Search Results (10,293)

Inflammatory bowel disease (IBD) is characterized by chronic inflammation of the gastrointestinal tract. Although the aetiology of IBD remains largely unknown, several studies suggest that an individual’s genetic susceptibility, external environmental factors, intestinal microbial flora, and immune responses are all factors involved in and functionally linked to the pathogenesis of IBD. Beyond the gastrointestinal manifestations, IBD patients frequently suffer from psychiatric comorbidities, particularly depression and anxiety. It remains unclear whether these disorders arise solely from reduced quality of life or whether they share overlapping biological mechanisms with IBD. This review aims to explore the bidirectional relationship between IBD and depressive disorders (DDs), with a focus on four key shared mechanisms: immune dysregulation, genetic susceptibility, alterations in gut microbiota composition, and dysfunction of the hypothalamic–pituitary–adrenal (HPA) axis. By examining recent literature, we highlight how these interconnected systems may contribute to both intestinal inflammation and mood disturbances. Furthermore, we discuss the reciprocal pharmacologic interactions between IBD and DDs: treatments for IBD, such as TNF-alpha and integrin inhibitors, have demonstrated effects on mood and anxiety symptoms, while certain antidepressants appear to exert independent anti-inflammatory properties, potentially reducing the risk or severity of IBD. Overall, this review underscores the need for a multidisciplinary approach to the care of IBD patients, integrating psychological and gastroenterological assessment. A better understanding of the shared pathophysiology may help refine therapeutic strategies and support the development of personalized, gut–brain-targeted interventions. Full article

Premature ovarian insufficiency (POI) is an important factor in female infertility and is often associated with oxidative stress. Alginate oligosaccharides (AOSs), derived from the degradation of alginate, have been demonstrated to have protective effects against various oxidative stress-related diseases. However, the impact of AOSs on POI has not been previously explored. The current study explored the effects of AOSs on ovarian dysfunction in a mouse model of POI induced by D-galactose (D-gal). Female C57BL/6 mice were randomly divided into five groups: the control (CON), POI model (D-gal), and low-, medium-, and high-dose AOS groups (AOS-L, 100 mg/kg/day; AOS-M, 150 mg/kg/day; AOS-H, 200 mg/kg/day). For 42 consecutive days, mice in the D-gal, AOS-L, AOS-M, and AOS-H groups received daily intraperitoneal injections of D-gal (200 mg/kg/day), whereas those in the CON group received equivalent volumes of sterile saline. Following D-gal injection, AOSs were administered via gavage at the specified doses; mice in the CON and D-gal groups received sterile saline instead. AOS treatment markedly improved estrous cycle irregularities, normalized serum hormone levels, reduced granulosa cell apoptosis, and increased follicle counts in POI mice. Moreover, AOSs significantly reduced ovarian oxidative stress and senescence in POI mice, as indicated by lower levels of malondialdehyde (MDA), higher activities of catalase (CAT) and superoxide dismutase (SOD), and decreased protein expression of 4-hydroxynonenal (4-HNE), nitrotyrosine (NTY), 8-hydroxydeoxyguanosine (8-OHdG), and p16 in ovarian tissue. Analysis of the gut microbiota through 16S rRNA gene sequencing and short-chain fatty acid (SCFA) analysis revealed significant differences in gut microbiota composition and SCFA levels (acetic acid and total SCFAs) between control and D-gal-induced POI mice. These differences were largely alleviated by AOS treatment. AOSs changed the gut microbiota by increasing the abundance of Ligilactobacillus and decreasing the abundance of Clostridiales, Clostridiaceae, Marinifilaceae, and Clostridium_T. Additionally, AOSs mitigated the decline in acetic acid and total SCFA levels observed in POI mice. Notably, the total SCFA level was significantly correlated with the abundance of Ligilactobacillus, Marinifilaceae, and Clostridium_T. In conclusion, AOS intervention effectively mitigates ovarian oxidative stress, restores gut microbiota homeostasis, and regulates the microbiota–SCFA axis, collectively improving D-gal-induced POI. Therefore, AOSs represent a promising therapeutic strategy for POI management. Full article

While the gut microbiota of obese children in Mexico has been studied, its relationship with depressive and anxiety symptoms in obese adults remains unexplored. The aim of this study was to describe the gut microbiota profile of Mexican adults with obesity and its association with depression and anxiety. We sequenced the V3-V4 region of the 16S rRNA gene from stool samples of obese adults categorized into four groups: control (OCG), with depressive symptoms (OD), with anxiety symptoms (OAx), or with both (ODAx). Alpha diversity was assessed using t-tests, beta diversity was assessed with PERMANOVA, and taxonomic differences was assessed with LEfSe. Associations between bacterial genera and clinical variables were analyzed using the Maaslin2 library. Bacteroidota was the most prevalent phylum, and Prevotella was the dominant enterotype across all groups. Although overall diversity did not differ significantly, 30 distinct taxonomic biomarkers were identified among groups as follows: 4 in OCG (Firmicutes), 5 in OD (Firmicutes, Bacteroidota), 13 in OAx (Firmicutes, Bacteroidetes, Fusobacteroidota, Proteobacteria), and 8 in ODAx (Firmicutes). This is the first study to identify distinct gut microbiota profiles in obese Mexican adults with depressive and anxiety symptoms. These findings suggest important microbial biomarkers for improving the diagnosis and treatment of mental health conditions in obesity. Full article

Early weaning of piglets elicits weaning stress, which in turn induces oxidative stress and consequently impairs growth and development. Hydrogen-rich water (HRW), characterized by selective antioxidant properties, mitigates oxidative stress damage and serves as an ideal intervention. This study aimed to evaluate the effects of HRW on weaned piglets, specifically investigating its impact on growth performance, diarrhea incidence, antioxidant function, intestinal morphology, gut microbiota, and hepatic metabolites. The results demonstrate that HRW significantly increased the average daily feed intake and significantly reduced the diarrhea rate in weaned piglets. Analysis of serum oxidative stress indicators revealed that HRW significantly elevated the activities of total antioxidant capacity and total superoxide dismutase while significantly decreasing malondialdehyde concentration. Assessment of intestinal morphology showed that HRW significantly increased the villus height to crypt depth ratio in the duodenum, jejunum, and ileum. Microbial analysis indicated that HRW significantly increased the abundance of Prevotella in the colon. Furthermore, HRW increased the abundance of beneficial bacteria, such as Akkermansia, in the jejunum and cecum, while concurrently reducing the abundance of harmful bacteria like Escherichia. Hepatic metabolite profiling revealed that HRW significantly altered the metabolite composition in the liver of weaned piglets. Differentially abundant metabolites were enriched in oxidative stress-related KEGG pathways, including ABC transporters; pyruvate metabolism; autophagy; FoxO signaling pathway; glutathione metabolism; ferroptosis; and AMPK signaling pathways. In conclusion, HRW alleviates diarrhea and promotes growth in weaned piglets by enhancing antioxidant capacity. These findings provide a scientific foundation for the application of HRW in swine production and serve as a reference for further exploration into the mechanisms underlying HRW’s effects on animal health and productivity. Full article

Ultrafine bubbles (UFBs) represent an emerging technology with unique physicochemical properties. This study investigated the effects of air-filled UFBs infused in drinking water on gut microbiota composition and the associated health markers in Sprague Dawley rats over a 12-week period. Using a two-phase design, UFB concentration was increased from 1.7 × 10⁶ to 6.5 × 10⁹ UFBs/mL at week 7 to assess dose-dependent effects. Administration of UFBs in drinking water induced significant shifts in gut microbiome populations, characterized by increased Bacteroidetes (+122% weeks 8–12) and decreased Firmicutes (−43% weeks 8–12) compared to controls. These microbial shifts coincided with enhanced short-chain fatty acid production (butyrate +56.0%, p ≤ 0.001; valerate +63.1%, p ≤ 0.01) and reduced inflammatory markers (TNF-α −84.0%, p ≤ 0.05; IL-1β −41.0%, p ≤ 0.05; IL-10 −69.8%, p ≤ 0.05). UFB effects demonstrated systematic concentration-dependent threshold responses, with 85.7% of parameters exhibiting directional reversals between low (1.7 × 10⁶ UFBs/mL) and high (6.5 × 10⁹ UFBs/mL) concentration phases rather than linear dose–response relationships. The systematic nature of these threshold effects, with 71.4% of parameters achieving statistical significance (p ≤ 0.05), indicates concentration-dependent biological mechanisms rather than random effects on gut biology. Despite current metagenomic techniques identifying only 25% of the total gut microbiome, the observed changes in characterized species and metabolites demonstrate UFB technology’s therapeutic potential for conditions requiring microbiome modulation, providing new insights into UFB influence on complex biological systems. Full article

Low-dose carrot rhamnogalacturonan-I (cRG-I) has shown consistent modulatory effects on the gut microbiota and immune function in humans. In this study we investigated its effects on the microbial composition and metabolite production of the gut microbiota of small (5–10 kg), medium-sized (10–27 kg), and large (27–45 kg) dogs, using inulin and xanthan as comparators. Fecal samples from six dogs of each size group were evaluated. Overall microbiome composition, assessed using metagenomic sequencing, was shown to be driven mostly by dog size and not treatment. There was a clear segregation in the metabolic profile of the gut microbiota of small dogs versus medium-sized and large dogs. The fermentation of cRG-I specifically increased the levels of acetate/propionate-producing Phocaeicola vulgatus. cRG-I and inulin were fermented by all donors, while xanthan fermentation was donor-dependent. cRG-I and inulin increased acetate and propionate levels. The responses of the gut microbiota of different sized dogs to cRG-I were generally consistent across donors, and interindividual differences were reduced. This, together with the significant increase in P. vulgatus during fermentation in both this study and an earlier human ex vivo study, suggests that this abundant and prevalent commensal species has a core capacity to selectively utilize cRG-I. Full article

Autism Spectrum Disorder (ASD) is frequently accompanied by gastrointestinal disturbances, dietary selectivity, and altered stress responses, with growing evidence pointing to gut–brain axis involvement. While intestinal microbiota has been extensively studied, the role of the oral microbiota remains underexplored. This study investigates the associations between oral microbiota composition and behavioral, gastrointestinal, dietary, and neuroendocrine parameters in children with ASD. A total of 45 children aged 2–18 years comprised the study group. Data collection included oral swabs for 16S rRNA gene sequencing, salivary cortisol sampling, dietary records, and standardized behavioral assessments using the Vineland Adaptive Behavior Scale. A total of 363 microbial species across 11 phyla were identified. Significant correlations were observed between specific bacterial taxa and functional gastrointestinal disorders (FGIDs), dietary patterns, salivary cortisol rhythms, and functioning. Children with FGIDs, food selectivity, or macronutrient imbalances exhibited enriched pro-inflammatory taxa (e.g., Selenomonas, Megasphaera), whereas those with typical cortisol secretion or higher adaptive functioning showed greater microbial diversity and abundance of health-associated genera (e.g., Bifidobacterium dentium). These findings suggest that oral microbiota profiles may reflect systemic physiological and neurobehavioral traits in children with ASD. Further longitudinal studies are needed to clarify causal relationships and support the development of microbiota-targeted interventions. Full article

Background: Artificial non-nutritive sweeteners (NNSs), such as sucralose, have been associated with gut microbiota (GM) alterations. However, the impact of rebaudioside A (reb A), a natural NNS, on GM has received limited scrutiny. Objective: The objective of this study was to examine the response of GM composition to sucralose and reb A in rats under two dietary conditions. Methods: Male Wistar rats (150–200 g) fed with a normal diet (ND) or a high-fat diet (HFD) were randomly assigned to receive sucralose (SCL), reb A (REB), glucose (GLU, control), or sucrose (SUC). The NNS interventions were administered in water at doses equivalent to the acceptable daily intake (ADI). After eight weeks, the GM composition in fecal samples was analyzed through 16S ribosomal RNA gene sequencing. Results: The NNSs did not modify the diversity, structure, phylum-level composition, or Firmicutes/Bacteroidetes (F/B) ratio of the GM in rats under ND or HFD. However, REB with HFD decreased Bacilli and increased Faecalibacterium abundance at the class level. SCL and REB in rats receiving ND reduced the genera Romboutsia and Lactobacillus. Conclusions: Our study suggests that when sucralose or reb A is consumed at recommended doses, there is no alteration in the diversity or the composition of the GM at the phylum level. The clinical relevance of these findings lies in the potential modifications of the GM at specific taxonomic levels by the consumption of these NNSs. Further research involving humans and including a broader range of microbial analyses is warranted. Full article

Diabetic retinopathy (DR) is a progressive, multifactorial complication of diabetes and one of the major global causes of visual impairment. Its pathogenesis involves chronic hyperglycaemia-induced oxidative stress, inflammation, mitochondrial dysfunction, neurodegeneration, and pathological angiogenesis, as well as emerging systemic contributors such as gut microbiota dysregulation. While current treatments, including anti-vascular endothelial growth factor (anti-VEGF) agents, corticosteroids, and laser photocoagulation, have shown clinical efficacy, they are largely limited to advanced stages of DR, require repeated invasive procedures, and do not adequately address early neurovascular and metabolic abnormalities. Resveratrol (RSV), a naturally occurring polyphenol, has emerged as a promising candidate due to its potent antioxidant, anti-inflammatory, neuroprotective, and anti-angiogenic properties. This review provides a comprehensive analysis of the molecular mechanisms by which RSV exerts protective effects in DR, including modulation of oxidative stress pathways, suppression of inflammatory cytokines, enhancement of mitochondrial function, promotion of autophagy, and inhibition of pathological neovascularisation. Despite its promising pharmacological profile, the clinical application of RSV is limited by poor aqueous solubility, rapid systemic metabolism, and low ocular bioavailability. Various routes of administration, including intravitreal injection, topical instillation, and oral and sublingual delivery, have been investigated to enhance its therapeutic potential. Recent advances in drug delivery systems, including nanoformulations, liposomal carriers, and sustained-release intravitreal implants, offer potential strategies to address these challenges. This review also explores RSV’s role in combination therapies, its potential as a disease-modifying agent in early-stage DR, and the relevance of personalised medicine approaches guided by metabolic and genetic factors. Overall, the review highlights the therapeutic potential and the key translational challenges in positioning RSV as a multi-targeted treatment strategy for DR. Full article

Nonalcoholic fatty liver disease (NAFLD) is a clinicopathological syndrome characterised by hepatic steatosis in the absence of significant alcohol consumption or other specific causes of liver injury. It has become one of the leading causes of liver dysfunction worldwide. However, the precise pathophysiological mechanisms underlying NAFLD remain unclear, and effective therapeutic strategies are still under investigation. Autophagy, a vital intracellular process in eukaryotic cells, enables the degradation and recycling of cytoplasmic components through a membrane trafficking pathway. Recent studies have demonstrated a strong association between impaired or deficient autophagy and the development and progression of NAFLD. Restoring autophagic function may represent a key approach to mitigating hepatocellular injury. Nevertheless, due to the complexity of autophagy regulation and its context-dependent effects on cellular function, therapeutic strategies targeting autophagy in NAFLD remain limited. This review aims to summarise the relationship between autophagy and NAFLD, focusing on autophagy as a central mechanism. We discuss the latest research advances regarding interventions such as diet and exercise, pharmacological therapies (including modern pharmacological therapy and plant-derived compounds), and other approaches (such as hormones, nanoparticles, gut microbiota, and vitamins). Furthermore, we briefly highlight potential autophagy-related molecular targets that may offer novel therapeutic insights for NAFLD management. Full article

Background/Objectives: Primary liver cancer (PLC), encompassing hepatocellular carcinoma (HCC) and cholangiocarcinoma (CCA), constitutes a growing global health concern. Metabolic dysfunction-associated Steatotic Liver Disease (MASLD) and Type 2 diabetes mellitus (T2DM) represent a recurrent epidemiological overlap. Individuals with MASLD and T2DM (MASLD-T2DM) are at a higher risk of PLC. This scoping review highlights the epidemiological burden, the classic and novel pathogenetic frontiers, and the potential strategies optimizing the management of PLC in MASLD-T2DM. Methods: A systematic search of the PubMed, Medline, and SCOPUS electronic databases was conducted to identify evidence investigating the pathogenetic mechanisms linking MASLD and T2DM to hepatic carcinogenesis, highlighting the most relevant targets and the relatively emerging therapeutic strategies. The search algorithm included in sequence the filter words: “MASLD”, “liver steatosis”, “obesity”, “metabolic syndrome”, “body composition”, “insulin resistance”, “inflammation”, “oxidative stress”, “metabolic dysfunction”, “microbiota”, “glucose”, “immunometabolism”, “trained immunity”. Results: In the MASD-T2DM setting, insulin resistance (IR) and IR-induced mechanisms (including chronic inflammation, insulin/IGF-1 axis dysregulation, and autophagy), simultaneously with the alterations of gut microbiota composition and functioning, represent crucial pathogenetic factors in hepatocarcinogenesis. Besides, the glucose-related metabolic reprogramming emerged as a crucial pathogenetic moment contributing to cancer progression and immune evasion. In this scenario, lifestyle changes, simultaneously with antidiabetic drugs targeting IR-related effects and gut-liver axis, in parallel with novel approaches modulating immunometabolic pathways, represent promising strategies. Conclusions: Metabolic dysfunction, classically featuring MASLD-T2DM, constitutes a continuously expanding global issue, as well as a critical driver in PLC progression, demanding integrated and personalized interventions to reduce the future burden of disease. Full article

This comprehensive study investigates the spatial distribution of metals in surface water, their accumulation in fish tissues, and their impact on the gut microbiome dynamics of fish in the Qi River, Huanggang City, Hubei Province. Three distinct sampling regions were established: the mining area (A), the transition area (B), and the distant area (C). Our results revealed that metal concentrations were highest in the mining area and decreased with increasing distance from it. The bioaccumulation of metals in fish tissues followed the order of gut > brain > muscle, with some concentrations exceeding food safety standards. Analysis of the gut microbiota showed that Firmicutes and Proteobacteria dominated in the mining area, while Fusobacteriota were more prevalent in the distant area. Heavy metal pollution significantly altered the composition and network structure of the gut microbiota, reducing microbial associations and increasing negative correlations. These findings highlight the profound impact of heavy metal pollution on both fish health and the stability of their gut microbiota, underscoring the urgent need for effective pollution control measures to mitigate ecological risks and protect aquatic biodiversity. Future research should focus on long-term monitoring and exploring potential remediation strategies to restore the health of affected ecosystems. Full article

The enteroendocrine system of the gastrointestinal (GI) tract is the largest endocrine organ in the human body, playing a central role in the regulation of hunger, satiety, digestion, and energy homeostasis. Numerous factors—including dietary components, physical activity, and the gut microbiota—affect the secretion of GI hormones. This study aims to analyze how these factors modulate enteroendocrine function and influence systemic metabolic regulation. This review synthesizes the current scientific literature on the physiology and distribution of enteroendocrine cells and mechanisms of hormone secretion in response to macronutrients, physical activity, and microbial metabolites. Special attention is given to the interactions between gut-derived signals and central nervous system pathways involved in appetite control. Different GI hormones are secreted in specific regions of the digestive tract in response to meal composition and timing. Macronutrients, particularly during absorption, stimulate hormone release, while physical activity influences hormone concentrations, decreasing ghrelin and increasing GLP-1, PYY, and leptin levels. The gut microbiota, through fermentation and metabolite production (e.g., SCFAs and bile acids), modulates enteroendocrine activity. Species such as Akkermansia muciniphila are associated with improved gut barrier integrity and enhanced GLP-1 secretion. These combined effects contribute to appetite regulation and energy balance. Diet composition, physical activity, and gut microbiota are key modulators of gastrointestinal hormone secretion. Their interplay significantly affects appetite regulation and metabolic health. A better understanding of these relationships may support the development of personalized strategies for managing obesity and related disorders. Full article

Triatoma pallidipennis, the main vector of Chagas disease in central Mexico, hosts a diverse and complex gut bacterial community shaped by environmental and physiological factors. To gain insight into these microbes’ dynamics, we characterised the gut bacterial communities of wild and insectary insects under different feeding and Trypanosoma cruzi infection conditions, using 16S rRNA gene sequencing. We identified 91 bacterial genera across 8 phyla, with Proteobacteria dominating most samples. Wild insects showed greater bacterial diversity, led by Acinetobacter and Pseudomonas, while insectary insects exhibited lower diversity and were dominated by Arsenophonus. The origin of the insects, whether they were reared in the insectary (laboratory) or collected from wild populations, was the principal factor structuring the gut microbiota, followed by feeding and T. cruzi infection. A stable core microbiota of 12 bacterial genera was present across all conditions, suggesting key functional roles in host physiology. Co-occurrence and functional enrichment analyses revealed that feeding and infection induced condition-specific microbial interactions and metabolic pathways. Our findings highlight the ecological plasticity of the triatomine gut microbiota and its potential role in modulating vector competence, providing a foundation for future microbiota-based control strategies. Full article

The gross benefit of feeding multi-species probiotics has been reported, but the effect on the gut microbiota in pre-weaned dairy calves has not been elucidated. To address this gap, a randomized controlled trial was conducted in California, USA, to investigate the effect of feeding probiotics on the fecal microbiota of pre-weaned dairy calves. A total of 30 neonatal calves were randomly assigned to either the probiotic (PRO) or control (CON) treatment. Fecal samples were collected at four age timepoints: days 7, 14, 21, and 42. Fecal bacterial population was analyzed using 16S rRNA amplicon sequencing. Differential abundance analysis was conducted to investigate the difference between the PRO and CON treatments, and diarrheic and non-diarrheic calves in each PRO and CON group. The PRO group had decreased Clostridium perfringens and Fusobacterium varium compared to the CON at 7 days of age. At 7 days of age, diarrheic calves in CON had more abundant F. varium compared to non-diarrheic calves, but there was no difference between diarrheic and non-diarrheic calves in the PRO group. In conclusion, probiotics administration decreased the population of pathogenic bacteria in feces from pre-weaned dairy calves on Day 7 of age. However, the treatment did not have an impact on bacterial diversity. These results suggest that the administration of probiotics has the potential to control gastrointestinal pathogens. Full article