the acquired TMZ resistance. Using untargeted metabolomics, we explored the metabolic rewiring in TMZ-resistant GBM cells and identified key alterations in glycolysis, the tricarboxylic acid (TCA) cycle, fatty acid metabolism, and amino acid metabolism, all might be linked to cellular proliferation. Our findings suggest that while glycolysis remains important, increased TCA cycle activity contributes to the drug resistance, supported by increased levels of mitochondrial mass and mitochondrial membrane potential. We observed significantly elevated glutamine levels, which may enhance mitochondrial activity, thereby supporting increased energy production. Furthermore, resistant cells exhibited enhanced NRF2 level in parallel with higher levels of antioxidants, including glutathione and catalase enzyme, and a concomitant decrease in the level of its negative regulator, KEAP1. These factors collectively may contribute to drug resistance by mitigating oxidative stress. These findings indicate that mitochondrial metabolic reprogramming and NRF2/KEAP1-mediated antioxidant defense mechanisms play a crucial role in TMZ resistance, and targeting these pathways may offer a novel strategy to overcome resistance in GBM therapy.

Sleep disturbances are common in individuals with inflammatory bowel disease (IBD) and may worsen its progression. This study investigates the bidirectional association between unhealthy sleep and IBD and explores proteomic mechanisms underlying this relationship. Data from 381,228 UK Biobank participants were analyzed to calculate adjusted odds ratios (ORs) for prevalent IBD and hazard ratios (HRs) for IBD incidence in relation to sleep patterns. A subset of 40,392 participants underwent plasma proteomic profiling, where differential expression analysis and weighted gene co-expression network analysis (WGCNA) identified key protein modules. A prognostic risk model for IBD was developed using least absolute shrinkage and selection operator (LASSO)-Cox regression. At baseline, 26.4% of participants exhibited unhealthy sleep, which was significantly associated with higher odds of prevalent IBD (OR = 1.250, 95% CI 1.165-1.340, p < 0.001) and an increased risk of developing IBD (HR = 1.237, 95% CI 1.136-1.348, p < 0.001). Proteomic profiling revealed 182 differentially expressed proteins common to both unhealthy sleep and IBD, with WGCNA identifying modules enriched in pathways related to cell activation, chemotaxis, and amino acid and organic acid metabolism. The proteomic risk model achieved an AUC of 0.81 for predicting 2-year IBD onset. Participants with both unhealthy sleep and high proteomic risk scores had a markedly increased risk of incident IBD (HR = 3.370, 95% CI 2.300-4.938, p < 0.001). Unhealthy sleep and IBD are bidirectionally linked, with inflammatory and metabolic processes mediating this association. These findings highlight potential biomarkers and therapeutic targets, underscoring the importance of integrating sleep assessments into IBD management strategies.

Understanding and overcoming protein production bottlenecks in plants.

YY1: Master regulator of metabolic reprogramming in cancer.

Diabetes mellitus (DM) is a clinical syndrome characterized by disturbance in carbohydrate, fat and protein metabolism due to either insulin deficiency or insulin resistance. Oral medications and insulin injections have typically been the conventional delivery modalities of diabetes treatment for both type 1 and patients with advanced type 2 diabetes. In spite of this, these treatments have some drawbacks, including low efficacy, unwanted side effects and the possibility of hypoglycemia. New developments in medication delivery techniques, such as insulin pumps, inhalers and patches, have been made with the intention of enhancing the efficacy of the treatment. Insulin pumps allow for precise and flexible administration of insulin, which, in turn, reduces the number of episodes of low blood sugar. The use of inhalers provides a non-invasive alternative that facilitates rapid glycemic management and increases patient satisfaction. Currently in the process of being developed, insulin patches provide a means of administering insulin that is both simple and painless. In this review, we investigate the efficacy, safety and practicability of various technological breakthroughs, such as insulin pumps, smart insulin pens and continuous glucose monitoring systems. In addition to this, it addresses the challenges that are preventing a wider acceptance, such as the costs, the availability and the requirements for training. In order to enhance patient outcomes and usher in a new era of diabetes care that is increasingly driven by technology, the report places a strong emphasis on the necessity of continued research and innovation.

Sulforaphane is a beneficial but unstable bioactive compound that can be converted from glucoraphanin by Lactiplantibacillus plantarum. However, the sulforaphane conversion rate is low, and the conversion mechanism of L. plantarum remains unclear. This research utilized the adaptive laboratory evolution technology to enhance the sulforaphane conversion rate of L. plantarum. The results showed that an increase in the glucose replacement ratio significantly downregulated carbohydrate metabolism and upregulated amino acid metabolism. Transcriptomic analysis showed that the ALE-adapted strain significantly upregulated carbohydrate metabolism and amino acid metabolism. In the conversion pathway, glucoraphanin is imported into L. plantarum cells, and its glucose moiety is phosphorylated by bglF (the phosphate group may be derived from phosphoenolpyruvate via the phosphotransferase system). Subsequently, the S-glycosidic bond of phosphorylated glucoraphanin is hydrolyzed by bglA (6-phospho-β-glucosidase), followed by nonenzymatic rearrangement and sulfate elimination, ultimately yielding sulforaphane. This research can contribute to revealing the interaction mechanism between microorganisms and natural active substances.

Abstract Immune escape is a critical hallmark of cancer, driving disease progression, poor prognosis, and resistance to therapies. However, how immune escape evolves in cancer is poorly understood. Existing studies are limited by a narrow focus on escape mechanisms and the inability of conventional methods to resolve the temporal order of clonal mutations. To overcome these challenges, we developed an integrative approach that combines systematic mining of immunomodulatory genes and novel computational reconstruction of tumor evolution history. Using this framework, we generated the first pan-cancer atlas of genetic evolution of immune escape. We find that immunomodulatory pathways are mutated at varying frequencies across cancers. For example, antigen presentation machinery is highly mutated in chromophobe renal cell carcinoma and lung squamous cell carcinoma, while the protein methylation pathway is highly mutated in bladder transitional cell carcinoma. Furthermore, cancers exhibit distinct evolutionary trajectories of immune escape. Pancreatic adenocarcinoma acquires late mutations in amino acid metabolism, esophageal adenocarcinoma shows early mutations in neuroactive ligand−receptor interaction and IFNγ signaling, and breast adenocarcinoma has late mutations in protein methylation. These findings systematically map the genetic evolution of immune escape across cancer types and lay the groundwork for novel approaches in early detection, immunoprevention, and therapeutic intervention. Citation Format: Wenjie Chen, Toby Baker, Zhihui Zhang, Huw Alexander. Ogilvie, Peter Van Loo, Shengqing Gu. Genetic evolution of immune escape across cancers [abstract]. In: Proceedings of the AACR Special Conference in Cancer Research: Cancer Evolution: The Dynamics of Progression and Persistence; 2025 Dec 4-6; Albuquerque, NM. Philadelphia (PA): AACR; Cancer Res 2025;85(23_Suppl):Abstract nr B022.

Depression is a mental disorder, and the complexity of its pathogenesis affects the treatment and prevention of depression. Flavonoids possess a variety of biological effects, including antidepressant properties. Quercetin, a natural flavonoid, exhibits antioxidant, antidepressant and anti-inflammatory effects. This research investigated the antidepressant properties of quercetin on rats induced by chronic unpredictable mild stress through untargeted metabolomics. A total of 96 rats were randomly allocated across six groups: control group, quercetin-treated groups receiving distinct dosages (10 and 50 mg/kg bw, respectively), depression model group, and different dosages of quercetin intervention in the depression model. During the 8 wk chronic unpredictable mild stress modeling process, quercetin was administered to the rats via gavage once daily. After 8 wk modeling, rat urine samples and prefrontal cortex were collected for untargeted metabolomics research and related detection, respectively. 19 differential metabolites were identified in the urine of chronic unpredictable mild stress-induced rats, and pathway analysis indicated metabolic disorders in rats, including arachidonic acid metabolism and amino acid metabolism. This study found that the elevation of urinary PGE2 and LTB4 is closely associated with the activation of the NF-κB/NLRP3 pathway in the PFC of chronic unpredictable mild stress-induced rats. Metabolomics reveals that quercetin can ameliorate metabolic disorders induced by chronic unpredictable mild stress through multiple pathways, and inhibit the activation of the NF-κB/NLRP3 pathway in the PFC by exerting anti-inflammatory and antioxidant effects. This study offers novel insights into the role of quercetin for the prevention and management of depression.

ContextCotton stalk valorization is limited by high lignification, resulting in waste and environmental issues. Biochar, a pyrolysis-derived material, shows promise in reducing ruminant methane emissions. Aims: This study investigates the effects of cotton stalk biochar (CSB) as a feed additive on rumen fermentation, methane emissions, microbial communities, and nutrient degradation in dairy cows.MethodsCotton stalks were air-dried, cut into 2–3 cm segments, oven-dried at 105°C for 6 h, ground through an 80-mesh sieve, and pyrolyzed under N2 (0.5 L/min) at 13.3°C/min to 400°C with a 3 h hold to produce CSB. CSB was added to diets at 0%, 3%, and 6% levels. Each treatment was conducted in triplicate, with two fermentation bottles for each replicate. Rumen fermentation was simulated using an in vitro static culture method with rumen fluid from Holstein dairy cows. Fermentation parameters, gas production, nutrient disappearance, microbial populations, and metabolites were analyzed.Key ResultsCSB addition increased rumen pH and significantly reduced total gas, CH4, CO2, and H2 production (P < 0.05). Total volatile fatty acid concentration decreased with increasing CSB levels. However, no significant changes were observed in microbial diversity or total DNA copy numbers of bacteria and methanogens. Metabolomics revealed that CSB altered key metabolites involved in amino acid (such as citrulline) and fatty acid metabolism (such as pyruvic acid and undecanoic acid). As CSB levels increased, cellulase activity decreased, thereby inhibiting dry matter and fiber loss rates and further reducing gas production. Conclusions: In conclusion, the addition of 3% or 6% biochar to the feed of cows was able to minimise ruminal gas production. However, it may act by inhibiting the ruminal fermentation (NDF degradation) pathway.Implication.The addition of 3% CSB can reduce in vitro gas production in the rumen of dairy cows.

BackgroundEnvironmental pollutants have a profound impact on microbial dynamics. This study highlights the influence of anthropogenic activity on the shift in bacterial diversity in the catchment area compared to upstream and downstream at Kathajodi, using a metagenomic approach for the first time in River Kathajodi.MethodsWater samples were collected from upstream, catchment, and downstream locations and transported at 4°C to the laboratory for DNA extraction, library preparation, sequencing, and physicochemical analysis employing inductively coupled plasma. The extracted DNA was sequenced via the Illumina HiSeq platform and analyzed through MG-RAST for taxonomic and functional classification using KEGG and COG annotations. Statistical diversity analysis, including rarefaction curves, alpha- and beta-diversity indices, and Venn diagrams, provided insights into microbial composition and community variations across sites.ResultsA significant abundance of pollution indicator members of phylum Bacteroidetes (29.82%) in the catchment (CM), highly contaminated with metals, fecal, and other organic pollutants, could be attributed to their high metabolic capabilities to degrade them. The pristine upstream (US) exhibited an abundance of Shewanella (25.04%), Pseudomonas (17.35%), and Synechococcus (5.62%). The CM, influenced by high anthropogenic activity, showed higher abundances of Flavobacterium (5.20%), Arcobacter (4.05%), and Bacteroides (3.88%). In contrast, downstream (DS), with fewer anthropogenic activities, displayed higher abundances of Aeromonas (4.40%), Acidovorax (0.52%), and Acidimicrobium (0.32%). The highest bacterial diversity of CM could be due to the influence of the physicochemical properties of city waste effluent. From the Venn diagram, 73 common OTUs at the genera level were observed in all three sites, which indicates that the native microflora of the river water niche remains unaffected irrespective of the temporary changes in the vicinity. The functional profiling through KEGG and COG revealed that CM was enriched in carbohydrate metabolism (12.11%), while DS exhibited higher contributions to amino acid metabolism, along with the highest relative abundance of general function prediction (R) (12.89%), all indicative of stress adaptation and metabolic flexibility under polluted conditions. The clean upstream is home to oxygen-loving helpful bacteria, the catchment supports nutrient-hungry and sewage-linked microbes, while the downstream is dominated by metal-tolerant and possibly harmful bacteria, showing the clear impact of human activities along the river.ConclusionsThe marked shift in bacterial diversity between US, CM, and DS regions highlights the ecological consequences of anthropogenic impact. These findings emphasize the need for effective environmental management to safeguard water quality and prevent undesirable health issues.Supplementary InformationThe online version contains supplementary material available at 10.1186/s44342-025-00054-3.

Normothermic machine perfusion (NMP) is being explored as a promising method to assess pretransplant viability and potentially enhance the functional performance of deceased-donor kidneys. To realize NMPs full potential, however, understanding ex vivo kidney metabolism and its differences from our clinical in vivo reference frame is essential. Here, a multiomics approach including metabolomics, transcriptomics, and proteomics analyses was used to explore metabolic differences between ex vivo and in vivo kidneys and assess the additional impact of warm ischemia on ex vivo kidney metabolism. Paired kidneys from laboratory pigs (n = 30) sustained either minimal or 75 min of warm ischemia. All kidneys underwent 6 h of oxygenated hypothermic machine perfusion followed by 6 h of NMP. Cortical tissue samples were collected in vivo, after cold preservation, and after NMP for metabolomics, transcriptomics, and proteomics analyses. Metabolomics analysis revealed increased branched-chain amino acid metabolism and decreased uracil- and cytidine-containing pyrimidine metabolism after NMP compared with in vivo. Subsequent analyses demonstrated enhanced glycolysis, decreased gluconeogenesis, impaired tricarboxylic acid cycle activity, and nicotinamide adenine dinucleotide depletion. Multiomics analysis showed associations between metabolic alterations and increased immune response and cell death processes during NMP. Together, our findings indicate substantial differences between in vivo and ex vivo kidney metabolism and reveal a link between metabolic alterations and potentially detrimental cellular processes.

Introduction Idiopathic pulmonary fibrosis (IPF) is a progressive lung disease with irreversible fibrosis and poor prognosis. Jiawei Buyang Huanwu Decoction (JBHD) has demonstrated therapeutic effects, but the exact mechanisms, particularly those mediated by the gut microbiota, remain largely unexplored. This study aimed to explore how JBHD modulates gut microbiota, and how these changes may influence host metabolic regulation in the context of IPF. Methods The IPF model was established via intratracheal bleomycin injection. After 28 days of treatment, feces samples were obtained for 16S rRNA gene sequencing, whereas serum and urine samples were collected for metabolomic analyses. Results Gut microbiota analysis showed that JBHD restored microbial dysbiosis in IPF rats. Differentially altered fecal microbes (DAFMs) reversed by JBHD included Lactobacillus, Clostridium sensu stricto 1, Turicibacter , and Christensenellaceae R-7 group at the genus level. The microbial functions reversed by JBHD in both KEGG Level 3 and COG analyses were related to amino acid metabolism, including Biosynthesis of amino acids (KEGG) and Amino acid transport and metabolism (COG). Serum and urine metabolomics showed that JBHD modified the metabolic profile of IPF rats. Among the differentially expressed metabolites (DEMs) altered by IPF, JBHD reversed 11 in serum and 13 in urine. Pathway analysis indicated that these DEMs were mainly associated with amino acid and lipid metabolism. The consistency between microbial functional predictions and host metabolomic findings in amino acid metabolism suggests that JBHD may influence host metabolic pathways through gut microbiota modulation. Functional prediction of the targets of reversed DEMs highlights signaling pathways related to immune regulation. Correlation and network analyses between DAFMs and DEMs reveal potential associations, implying that gut microbiota alterations may contribute to coordinated changes in host metabolism. Discussion JBHD may act by reshaping specific microbial communities, which in turn could help restore related metabolic disturbances. These findings suggest a possible microbiota-mediated mechanism through which JBHD may exert its effects along the gut–lung axis.

Rumen microbial nitrogen metabolism is crucial for animal health, productivity, and environmental sustainability in ruminants. Natural products like biochanin A are garnering interest as potential feed additives due to their beneficial effects and safety profiles. Here, we collected total mixed diet, plasma, milk, urine, and feces samples of dairy goats to evaluate the impact of biochanin A on nitrogen metabolism and elucidated regulatory mechanisms of nitrogen metabolism using multi-omics approaches by analyzing plasma metabolites and ruminal microbial communities. Supplementation with biochanin A significantly enhanced nitrogen utilization efficiency of dairy goats. Plasma metabolomics revealed that biochanin A altered pathways related to amino acid biosynthesis/metabolism and glycolysis/gluconeogenesis. In the rumen, biochanin A enriched microbial strains from the families Selenomonadaceae and Aminobacteriaceae. Up-regulated proteins predominantly associated with glycolysis were identified by metaproteomics. Integrated metagenomic and metaproteomic analyses demonstrated that biochanin A positively influenced carbohydrate metabolism, amino acid metabolism, and energy metabolism pathways. Biochanin A enhances nitrogen metabolism by regulating rumen microbial community function, supporting its potential as a natural feed additive to improve nitrogen utilization of ruminants. Video Abstract.

Background Abdominal massage is a therapeutic intervention in traditional Chinese medicine for managing insomnia; however, its underlying mechanisms remain incompletely understood. This study aimed to investigate the effects of abdominal massage on the gut microbiota and brain-gut peptides in a rat model of insomnia from the perspective of the microbiota–gut–brain axis. Methods Forty-eight male Wistar rats were randomized into control, model, abdominal massage (Abd massage), and zolpidem groups ( n = 12). An insomnia model was induced by intraperitoneal injection of 4-chloro-DL-phenylalanine (PCPA). The Abd massage group and the zolpidem group, respectively, received 14 days of abdominal massage and zolpidem treatment. Hippocampal histopathology was evaluated with hematoxylin and eosin (HE) staining. Serum levels of interleukin-1 beta (IL-1β), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF- α ), vasoactive intestinal peptide (VIP), growth hormone (GH), substance P (SP), and cholecystokinin-8 (CCK8) were measured by enzyme-linked immunosorbent assay (ELISA). The gut microbiota composition was examined using 16S rRNA sequencing. Results Behavioral experiments in a rat model of insomnia demonstrated that abdominal massage significantly extended sleep duration. The treatment alleviated histopathological damage in the hippocampus and regulated brain-gut peptide levels in both colon and brain tissues. Additionally, abdominal massage modulated gut microbiota structure, reducing the relative abundance of Bacteroidetes and Proteobacteria and increasing that of Firmicutes , Lachnospiraceae_NK4A136_group , Clostridia , and Clostridiales . Spearman correlation analysis revealed significant associations between microbial abundance and biochemical indicators. PICRUSt2 analysis further implicated carbohydrate metabolism, amino acid metabolism, and transcriptional regulation in the pathogenesis of insomnia. Conclusion The results of this study demonstrate that abdominal massage ameliorates insomnia and increases sleep duration. This effect is associated with the regulation of brain-gut peptide levels and the restoration of gut microbiota diversity and structure. These findings suggest that the microbiota-gut-brain axis may be involved in the therapeutic mechanism of abdominal massage for insomnia.

Multi-endpoint evaluation of PFOA toxicity in Danio rerio: Oxidative, genotoxic, and metabolomic responses.

Chronic obstructive pulmonary disease (COPD) is a prevalent chronic respiratory disease characterized by high prevalence, mortality, and disease burden. Current understanding of COPD pathogenesis primarily focuses on airway inflammation, immune dysfunction, oxidative stress, and protease-antiprotease imbalance. Notably, recent studies have increasingly highlighted the role of metabolic reprogramming in COPD. Metabolic reprogramming refers to cellular adaptation through metabolic pathway alterations in response to environmental stress, enabling physiological or pathological state transitions. This review systematically summarizes COPD pathogenesis, with particular focus on metabolic reprogramming features (glucose, lipid, and amino acid metabolism) in immune cells from COPD experimental models. Furthermore, we analyze the interactions between these metabolic alterations and chronic inflammatory responses, providing new insights into COPD pathogenesis.