Search Results (198)

Irritable bowel syndrome (IBS) is a gut–brain axis chronic disorder, characterized by recurrent abdominal pain and altered bowel habits in the absence of organic pathology. Nutrition plays a central role in symptom management, yet no single dietary strategy has demonstrated universal effectiveness. This narrative review critically evaluates current nutritional approaches to IBS. The low-Fermentable Oligo-, Di-, Mono-saccharides and Polyols (FODMAP) diet is the most extensively studied and provides short-term symptom relief, but its long-term effects on microbiota diversity remain concerning. The Mediterranean diet, due to its anti-inflammatory and prebiotic properties, offers a sustainable, microbiota-friendly option; however, it has specific limitations in the context of IBS, particularly due to the adverse effects of certain FODMAP-rich foods. A gluten-free diet may benefit individuals with suspected non-celiac gluten sensitivity, although improvements are often attributed to fructan restriction and placebo and nocebo effects. Lactose-free diets are effective in patients with documented lactose intolerance, while a high-soluble-fiber diet is beneficial for constipation-predominant IBS. IgG-based elimination diets are emerging but remain controversial and require further validation. In this review, we present the 10 dietary commandments for IBS, pragmatic and easily retained recommendations. It advocates a personalized, flexible, and multidisciplinary management approach, avoiding rigidity and standardized protocols, with the aim of optimizing adherence, symptom mitigation, and health-related quality of life. Future research should aim to evaluate, in real-world clinical settings, the impact and applicability of the 10 dietary commandments for IBS in terms of symptom improvement and quality of life Full article

Recent findings highlight that Reelin, a glycoprotein involved in neural development, synaptic plasticity, and neuroinflammation, plays some specific roles in neurodegenerative disorders associated with aging, such as age-related macular degeneration (AMD) and Alzheimer’s disease (AD). Reelin modulates synaptic function and guarantees homeostasis in neuronal-associated organs/tissues (brain and retina). The expression of Reelin is dysregulated in these neurological disorders, showing common pathways depending on chronic neurogenic inflammation and/or dysregulation of the extracellular matrix in which Reelin plays outstanding roles. Recently, the relationship between AMD and AD has gained increasing attention as they share many common risk factors (aging, genetic/epigenetic background, smoking, and malnutrition) and histopathological lesions, supporting certain pathophysiological crosstalk between these two diseases, especially regarding neuroinflammation, oxidative stress, and vascular complications. Outside the nervous system, Reelin is largely produced at the gastrointestinal epithelial level, in close association with innervated regions. The expression of Reelin receptors inside the gut suggests interesting aspects in the field of the gut–brain–eye axis, as dysregulation of the intestinal microbiota has been frequently described in neurodegenerative and behavioral disorders (AD, autism, and anxiety and/or depression), most probably linked to inflammatory, neurogenic mediators, including Reelin. Herein we examined previous and recent findings on Reelin and neurodegenerative disorders, offering findings on Reelin’s potential relation with the gut–brain and gut–brain–eye axes and providing novel attractive hypotheses on the gut–brain–eye link through neuromodulator and microbiota interplay. Neurodegenerative disorders will represent the ground for a future starting point for linking the common neurodegenerative biomarkers (β-amyloid and tau) and the new proteins probably engaged in counteracting neurodegeneration and synaptic loss. Full article

Gamma-aminobutyric acid (GABA) is a non-protein amino acid playing a significant role in the central nervous system and the gut–brain axis. This study investigated the potential to produce GABA by lactic acid bacteria (LAB) isolated from different varieties of organic tomatoes. The isolated LAB were taxonomically identified by 16S rRNA gene sequencing, the presence of the gadB gene (glutamate decarboxylase) was detected, and GABA production was quantified using HPLC. Levilactobacillus brevis CRAI showed the highest GABA production under optimised fermentation conditions with 4% monosodium glutamate (MSG). The genome sequencing of L. brevis CRAI revealed the presence of gadA and gadB isoforms and assessed the strain’s safety profile. The gene expression analysis revealed that the gadA and gadB genes were upregulated in the presence of 4% MSG. The probiotic potential of L. brevis CRAI was also assessed by functional assays. The strain showed strong antimicrobial activity against representative enteropathogens, i.e., Escherichia coli ETEC, Salmonella choleraesuis, and Yersinia enterocolitica, and anti-inflammatory effect, reducing nitric oxide production in LPS-stimulated RAW264.7 macrophages. In addition, its ability to adhere to intestinal epithelial Caco-2 cells was demonstrated. These results highlight L. brevis CRAI as a promising candidate for the development of GABA-enriched functional foods or probiotic supplements with the perspective to modulate the gut-brain axis. Full article

Background/Objectives: High-fat-diet (HFD) consumption drives chronic liver injury via gut dysbiosis and metabolic disturban. Apple cider vinegar, rich in polyphenols and organic acids, shows potential in metabolic regulation. This study aimed to investigate whether apple cider vinegar powder (ACVP) alleviates HFD-induced liver injury by modulating the gut–liver axis. Methods: For 12 weeks, C57BL/6 J mice received daily ACVP gavage while being fed a HFD. A series of biological assessments were conducted, including systemic metabolic evaluations (body weight, serum alanine aminotransferase (ALT)/aspartate aminotransferase (AST), and lipid/glucose levels), hepatic steatosis (hematoxylin and eosin (H&E) staining), intestinal microbiome characterization (16S rRNA gene genomic analysis), and comprehensive metabolite profiling of cecal contents (non-targeted metabolomics). Pearson correlation networks integrated multi-omics data. Results: ACVP attenuated HFD-induced weight gain by 26.3%, hepatomegaly and dyslipidemia, as well as reduced hepatic lipid vacuoles and serum ALT (48%)/AST (21.5%). ACVP restored gut microbiota diversity, enriching Muribaculaceae. Cecal metabolomics identified 38 HFD-perturbed metabolites reversed by ACVP, including indolelactate, hyocholate, and taurocholic acid. the Kyoto encyclopedia of genes and genomes (KEGG) analysis revealed ACVP-mediated recovery of linoleic acid metabolism. Correlation networks linked Akkermansia to anti-inflammatory metabolites (e.g., trans-ferulic), while Desulfobacterota correlated with pro-inflammatory oxylipins (e.g., 12,13-dihydroxy-9Z-octadecenoic acid (DHOME)). Conclusions: ACVP mitigates HFD-induced liver injury by remodeling gut microbiota, restoring microbial metabolites, and enhancing gut–liver crosstalk. Full article

The gut-brain axis (GBA) represents an operant acting in a two-direction communication system between the gastrointestinal tract and the central nervous system, mediated by the enteric nervous system (ENS), vagus nerve, immune pathways, and endocrine signaling. In recent years, evidence has highlighted the pivotal role of the gut microbiota in modulating this axis, forming the microbiota-gut-brain axis (MGBA). Our review synthesizes current knowledge on the anatomical and functional substrates of gut-brain communication, focusing on interoceptive signaling, the roles of intrinsic primary afferent neurons (IPANs) and enteroendocrine cells (EECs) and the influence of microbial metabolites, including short-chain fatty acids (SCFAs), bile acids, and indoles. These agents modulate neurotransmission, epithelial barrier function, and neuroimmune interactions. The vagus nerve serves as a primary pathway for afferent sensory signaling from the gut influenced indirectly by the ENS and microbiota. Dysbiosis has been associated with altered gut-brain signaling and implicated in the pathophysiology of disorders ranging from irritable bowel syndrome to mood disorders and neurodegeneration. Microbial modulation of host gene expression via epigenetic mechanisms, including microRNAs, adds another layer of complexity. The gut has a crucial role as an active sensory and signaling organ capable of influencing higher-order brain functions. Understanding the MGBA has significant implications for new therapeutic interventions targeting the microbiome to manage neurogastroenterological and even neuropsychiatric conditions. Full article

Chronic kidney disease (CKD) has a high prevalence worldwide, with an increasing incidence. One of the mechanisms of CKD progression involves a disordered inter-organ relationship between the kidneys and the intestine, known as the kidney-gut axis. In CKD, two pathological gut conditions—disturbed gut microbiota composition called uremic dysbiosis and leaky gut—contribute to the progression of CKD. Dysbiosis is associated with the increased production of gut-derived uremic toxins, leaky gut, and chronic systemic inflammation, leading to worsening uremia, which in turn aggravates the gut condition. This vicious cycle should be a target of the therapeutic strategy against CKD. The modulation of uremic dysbiosis, including prebiotics, probiotics, and synbiotics, has been a typical treatment approach, although clinical evidence for their efficacy has been insufficient. Some non-antibiotic drugs have an impact on human gut bacteria that are believed to play a role in their clinical efficacy on kidney function. Nutrition therapies, including a low-protein diet, dietary fiber, a Mediterranean diet, and whole grains, positively influence gut microbiota composition and have been linked to a decreased risk of CKD. Novel strategies are currently being explored, involving the use of postbiotics, microbiome sequencing techniques, and fecal microbiota transplantation, although clinical application remains to be tested. Human trials investigating the above-mentioned interventions remain inconclusive due to several limitations, including dietary variability and genetic factors. Future research should focus on the development of more effective probiotics, prebiotics, and microbial metabolism-modifying drugs, not only for CKD but for other systemic diseases as well. Full article

Feed fermented by various strains of Lactobacillus plantarum (LP) produces distinct biologically active substances. This study systematically evaluates the growth performance, gut microbiota modulation, and immune response parameters in Muscovy ducks fed with LP81-fermented diets (LP81-FF) compared to conventional regimens. Our findings demonstrate that LP81-FF elicits dose-dependent improvements in Muscovy duck production parameters. Through a 70-day feeding trial, LP81-FF administration reduced feed intake by 3.1% and improved the average daily gain (ADG) and feed conversion ratio (FCR) by 9.18% and 6.65% (p < 0.05) compared to conventional feed. Systemic antioxidant capacity analysis revealed 25.99% elevation in total antioxidant capacity (T-AOC) (p < 0.05), accompanied by 14.37% and 30.79% increases in serum IgG and IgM levels, respectively. Immune organ indices showed dose-responsive enhancement, with the high-dose group (HD) achieving 47.27% and 28.92% increases in thymus and bursa of Fabricius indices (p < 0.05). Additionally, 16S rRNA sequencing revealed that LP81-FF optimized the intestinal microbial community structure of Muscovy ducks by promoting the abundance of Bacteroides, Butyricicoccus, and Ruminococcus (beneficial bacteria) (p < 0.05), while inhibiting the increase of Escherichia-Shigella and Rothia (harmful bacteria). It also promoted the secretion of beneficial metabolites such as Glutaric acid and 2,6-Diaminohexanoic acid in the intestine, inhibited the production of harmful substances dominated by Fexofenadine, and enhanced the strength of physical barrier-related factors such as intestinal mucosa villi and goblet cell count. These multi-omics insights establish that LP81-FF enhances growth performance through coordinated modulation of gut–liver axis homeostasis, mucosal immunity activation, and microbial-metabolic network optimization. Our results position LP81-FF as a sustainable alternative to antibiotic growth promoters in waterfowl production systems. Full article

The gut microbiome supports immune health and influences gut and heart functions through the gut-heart axis. Synbiotics (SBT), combining probiotics and prebiotics, help restore microbiome balance. Chemotherapy often disrupts this balance, leading to adverse effects on the gut and heart. This study explores the potential of SBT supplementation in reducing heart and gut inflammation caused by doxorubicin (DOX) chemotherapy. The gut microbiome plays a vital role in immune health, and metabolites produced by gut bacteria contribute to physiological functions through the gut-heart axis. Chemotherapy drugs often disrupt these processes, leading to adverse effects on internal organs. Using 24 ICR male mice divided into four groups, the experiment assessed the impact of SBT on DOX-induced damage. Results indicated that DOX treatment significantly worsened survival rates, physical performance, heart function, and gut microbiome stability. However, co-treatment with SBT improved these markers, suggesting that SBT may help mitigate chemotherapy-induced side effects in cancer patients. Full article

Until recently, it was believed that bacterial translocation occurs as a result of leaky gut syndrome or sepsis. To confirm or exclude the process of bacterial translocation, biomarkers can be used. One such biomarker is defensins, which indicate immune activity, as defensins are cationic peptides with antibacterial properties produced by intestinal epithelial cells. Also, fatty acid-binding proteins (I-FABP and L-FABP) can serve as useful serological markers for intestinal epithelial damage, indicating impaired intestinal permeability or organ damage, as high concentrations of them are found in tissues and low concentrations in blood serum. In the context of obesity, the integrity of the intestinal barrier, which can be disrupted by dietary fat, leads to increased intestinal permeability. Since bacterial translocation and microbiota contribute to obesity and Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD) associated with metabolic dysfunction, intestinal barrier markers can be used to study the role of the gut–liver axis. The aim of this study was to gain insight into the pathogenesis of MASLD and examine the impact of bacterial translocation markers and intestinal and hepatic fatty acid-binding proteins (I-FABP and L-FABP) in children with MASLD. Method: We examined 60 children with MASLD and overweight/obesity (MASLD was diagnosed based on increased liver echogenicity in ultrasound and elevated ALT activity), aged 14.5 years (range 8.5 to 15.8); 33 children with overweight/obesity without MASLD, aged 13.0 years (range 11.4 to 15.8); and 16 healthy controls aged 11.0 years (range 7.0 to 16.2). Defensin, I-FABP, and L-FABP levels were measured using commercial kits: ELISA kits (Drg Medtek) were used to assess α-5 and α-6 defensin concentrations (HBD5, HBD6). I-FABP and L-FABP concentrations were measured using commercial ELISA kits (Hycult Biotech Inc., Wayne, PA, USA). ANOVA analysis was used to compare results across the three study groups. Results: A significant difference was found for the following tests among children with MASLD, obesity, and healthy controls: defensin 6 (14.4 ng/mL vs. 6.13 ng/mL vs. 17.2 ng/mL, respectively), L-FABP (9168 pg/mL vs. 7954 pg/mL vs. 7620 pg/mL, respectively), and I-FABP (272 pg/mL vs. 321 pg/mL vs. 330 pg/mL, respectively). No differences were found in defensin 5 levels (median 567.2 pg/mL vs. 485.7 pg/mL vs. 601.8 pg/mL). No differences were observed in cholesterol levels (HDL, LDL) or triglyceride concentrations, as well as apolipoprotein levels. Conclusions: Based on our study, it was concluded that inflammation and intestinal barrier damage lead to increased L-FABP levels, as it is released from enterocytes in response to oxidative stress or tissue damage. Defensin 6 may indirectly affect L-FABP through microbiota regulation and protection of the intestinal barrier. Defensin 6 also exerts antimicrobial activity and may accompany liver inflammation, with its increased concentration in comparison to obesity explained by the activation of defense mechanisms. Full article

The existing body of evidence has highlighted gut microbiota as a versatile regulator of body wellness affecting not only multiple physiological metabolisms but also the function of remote organs. Emerging studies revealed a reciprocal relationship between physical exercise and intestinal microbiota, suggesting that physical exercise could enhance gut health, including regulating intestinal barrier integrity, increasing microbial diversity, and promoting beneficial microbial metabolism. Furthermore, the beneficial outcomes of exercise on the intestine may also promote brain health through the gut–brain axis. Diet is an important factor in boosting exercise performance and also greatly impacts the structure of gut microbiota. Abundant research has reported that diet alongside exercise could exert beneficial effects on metabolism, immune regulation, and the neuropsychiatric system. In this paper, we used a narrative review, primarily searching PubMed, Web of Science, and Elsevier, to review the existing research on how moderate-intensity exercise promotes gut health, and we introduced the effects of exercise on the nervous system through the gut–brain axis. We also proposed dietary strategies targeting the regulation of gut microbiota to provide guidelines for boosting brain health. This review highlights that moderate exercise and a healthy diet promote gut and brain health. Full article

Microplastics (MPs) and nanoplastics (NPs), formed through the degradation of larger plastic materials, are emerging pollutants of significant concern. While their impact on aquatic ecosystems is well documented, their effects on terrestrial, especially farm animals remain underexplored. This review assesses the potential threats of MPs and NPs to Bangladesh’s livestock sector by analyzing the results of experimental models and environmental studies. In Bangladesh, MPs and NPs have been detected in agricultural soils, air, water bodies, and aquatic organisms, indicating possible entry into animal systems through contaminated feed, water, and inhalation. Once internalized, these particles may trigger oxidative stress, inflammation, and tissue damage, impairing vital biological systems. Documented health consequences include reduced fertility, hematotoxicity, gut microbiota imbalance, gut–brain axis disruption, skeletal disorders, and metabolic dysfunction. Additionally, MPs and NPs can induce genomic changes, including altered gene expression and DNA hypomethylation, intensifying physiological damage and reducing productivity. Therefore, managing plastic contamination is vital in protecting animal health, ensuring food safety, and preserving human well-being around the globe, especially in vulnerable regions like Bangladesh. Given the critical role of livestock and poultry in ensuring food security and public health, the findings highlight an urgent need for comprehensive research and mitigation strategies. Full article

The gut microbiota represents a rich and adaptive microbial network inhabiting the gastrointestinal tract, performing key functions in nutrient processing, immune response modulation, intestinal wall protection, and microbial defense. Its composition remains highly personalized and responsive to external influences, including lifestyle patterns, physical activity, body composition, and nutritional intake. The interactions of the gut microbiota with bodily systems are conventionally interpreted as broad systemic impacts on organ balance. Yet, emerging research—exemplified by the gut microbiota–brain axis—suggests the potential existence of more targeted and direct communication mechanisms. Dysbiosis, characterized by microbial ecosystem disturbance, generates multiple metabolic compounds capable of entering systemic circulation and reaching distant tissues, notably including ocular structures. This microbial imbalance has been associated with both systemic and localized conditions linked to eye disorders. Accumulating scientific evidence now supports the concept of a gut–retina axis, underscoring the significant role of microbiota disruption in generating various retinal pathologies. This review comprehensively investigates gut microbiota composition, functional dynamics, and dysbiosis-induced alterations, with specific focus on retinal interactions in age-related macular degeneration, diabetic retinopathy, glaucoma, and retinal artery occlusion. Moreover, the review explores microbiota-targeted therapeutic strategies, including precision nutritional interventions and microbial transplantation, as potential modulators of retinal disease progression. Full article

Depression poses increasing public health challenges, and alternative dietary strategies are gaining attention for their potential therapeutic effects. This study evaluates a natural ingredient-based formula powder (FP) for its antidepressant effects in a chronic unpredictable mild stress (CUMS) mouse model under both a standard diet and high-fat high-sugar diet (HFHSD) conditions. Behavioral tests demonstrated that FP significantly reduced immobility time in the forced swimming test and tail suspension test, and improved anxiety-like behavior in the open field test, particularly by increasing the central zone activity in mice fed a standard diet. FP supplementation also mitigated CUMS- and HFHSD-induced organ damage, as indicated by increased small intestine and colon coefficients. At the molecular level, FP downregulated the expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) and upregulated brain-derived neurotrophic factor (BDNF) and tryptophan hydroxylase-2 (TPH2) in the hippocampus and colon. These findings suggest that FP exerts antidepressant-like effects by alleviating neuroinflammation and supporting the gut–brain axis, offering a promising functional food approach for managing depression. Full article

Recently, the gut microbiota has been found to be associated with multiple organs and systems in the human body, playing a key role in the occurrence and development of various diseases, such as the gut–brain axis and the gut–liver axis. However, its interaction with miscarriages remains poorly understood. This article reviews the characteristics of gut microbiota and its metabolites in patients with recurrent spontaneous abortion (RSA), the mechanism of gut microbiota inducing RSA, and potential therapeutic strategies. Therefore, it provides a new perspective on the gut microbiota in the pathogenesis and treatment of recurrent abortion, and the prospect of the future research direction of gut microbiota and recurrent abortion is proposed based on existing studies. Full article

The term “plastics” is an umbrella term generally referring to any material containing a high level of polymer content as an essential ingredient. Micro(nano)plastics (MNPs) are derived from the degradation of plastics, representing exogenous substances whose exposure can potentially interfere with different physiological processes. In this scenario, even considering the relative paramount detoxification role, the liver emerges as a key active organ in the relationship between plastic exposure and human disease. In industrialized countries, where plastics constitute largely diffused components of objects routinely adopted in daily/social life, including food packaging, Metabolic dysfunction-associated Steatotic Liver Disease (MASLD) represents the predominant hepatopathy and is progressively becoming the leading cause of cirrhosis and liver cancer, with an incompletely elucidated multifactorial pathogenesis. Notably, oral exposure to MNPs has been revealed to impact the gut–liver axis by influencing gut microbiota composition, gastrointestinal absorption, and, ultimately, determining hepatic accumulation. At the hepatic level, MNPs can contribute to the onset and worsening of steatosis by inducing metabolic dysfunction and inflammation. Plastics can also serve as vectors for different potentially toxic additives, with specific MNPs constituting a persistent source of release of bisphenol A (BPA), a well-recognized exogenous etiological factor contributing to MASLD genesis and worsening. Recently, exposure to MNPs and additives has demonstrated significant impacts on the immune system, oxidative stress, and metabolism. In particular, polystyrene-derived MNPs impair the mechanisms regulating hepatic lipid metabolism, simultaneously acting as antigens abnormally triggering the innate immune response. At the same time, environmental BPA exposure has been revealed to trigger trained immunity-related pathways, configuring novel pathogenetic drivers potentially promoting the progression of MASLD. The present review, after rapidly overviewing the main sources and toxicological properties of MNPs and related additives, explores plastic-related exposure’s potential implications in the genesis and progression of hepatic steatosis, highlighting the urgent need for further clarification of relative pathogenetic mechanisms. Full article