Functional dyspepsia (FD) and irritable bowel syndrome (IBS) are the most prevalent disorders of gut-brain interaction (DGBI), frequently overlapping and associated with complex pathophysiological mechanisms. Increasing evidence implicates gut microbiota alterations in driving symptoms via immune activation, altered motility, gut vascular barrier and gut-brain axis disruption. This review explores the role of gut microbiota in FD and IBS pathogenesis and symptomatology. A comprehensive literature search was conducted using PubMed, EMBASE, and Google Scholar databases, including studies published between January 2013 and March 2025. Particular focus is given to microbiota-targeted therapies such as prebiotics, probiotics, synbiotics, postbiotics, and fecal microbiota transplantation (FMT). The review also discusses multidimensional treatment strategies combining dietary and lifestyle modification, cognitive-behavioral therapy, and pharmacological neuromodulation. Recent advances in diagnostic methods, including capsule-based microbiota sampling and digital tools for remote psychogastroenterology care, are highlighted. Despite scientific progress, current DGBI management remains insufficiently personalized. Future approaches should integrate individualized microbiota profiling with targeted interventions and utilize innovative diagnostic and digital health technologies to enhance clinical outcomes in FD and IBS.

The gut microbiota, a complex community of microorganisms, plays a crucial role in gastrointestinal (GI) health, influencing digestion, metabolism, immune function, and the gut–brain axis. Dysbiosis, or an imbalance in microbiota composition, is associated with GI disorders, including irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and colorectal cancer (CRC). Conventional microbiota analysis methods, such as next-generation sequencing (NGS) and nuclear magnetic resonance (NMR), provide valuable insights but are often expensive, time-consuming, and destructive. Raman spectroscopy (RS) is a non-invasive, cost-effective, and highly sensitive alternative. This analytical technique relies on inelastic light scattering to generate molecular “fingerprints”, enabling real-time, marker-free analysis of microbiota composition and metabolic activity. This review explores the principles, sample preparation techniques, and advancements in RS, including surface-enhanced Raman spectroscopy (SERS), for microbiota research. RS facilitates identifying microbial species, analysing key metabolites like short-chain fatty acids (SCFA), and monitoring microbiota responses to dietary and therapeutic interventions. The comparative analysis highlights RS’s advantages over conventional techniques, such as the minimal sample preparation, real-time capabilities, and non-destructive nature. The integration of RS with machine learning enhances its diagnostic potential, enabling biomarker discovery and personalised treatment strategies for GI disorders. Challenges, including weak Raman signals and spectral complexity, are discussed alongside emerging solutions. As RS technology advances, mainly through portable spectrometers and AI integration, its clinical application in microbiota diagnostics and personalised medicine is poised to transform GI healthcare, bridging microbiota research with practical therapeutic strategies.

Background: Irritable Bowel Syndrome (IBS) is a complex disorder characterized by altered gut–brain interactions, with gastrointestinal microbiota and metabolic dysregulation playing key roles in its pathophysiology. Identifying specific metabolic alterations within the colonic mucosa may enhance our understanding of IBS and contribute to improved diagnostic and therapeutic approaches. Methods: This cross-sectional study analyzed the metabolomic profiles of colonic mucosal biopsies from 44 IBS patients assessed with ROME IV criteria and 69 healthy controls undergoing colonoscopy. Untargeted metabolomic profiling was conducted using liquid chromatography–mass spectrometry (LC-MS), and differential metabolite analysis was performed via fold-change calculations and machine learning-based classification. Results: IBS patients exhibited distinct mucosal metabolic profiles, with significantly elevated levels of N-acetylneuraminic acid and 1-palmitoylglycerol, suggesting compromised epithelial integrity and increased gut permeability. In contrast, cis-4-hydroxycyclohexanecarboxylic acid, a metabolite associated with protective mucosal functions, was reduced. Random Forest analysis identified these metabolites as key discriminatory features between IBS and control groups, reinforcing their potential role as biomarkers for IBS-related mucosal alterations. Conclusions: Our study highlights the unique metabolomic signatures of IBS at the mucosal level, emphasizing the role of microbial metabolites in disease pathology. These findings may facilitate the development of novel diagnostic tools and targeted therapeutic strategies, advancing personalized management for IBS patients.

Inflammatory bowel diseases (IBD) are increasingly acknowledged not merely as confined gastrointestinal disorders but as systemic immunometabolic syndromes. Central to this paradigm is the gut microbiota including non-bacterial components such as the virome, whose functional disruption marked by reduced short-chain fatty acids (SCFAs), increasingly implicated in pathogenic processes extending beyond intestinal mucosa. This review outlines how these alternations compromise the epithelial barrier and immune regulation, increasing the risk of recurrent Clostridioides difficile infections to anemia, neuropsychiatric comorbidities, and extraintestinal manifestations. We critically evaluate emerging microbiota-targeted strategies, including fecal microbiota transplantation (FMT), live biotherapeutic products (LBPs), and precision postbiotics, positioning them as potential adjuncts to conventional immunosuppression. Finally, we discuss the current barriers to clinical translation, such as safety and heterogeneity, and propose a future framework for personalized, functionally integrated IBD care aimed at restoring long-term microbiota homeostasis.

Colonoscopy is the gold standard for diagnosing and monitoring gastrointestinal diseases. However, bowel preparation, rather than the procedure itself, appears to be the main driver of transient gut microbiota disruption. Available evidence suggests that microbiota alterations after bowel preparation and colonoscopy may persist for days to weeks and may be associated with changes in barrier function, microbial metabolism, and symptom burden in susceptible individuals. This review summarizes current knowledge on the mechanisms underlying microbial disruption induced by bowel preparation, including loss of diversity, shifts in key taxa, impairment of metabolic pathways, and alterations in immunomodulatory metabolites. It also discusses potential clinical consequences and highlights nutritional strategies that may support microbiota recovery, including dietary fiber, polyphenols, and microbiota-targeted approaches. This review also highlights current research gaps and the need for well-designed clinical studies in this field.

Background/Objectives: Patient-reported outcomes (PROs) capture important dimensions of inflammatory bowel disease (IBD), including fatigue, questionnaire-defined mood-related symptom burden, pain, sleep disturbance, bowel urgency and impaired health-related quality of life, yet these outcomes are incompletely explained by conventional inflammatory markers. Metabolite-related measures may capture host–microbe co-metabolism relevant to patient-reported burden. Methods: This critical narrative review synthesized adult IBD literature linking metabolite-related measures with patient-reported symptom domains. PubMed/MEDLINE, Embase.com, Scopus and Web of Science Core Collection were searched through 11 June 2026; purposive source selection supported critical narrative synthesis rather than exhaustive enumeration. Results: Our structured search identified only a small number of human studies, mainly in fatigue and questionnaire-defined mood-related symptom burden. Studies included serum, plasma or fecal metabolite measurements, exploratory multi-omics, inferred microbial metabolic functions and interventional pathway testing. Fatigue was associated with serum amino-acid-related changes, plasma lipidomic alterations and fecal untargeted metabolomic and microbiome differences; inferred microbial functional modules were also reported. Mood-related burden was associated with serum and fecal metabolomic changes, bile-acid profiles and microbiota-derived functional signals. Within our search and eligibility criteria, no human studies paired measured metabolites with sleep-, pain- or urgency-specific patient-reported outcome measures (PROMs); evidence for multidimensional clusters was insufficient. Conclusions: We did not identify a metabolite-related signature for the assessment of patient-reported burden that had undergone both analytical and clinical validation; findings support candidate associations and exploratory signatures. Future work requires longitudinal, phenotype-stratified cohorts, validated PROMs, rigorous metabolomics methodology, causal modeling, inflammatory and dietary metadata, multiple-testing control and independent validation for clinical translation.