Search Results (691)

Background: D-amino acids are increasingly recognized as bioactive molecules with diverse physiological and pathological roles in humans, particularly in the gut, kidneys, and nervous system. Advances in analytical techniques have revealed their widespread presence in biological fluids, including plasma, urine, cerebrospinal fluid, amniotic fluid, and saliva, challenging the long-standing assumption that D-amino acids are absent or biologically insignificant in mammals. Scope: This review systematically summarizes the current knowledge on D-amino acid sources, distribution, metabolic regulation, and biological functions, with emphasis on their roles in human physiology and disease. Key findings: Accumulating evidence indicates that major D-amino acids, including D-serine, D-aspartate, and D-alanine, are derived from multiple sources such as diet, intestinal microbiota, and endogenous racemization processes. Rather than being passive metabolic byproducts, D-amino acids are now understood to participate in host–microbe interactions, neurotransmission, and renal physiology. Importantly, a consistent trend across studies is their dual and concentration-dependent nature, exhibiting beneficial effects under physiological conditions but potential cytotoxic effects at elevated levels. Conclusions and perspectives: Overall, D-amino acids represent multifunctional biomolecules with tightly regulated physiological roles and context-dependent pathological implications. However, major gaps remain in understanding their quantitative dynamics, tissue-specific regulation, and microbiota-dependent metabolism. Future studies addressing these mechanisms will be essential for establishing their clinical utility as biomarkers and for developing D-amino acid-based therapeutic and nutritional strategies. Full article

Triplophysa yarkandensis (Cypriniformes: Nemacheilidae), a rare endemic fish in the Tarim River Basin, Xinjiang, China, plays a pivotal role in maintaining the stability of plateau saline–alkaline aquatic ecosystems, yet its survival is increasingly threatened by habitat salinization. However, the multi-dimensional synergistic adaptation mechanisms linking its phenotypic variation, intestinal structure, and associated microbial communities to extreme saline–alkaline stress remain poorly understood. In this study, we innovatively integrated morphological/intestinal histological characterization, 16S rRNA gene sequencing, and microbial ecological analyses (co-occurrence networks and assembly processes) to systematically decode its adaptive strategies. Results revealed that T. yarkandensis exhibits a streamlined body shape, morphological variability, and elongated intestinal villi that may support locomotion and nutrient/ion uptake under osmotic stress. Its gut exerts a stringent selective filter, driving distinct differentiation between water and gut microbial communities—with gut-enriched core taxa (Aurantimicrobium and Aestuariivirga) and functional pathways (unsaturated fatty acid biosynthesis and ABC transporters) specialized for osmoregulation. Notably, the water microbial assembly is dominated by stochastic processes, while the gut assembly relies on host-driven deterministic selection, forming a habitat-specific adaptive pattern. These findings uncover the synergistic adaptation system of host phenotype and gut microbiota for survival in extreme saline–alkaline habitats, advancing our understanding of fish–microbe co-evolution in extreme ecosystems and providing critical theoretical support for the conservation of rare plateau fish, as well as guidance for the utilization of saline–alkaline water resources in aquaculture. Full article

Increasing evidence suggests pancreatic cancer develops within a host–microbe ecosystem in which microbial communities across anatomical niches interact with tumour biology, immune regulation, metabolism, and therapeutic response. This review examines pancreatic cancer through the lens of humans as holobionts, integrating evidence from the oral, gut, biliary, and intratumoural microbiomes. Epidemiological and sequencing studies demonstrate consistent microbial alterations across these niches in pancreatic cancer, including oral dysbiosis associated with periodontal pathogens, gut microbial shifts toward pro-inflammatory taxa, disease-specific biliary microbial signatures, and the presence of distinct intratumoural microbial communities. Mechanistic studies indicate that intestinal barrier disruption, microbial translocation, immune and metabolite signalling can influence tumour immune architecture, macrophage polarisation, T-cell infiltration, oncogenic signalling pathways, and chemotherapeutic metabolism, particularly inactivation by tumour-associated bacteria. Microbiome-driven shifts in immunometabolism can reprogramme immune-cell metabolic pathways, impairing effective T-cell activation, promoting tumour-supportive macrophage phenotypes. Emerging therapeutic strategies aim to modulate the microbiome–tumour axis, including dietary interventions, probiotics and immunonutrition, faecal microbiota transplantation, engineered microbial therapies, and microbiome-informed antibiotic strategies. While pre-clinical findings are compelling and early-phase clinical studies suggest feasibility, most evidence remains associative and heterogeneous across cohorts and methodologies. Understanding pancreatic cancer as a multi-site ecological system may help explain inter-patient variability in disease progression and treatment response. This could usher in a new era for therapeutic manipulation where future progress will depend on longitudinal, multi-omic, and interventional studies to determine whether microbiome-targeted strategies can produce clinically meaningful improvements in pancreatic cancer outcomes. Full article

Probiotics are commonly applied to maintain the balance of gut microbiota and regulate the intestinal metabolic function of companion animals. In the present study, complex probiotics (Bacillus coagulans SNZ-1969, Bacillus subtilis, and Bacillus licheniformis) were added into the basal diet of domestic cats to investigate their influence on the intestinal microbiome and metabolic characteristics. Results revealed that the alpha diversity of the gut microbiota in the probiotic group was enhanced when compared to the control group. The beta diversity of the gut microbiota was also altered by the oral consumption of the complex probiotics. Compared to the control group, the relative abundance of beneficial microbes (such as Clostridium, Bacteroides, Phocaeicola, and Ruminococcus) in the probiotic group was enhanced, while the relative abundance of opportunistic pathogens (such as Escherichia, Gallibacter, Corynebacterium) was decreased. Additionally, the intestinal metabolic characteristics of domestic cats were also changed. The metabolomic analysis identified 408 differential metabolites between the two groups, and the KEGG function pathway analysis proved that the dominant pathway related to the differential metabolites were the amino acid metabolism, lipid metabolism, carbohydrate metabolism, energy metabolism, endocrine system, digestive system, immune system, and other metabolic pathways. Spearman’s correlation analysis revealed that the beneficial microbes had positive correlations with the differential metabolites. In conclusion, the current study demonstrated that oral administration of complex probiotics could regulate overall health and well-being in domestic cats through modulating the gut microbiome and metabolic characteristics. Full article

Background: The prevalence of neurodegenerative diseases like Alzheimer’s and mental disorders like depression or anxiety appears higher in patients with gastrointestinal tract diseases like inflammatory bowel disease (IBD). Conversely, depressed patients have higher rates of gastrointestinal disorders. These observations suggest bidirectional communication between the brain and the gastrointestinal tract, the so-called “gut–brain axis”. Moreover, an altered microbiota, called “dysbiosis”, has been reported in these diseases, highlighting the network between gut microbes and their host. The emergence of the microbiota as a key regulator of the gut–brain dialog has led to the establishment of the concept of the “microbiota–gut–brain axis”. Objectives: In this narrative review, we outline the main interaction channels between the gastrointestinal tract and the brain. Then, we summarize current knowledge of two major diets (i.e., Western and Mediterranean diets) and the principal dietary components that modulate the microbiota–gut–brain axis to discuss the mechanisms putatively involved in intestinal, psychiatric, and neurological disorders. Conclusions: Diet is a major factor influencing the gut microbiota, and consequently, also putatively systemic mechanisms through the microbiota–gut–brain axis. Indeed, the composition of the diet is crucial for health and disease. Despite the main role of diet, the physiological, cellular, or molecular mechanisms involved in the complex communication between the microbiome, gut, and brain are still poorly understood. Full article

Background: Prostate cancer (PCa) arises from complex interactions among host genetics, androgen signaling, and microbial communities. Emerging genomic evidence supports the presence of microbial consortia within prostate tissue, suggesting that microbial genes, metabolites, and host–microbe interactions may contribute to chronic inflammation, oncogenic signaling, and therapeutic resistance. Methods: We conducted a narrative review using targeted searches of PubMed and Google Scholar for studies published between 2020 and 2025, complemented by selected mechanistic reports published in March 2026. Human studies and experimental research providing mechanistic insights into prostate models were prioritized. Due to the heterogeneous methodologies, evidence was synthesized qualitatively, with an emphasis on genomic and signaling perspectives. Results: Low-biomass microbial DNA is consistently detected in prostate tissue. Proteomic analyses of Corpora amylacea suggest a “fossil record” of past infections through sequestered microbial DNA and antimicrobial proteins, potentially priming tissue for long-term carcinogenic processes, although contamination remains a key limitation. Recurrent bacterial and viral signals, including Cutibacterium acnes, Escherichia coli, Pseudomonas, Acinetobacter, human papillomavirus, Epstein–Barr virus, and cytomegalovirus, appear to converge on a restricted set of tumor-relevant pathways, including TLR–NF-κB, MAPK, PI3K/AKT/mTOR, cGAS–STING, and p53/pRb disruption. These interactions may promote cytokine production, oxidative stress, DNA damage, epithelial–mesenchymal transition, extracellular matrix remodeling, immune evasion, and resistance to therapy. The gut–prostate axis further links intestinal dysbiosis and microbial metabolites with systemic IGF-1 signaling and castration resistance. Conclusions: Microbial genomic consortia in the prostate and gut may shape inflammatory, metabolic, and immune networks that influence PCa initiation and progression. However, most available data remain correlative and are limited by low-biomass sampling, contamination risk, and heterogeneous study designs. Future research should prioritize rigorous contamination control, longitudinal and prostate-specific mechanistic studies, and integrated multi-omic approaches to clarify causality and identify actionable microbial targets for prevention, diagnosis, and therapy. Full article

Recently, an oral–gut communication axis has been proposed. Herein, we review clinical studies reporting differences in oral microbial communities in inflammatory bowel diseases (IBDs), with a focus on Crohn’s Disease (CD), as well as evidence from experimental models. While available studies support evidence for the direct transmission of oral-derived bacteria to gut, further work is needed to clarify whether such transmission results in stable colonization of intestinal niches and the establishment of a persistent host–microbe state that influences host physiology. To date, evidence from clinical and murine studies suggests three routes of the oral–gut axis, which in turn directly or indirectly exacerbate intestinal inflammation and contribute to IBD pathogenesis: (i) direct invasion of pathobionts through swallowing, (ii) migration of the oral pathogen activated pro-inflammatory immune cells, (iii) systemic inflammation triggered by oral pathogens such as Porphyromonas gingivalis. Although the role of oral microbiome in systemic diseases is becoming more apparent, sophisticated clinical and experimental studies are needed to elucidate the direct and indirect oral–gut communication mechanisms, including the contribution of oral microbial metabolites. Future directions may include evaluating the diagnostic and therapeutic potential of the oral microbiome and metabolome. Full article

This study investigates the effects of N-acetylneuraminic acid (Neu5Ac) on intestinal microbial composition and metabolic activity in piglets using two complementary approaches: in vitro fermentation and in vivo dietary supplementation with coated Neu5Ac. In vitro fermentation results demonstrated that Neu5Ac stimulates higher production of formate and acetate by piglet intestinal microbiota compared with other human milk-derived monosaccharides (p < 0.05). In vivo feeding trials showed that dietary coated Neu5Ac significantly increased microbial α-diversity and altered the overall microbial composition in both the jejunum and colon (p < 0.05). For instance, coated Neu5Ac reduced the relative abundances of ASV1 Clostridium and ASV17 Clostridium in the jejunum, while raising the relative abundances of ASV3 Veillonella, ASV4 Veillonella, ASV7 Lactobacillus salivarius, ASV11 Actinobacillus porcitonsillarum in the jejunum, and ASV41 Xylanibacter in the colon (p < 0.05). Furthermore, coated Neu5Ac significantly elevated formate and acetate concentrations in the jejunum (p < 0.05) and exhibited a trend toward increased acetate levels in the colon (0.05 < p < 0.1). Collectively, using piglets as a model, this study demonstrates that Neu5Ac facilitates the intestinal colonization of beneficial microbes (e.g., Lactobacillus), leading to enhanced production of microbial metabolites, particularly formate and acetate, which may contribute to improved gut homeostasis in early life. Full article

Prostate cancer (PCa) is one of the most common malignancies in men, and growing evidence implicates the gut microbiome as a significant, modifiable contributor to disease evolution and management. Dysbiosis influences PCa biology through effects on inflammation, immune regulation, metabolism, and hormone signaling. Microbial imbalance can promote systemic inflammation and increase intestinal permeability, activating immune signaling pathways such as NF-κB–IL-6–STAT3. In parallel, microbiome-driven metabolic effects, including IGF-1 signaling and microbial androgen synthesis or recycling, may contribute to resistance to androgen deprivation therapy (ADT). Microbial metabolites, notably short-chain fatty acids (SCFAs) and trimethylamine N-oxide (TMAO), exert context-dependent effects on tumor growth, treatment resistance, and progression. Conversely, beneficial microbes have been associated with improved treatment sensitivity and immune regulation. Together, these insights support the gut microbiome as a potential biomarker and emerging therapeutic target in PCa. Modulation strategies, including diet, probiotics, antibiotics, and fecal microbiota transplantation (FMT), are being explored to improve treatment response and address resistance. As mechanistic evidence continues to grow, ongoing monitoring of the gut microbiome may help inform risk stratification and treatment optimization in prostate cancer. Full article

Deleterious crosstalk between the gut and distant organs is a key factor behind disease progression. Currently, the molecular signals mediating this communication remain elusive. We hypothesized that systemic oxidative stress and oxidatively modified serum proteins transmit injury signals from extraintestinal sites to the gut. In various murine models of organ injury, primary damage was consistently associated with systemic oxidative stress and intestinal damage. Specifically, ischemia/reperfusion (I/R)-induced acute kidney injury caused profound colonic barrier defects. Depleting the microbiota with antibiotics markedly improved survival and attenuated both renal and colonic injury, implicating translocated microbes in exacerbating pathology. Mechanistically, these changes were linked to systemic oxidative stress and were largely prevented by the antioxidant N-acetylcysteine. Furthermore, serum from I/R mice disrupted epithelial barrier integrity and induced cell death in vitro, effects that were recapitulated by exposure to oxidized serum proteins. Characterization of serum components identified albumin as the predominantly oxidized protein, which displayed potent cytotoxicity toward cultured intestinal epithelial cells. Our findings establish oxidative stress and oxidized serum albumin as key pathogenic factors mediating the detrimental interaction between remote organs and the gut. These data suggest that targeting oxidative modifications offers a promising therapeutic strategy to disrupt this pathological loop in critical illness. Full article

Runting and stunting syndrome (RSS) has been reported worldwide in commercial aquaculture and is frequently observed in juvenile-rearing ponds of Apostichopus japonicus. The objective of this study was to use commercially cultured A. japonicus naturally affected by RSS under high-density culture conditions as the study subjects. Different nutritional additive treatments, including marine mud, effective microorganisms (EM; photosynthetic bacteria, lactic acid bacteria, yeasts, and actinomycetes), yeast, kelp powder, and fermented kelp powder, were applied, and growth performance during recovery, the activities of intestinal digestive enzymes (protease, alginate lyase and cellulase), and heterotrophic bacterial counts were systematically evaluated. The results showed that the recovery rate of RSS in A. japonicus decreased in the following order: the EM group (90.91 ± 1.15%), the fermented kelp group (90.91 ± 4.96%), the yeast group (81.82 ± 5.99%), the kelp group (72.73 ± 1.35%), the marine mud group (63.64 ± 1.41%), and the control group (54.55 ± 1.47%). Moreover, increased intestinal digestive enzyme activities, elevated heterotrophic bacterial counts, and a reduced relative abundance of Vibrio were identified as key factors associated with RSS recovery in A. japonicus, with the EM and fermented kelp groups showing the most pronounced effects. High-throughput sequencing further revealed that nutritional additive treatments differed in their effects on the intestinal microbial community structure of RSS-affected A. japonicus. At the phylum level, Bacillota (26.45–48.08%), Actinomycetota (13.96–44.99%), and Pseudomonadota (9.15–56.46%) were the dominant phyla in the intestine of A. japonicus. At the genus level, a lower relative abundance of Vibrio was associated with improved recovery, and groups with lower Vibrio levels generally exhibited better recovery outcomes; notably, the EM group showed the lowest relative abundance of Vibrio (1.37%). Overall, these community shifts may contribute to recovery by supporting potential energy supply, immune regulation, and functional restoration. Therefore, these findings provide new insights into the treatment of RSS in A. japonicus through the development of beneficial microbes and the targeted suppression of potential pathogens. Full article

The rising cost of conventional protein sources such as soybean meal has prompted the search for sustainable and economical alternatives in aquafeeds. Sugar beet pulp (SBP), an abundant by-product of the sugar industry, possesses nutritional potential but is limited by its high fiber and anti-nutritional factors. Solid-state fermentation (SSF) offers a promising approach to enhance its nutritive value and functional properties. This study evaluated the effects of dietary inclusion of mixed microbial solid-state fermented beet pulp (FBP) on the growth, systemic health and intestinal function of juvenile yellow catfish (Pelteobagrus fulvidraco). First, orthogonal optimization determined Lactiplantibacillus plantarum:Saccharomycopsis fibuligera:Bacillus subtilis = 1:3:3 as the optimal ratio, significantly improving the nutritional profile of FBP. Based on this optimized FBP, an 8-week feeding trial, five isonitrogenous and isolipidic diets were formulated by replacing 0–12% soybean meal with FBP. The results demonstrated that 9% FBP inclusion yielded optimal growth performance and significantly improved muscle texture. At the systemic level, FBP supplementation reduced serum lipid markers and liver enzyme activities while enhancing antioxidant capacity. At the intestinal level, FBP promoted intestinal health by increasing key digestive enzyme (lipase, trypsin, amylase) activities, stimulating villus development, and improving intestinal antioxidant status. Furthermore, gut microbiota analysis revealed that dietary FBP supplementation significantly modulated intestinal microbial composition, with notable enrichment of genera such as Leucobacter. In conclusion, FBP is a multi-functional ingredient that enhances growth, product quality, systemic physiology, and intestinal health in yellow catfish aquaculture. These findings provide a viable strategy for the sustainable utilization of agricultural by-products in aquafeeds. Full article

Obesity has become a major disease in dogs and cats. Dietary management is a preventive measure because controlling energy intake (e.g., portion size and diet energy density) helps maintain an ideal BCS and reduces the likelihood of progressive weight gain and associated metabolic abnormalities. This study evaluated a low-fat diet, with or without plant-extract supplementation, and its effects on serum biochemistry, lipid metabolism, gut microbiota, and metabolic profiles in healthy beagles. Thirty beagles were randomly divided into three groups (n = 10 per group): a conventional diet (Group A), a low-fat diet (Group B), and a low-fat diet supplemented with plant extract (Group C). The experiment lasted for a total of 9 weeks, comprising an adaptation period of one week and an experimental period of eight weeks. Results showed that, compared with Group A, the low-fat diet interventions (Groups B and C) significantly reduced serum levels of triglycerides, low-density lipoprotein, and total bile acids (p < 0.05). Furthermore, superoxide dismutase activity was significantly higher in Groups B and C than in Group A (p < 0.05). Compared with both Groups A and B, Group C exhibited significantly lower malondialdehyde levels, reduced proinflammatory cytokines (tumor necrosis factor-α, interleukin-1β, interleukin-6; p < 0.05), and decreased serum diamine oxidase activity and lipopolysaccharide levels (p < 0.05). The gut microbiota analysis revealed that Group C had a significantly increased relative abundance of beneficial bacteria, such as Lactobacillus (p < 0.05). Metabolomic analysis further indicated that beneficial metabolites, including γ-aminobutyric acid and glutamine, were significantly upregulated in Group C (p < 0.05). In conclusion, while a low-fat diet effectively regulated serum lipids in healthy dogs, the supplementation of a blended extract from Atractylodes lancea, Magnolia officinalis, and Citrus reticulata Blanco demonstrated broader efficacy. It further improved lipid metabolism, systemic antioxidant status, and intestinal barrier function, while attenuating inflammation and enriching beneficial gut microbes (Lactobacillus) and metabolites (GABA and glutamine). These findings suggest that while a low-fat diet alone is beneficial, its combination with plant extract provides a novel dietary strategy for promoting lipid metabolism and potentially reducing obesity-related disease risk in dogs. Full article

The gut microbiota plays a key role in the health of wild birds, reflecting the influence of diet, habitat, and social behavior. Migratory and highly gregarious species such as the yellow-headed blackbird (Xanthocephalus xanthocephalus) provide valuable opportunities to explore host–microbe–environment interactions within a One Health framework. During migration, birds are exposed to diverse environments and dietary sources, which can promote highly diverse intestinal microbial communities and facilitate transient acquisition of environmental microorganisms. Here, we present the first taxonomic characterization of the fecal bacterial microbiota of X. xanthocephalus in northern Mexico based on 16S rRNA gene sequencing of the V3–V4 region. In addition, we performed a conservative screening to assess whether any bacterial taxa tentatively assigned at the species level have been previously reported as human pathogens or as having potential zoonotic relevance. Fecal samples were collected noninvasively from communal roosts within an urban–agricultural landscape of the Comarca Lagunera region during a winter season. A highly diverse bacterial community (39 phyla, 369 families, and 1195 bacterial species) was identified. Firmicutes_D, Actinobacteriota, and Campylobacterota were the dominant phyla. Among the bacterial taxa tentatively assigned at the species level, only three have been reported to exhibit zoonotic potential in the literature; however, none corresponded to avian-adapted pathogens or bacterial species historically associated with major zoonotic outbreaks, and all were detected at very low relative abundances. Overall, our findings establish an initial microbiological baseline for X. xanthocephalus and underscore the role of migratory birds as indicators of environmental microbial dynamics rather than direct sources of zoonotic risk in semiarid regions of northern Mexico. Full article

Irritable bowel syndrome (IBS) and small intestinal bacterial overgrowth (SIBO) share symptoms such as abdominal pain, bloating, and altered bowel habits. Both are linked to dysbiosis and gut–brain axis dysfunction. IBS is a multifactorial disorder characterized by abnormal motility, visceral hypersensitivity, low-grade inflammation, and alterations in the microbiota. In contrast, SIBO is defined by excessive bacterial colonization of the small intestine that can mimic or worsen IBS symptoms. Gut microbes and their metabolites influence motility, immune activation, barrier integrity, and gas production; methanogen overgrowth is associated with constipation-predominant presentations, while hydrogen- and hydrogen sulfide-related pathways may contribute to diarrhea and bloating. Because recurrent or empiric antibiotic use is common—particularly in suspected SIBO—yet carries risks of resistance, microbiome disruption, and relapse, there is a strong rationale to prioritize effective non-antibiotic strategies. Accordingly, this review synthesizes current evidence on IBS/SIBO pathophysiology and microbiota interactions. It evaluates non-pharmacological interventions including dietary approaches, probiotics/prebiotics, herbal therapies, and mind–body treatments (e.g., cognitive behavioral therapy and gut-directed hypnotherapy). We emphasize an integrative framework that supports symptom control and quality of life while helping reduce unnecessary antibiotic exposure. Full article