Search Results (739)

Chronic kidney disease (CKD) is increasingly linked to intestinal barrier dysfunction, which contributes to systemic inflammation and disease progression. We investigated whether 2′-fucosyllactose (2′-FL), a human milk oligosaccharide, could modulate intestinal epithelial barrier function under uremic toxin exposure and examined the role of the aryl hydrocarbon receptor (AhR). Using wild-type (WT) and AhR knockout (AhR KO) Caco-2 cell lines, we assessed barrier function and cellular responses through transepithelial electrical resistance (TEER), paracellular permeability (Papp), tight junction (TJ) gene expression, AhR target gene activation, and metabolic assays. AhR deficiency impaired epithelial maturation, confirming its role in barrier development. Short-term exposure to uremic toxins (UTs) did not significantly affect TEER or paracellular permeability under the conditions tested. However, 2′-FL reduced paracellular permeability in both WT and AhR KO cells in the presence of FCS. These effects occurred without changes in TJ gene expression, indicating mechanisms beyond transcriptional regulation. AhR target genes were not induced by UTs, suggesting limited receptor activation, and metabolic activity was unaffected. Overall, 2′-FL reduced paracellular permeability under selected experimental conditions, while the impaired barrier development observed in AhR-deficient cells supports a role for AhR in intestinal epithelial barrier development. Full article

Background/Objectives: Cancer-related fatigue (CRF) is one of the most prevalent and disabling symptoms among patients with cancer, but its underlying mechanisms and effective management strategies have not yet been fully elucidated. Increasing evidence suggests that the microbiota–gut–brain axis (MGBA) may contribute to the pathogenesis of CRF by integrating nutritional status, intestinal barrier integrity, microbial metabolites, immune responses, and host energy metabolism. However, direct causal evidence in human CRF remains limited, and several mechanistic insights are extrapolated from other disease models. This narrative review aims to synthesize evidence for nutritional MGBA–CRF regulatory mechanisms, focusing on microbiota-associated biomarkers and microbiome-targeted dietary interventions, and to distinguish directly observed in a CRF population from indirect hypothetical mechanisms. Methods: This review synthesizes current evidence on the nutritional regulatory mechanisms linking the MGBA to CRF, with particular attention to microbiota-associated biomarkers and dietary or microbiome-targeted interventions. Results: Microbiota dysbiosis, reduced production of short-chain fatty acids, disrupted tryptophan metabolism, and increased intestinal permeability may lead to systemic inflammation, neuroendocrine dysfunction, and impaired mitochondrial function, thereby exacerbating fatigue. Moreover, nutritional factors, dietary patterns, and microbiota-targeted interventions may help restore microbiota homeostasis and alleviate fatigue-related biological dysregulation. Conclusions: A deeper understanding of MGBA may help in developing personalized nutritional strategies for patients with cancer experiencing fatigue symptoms and support more effective management of CRF. Full article

Cold exposure is an important environmental stressor that can disrupt physiological homeostasis and induce complex metabolic, immune, oxidative, and gastrointestinal responses. Increasing evidence indicates that the intestine is a sensitive target of cold exposure, yet the underlying mechanisms and their interrelationships remain incompletely understood. This review summarizes and critically evaluates current evidence on cold exposure-induced intestinal dysfunction and adaptation, with emphasis on intestinal barrier integrity, mucus and digestive function, inflammatory and oxidative responses, pyroptosis-related signaling, gut microbiota remodeling, animal models, and potential intervention strategies. Experimental studies in rodents, pigs, poultry, and fish indicate that cold exposure can induce intestinal morphological alterations, epithelial barrier disruption, increased permeability, tight-junction remodeling, mucus and digestive dysfunction, inflammatory activation, oxidative stress, apoptosis, and, under specific conditions, inflammasome-associated pyroptosis. Concurrent alterations in gut microbial composition and metabolites may interact with epithelial and immune responses, although the temporal and causal relationships among these processes remain insufficiently defined. Importantly, intestinal responses to cold are highly context-dependent and vary according to exposure temperature, duration, pattern, species, nutritional status, acclimation history, and pre-existing disease. Evidence from experimental colitis models further suggests that controlled cold exposure may promote mucosal repair and antimicrobial defense under selected conditions, indicating that cold exposure is not universally detrimental to intestinal health. This review also evaluates nutritional and food-derived strategies, including rutin, plant-derived preparations, dietary glucose, sodium butyrate, vitamin D3, probiotics, prebiotics, and other microbiota-targeted approaches, which have shown potential in mitigating cold-associated intestinal disturbances. Finally, major methodological and translational challenges are discussed, including the need for standardized cold-exposure protocols, causal and longitudinal studies, functional microbiome analysis, and better translation from animal models to human health. Collectively, current evidence supports a multidimensional and context-dependent framework for understanding how cold exposure influences intestinal homeostasis and highlights nutritional and food-derived interventions as promising strategies for maintaining intestinal health under cold environmental conditions. Full article

Background/Objectives: Mesalazine (MSZ), the first-line therapy for ulcerative colitis (UC), is a BCS Class IV drug limited by poor aqueous solubility and low intestinal permeability, which together restrict colonic drug delivery and therapeutic efficacy. This study aimed to develop a co-amorphous (CAM) system of MSZ and aloperine (ALO) to enhance MSZ dissolution and permeation while achieving anti-UC synergy. Methods: The MSZ-ALO CAM system was prepared via solvent evaporation and characterized by PXRD, DSC, FTIR, and ¹H NMR. Equilibrium solubility, intrinsic dissolution rate (IDR), and in vitro permeability were assessed under biorelevant pH conditions. Physical stability was evaluated under long-term and accelerated conditions. Network pharmacology predicted potential therapeutic targets and synergistic mechanisms. Results: Solid-state characterization confirmed a homogeneous single-phase CAM system stabilized mainly by a carboxylate–ammonium ionic bond and hydrogen bonding. At pH 4.5, where MSZ solubility was lowest, equilibrium solubility and IDR increased up to 71.9-fold and 35.8-fold, respectively. In vitro permeability at pH 6.5 increased 2-fold. The system remained physically stable for eight months under dry conditions and withstood accelerated stresses without recrystallization. Network pharmacology identified 51 shared targets among MSZ, ALO, and UC, enriched in MAPK, HIF-1, and AMPK pathways; core hubs included HSP90AA1, SRC, CASP3, GSK3B, and ALB. Conclusions: This study presented the first MSZ-ALO CAM system that simultaneously addresses the dual solubility and permeability barriers of MSZ and provided a multi-target pharmacological basis for synergistic UC therapy, offering a promising pharmaceutical strategy for colon-targeted delivery. Full article

Polycystic ovary syndrome is a heterogeneous endocrine and metabolic disorder diagnosed when at least two of three features—chronic anovulation, hyperandrogenism, and polycystic ovarian morphology—are present, according to the Rotterdam criteria endorsed by the 2023 International Evidence-Based Guideline. Its metabolic burden extends well beyond reproduction. Insulin resistance, low-grade systemic inflammation, and central adiposity are common, and recent work links the composition of the gut microbiota and the integrity of the intestinal barrier to each of these features, the association between dysbiosis and the pathogenesis of the syndrome having been reviewed in detail. The same gut-related disturbances are now being connected to a second, less recognized consequence of the syndrome: impaired skeletal muscle health. In one cohort, an increased prevalence of sarcopenic obesity has been reported in PCOS despite the anabolic potential of androgen excess, and this review proposes that the two observations are mechanistically linked. Two candidate pathways connect the gut to muscle in PCOS. The first runs from increased intestinal permeability to circulating lipopolysaccharide, which activates Toll-like receptor 4 and a cascade of pro-inflammatory cytokines that blunt insulin signalling in skeletal myocytes. The second runs through bile acids: PCOS is characterized by a distinct circulating bile acid profile, currently described in a preprint that has not undergone peer review, while peer-reviewed profiling has confirmed altered circulating bile acid signatures and links to hyperandrogenism in women with PCOS. Signalling through the farnesoid X receptor and Takeda G protein-coupled receptor 5 has been shown to regulate muscle insulin sensitivity, mitochondrial oxidative capacity, and protein turnover in experimental systems, although direct demonstration in human PCOS muscle is lacking. Both pathways are predicted to converge on the IRS-1–PI3K–Akt–mTORC1 axis, the signalling hub through which muscle cells normally translate insulin into glucose uptake and protein synthesis. After reviewing the evidence for gut barrier dysfunction and skeletal muscle impairment in PCOS, we propose a dual-axis model linking intestinal permeability, bile acid signalling, and sarcopenic obesity. We then consider the therapeutic potential of interventions targeting the microbiota, bile acid receptors, inflammation, and muscle function, and outline the study designs that could test the model directly. Full article

Pancreatic diseases, including acute pancreatitis (AP) and chronic pancreatitis (CP), pancreatogenic diabetes mellitus (T3cDM), autoimmune pancreatitis (AIP), and pancreatic cancer (PDAC), are associated with metabolic, inflammatory, and nutritional disturbances. Increasing evidence indicates a bidirectional relationship between pancreatic diseases and the gut microbiota. On the one hand, alterations in microbial composition and function, intestinal barrier dysfunction, and bacterial translocation may contribute to their pathogenesis and progression. On the other hand, pancreatic diseases and associated changes in nutrition and treatment may affect the composition and function of the gut microbiota. This narrative review aimed to discuss the role of the gut microbiota and nutritional aspects in selected pancreatic diseases. PubMed/MEDLINE was searched up to May 2026 for English-language publications, with emphasis on studies from the previous 10 years, while earlier relevant studies were also considered. Google Scholar was used as a supplementary source. Human observational, experimental and mechanistic studies, as well as secondary literature, were considered, addressing pancreatic microbiota, intestinal permeability, bacterial translocation, nutrition, and microbiota-targeted interventions. Available evidence indicates that pancreatic diseases are associated with alterations in gut and pancreatic microbial communities, although the reported patterns vary between diseases and studies. These changes may be relevant to intestinal barrier integrity, inflammatory signaling, microbial metabolite production, and, in pancreatic cancer, the tumor microenvironment and treatment response. Nutritional management remains an important component of care, particularly in patients with exocrine pancreatic insufficiency and those at risk of malnutrition. However, the causal relationships between pancreatic diseases and microbiota alterations remain incompletely established, and evidence for microbiota-targeted interventions is limited and heterogeneous. Further clinical studies are needed to clarify these interactions and their potential diagnostic and therapeutic relevance. Full article

Background/Objectives: Cecal ligation and puncture (CLP)-induced sepsis is accompanied by intestinal tight-junction disruption, circulating markers of barrier dysfunction, oxidative stress, bacterial dissemination, and multi-organ injury. This study evaluated the protective effects of chemically characterized pomegranate peel extract (PPE) and punicalagin (PUN) in a rat CLP model. Methods: Forty-eight female Wistar rats were randomized into six groups (n = 8): Sham, CLP, CLP + PPE 150 mg/kg, CLP + PPE 300 mg/kg, CLP + PUN 50 mg/kg, and non-septic PPE 300 mg/kg. Treatments were administered orally 1 h after surgery. Animals were monitored for 48 h and sampled at a predefined humane endpoint or at 48 h. Results: CLP reduced ileal ZO-1 and occludin abundance and increased serum diamine oxidase, D-lactate, and plasma endotoxin (all omnibus p < 0.001). Relative to untreated CLP, PPE 300 mg/kg increased ZO-1 and occludin by 219% and 236%, respectively, and reduced circulating markers consistent with intestinal barrier dysfunction, oxidative stress, lactate, and multi-organ injury. PPE 300 mg/kg and PUN 50 mg/kg were also associated with higher hepatic SIRT1/PGC-1α expression, lower recoverable aerobic bacterial burden, less histological injury, and higher observed 48 h survival (7/8 and 8/8 vs. 2/8 in CLP). Conclusions: PPE and PUN produced coordinated protective changes in this experimental CLP model. These biomarker-based and survival findings support further preclinical investigation of standardized pomegranate-derived preparations as potential adjunctive interventions; they do not establish direct intestinal permeability, mitochondrial restoration, clinical therapeutic efficacy, or a punicalagin-mediated mechanism. Full article

The consumption of Brassica spp. vegetables has been associated with antioxidant, anti-inflammatory, and prebiotic effects, mainly attributed to glucosinolates and polyphenols which are abundant in sprouts. Although broccoli sprouts are a recognized source of these bioactive compounds, other Brassicaceae sprouts remain comparatively understudied, particularly in relation to gastrointestinal disorders. In this in vitro study, hydroalcoholic extracts from red cabbage (CR) and pak-choi (PC) sprouts were compared with broccoli (BR) for their phytochemical composition, anti-inflammatory and intestinal barrier-protective activities. Caco-2 cells were stimulated with IL-1β, IFN-γ, and digested gliadin, while a Caco-2/THP-1 co-culture stimulated with LPS and IFN-γ was used to mimic intestinal permeability. CR contained the highest amounts of glucoraphanin (GFN, 22.133 ± 0.212 mg/g of extract) and sulforaphane (SFN, 9.517 ± 0.661 mg/g of extract), whereas BR showed the lowest levels. Polyphenol contents were comparable among the three extracts (3.5–4.5%). At 50 µg/mL, CR and PC extracts inhibited MCP-1 release (–37% and –48%, respectively), followed by BR (–31%), and this inhibitory effect was maintained after simulated gastrointestinal digestion. None of the extracts impaired the NF-κB-driven transcription, whereas only PC significantly enhanced the activity of Nrf-2. In the co-culture model, CR preserved epithelial barrier integrity measured by TEER and Lucifer Yellow assays (25–100 µg/mL). A PCR array showed that PC and CR (50 µg/mL) modulated genes involved in inflammation and barrier function, with a partial overlap with GFN. At the nominal p-value level, CR reduced CLDN1 and STAT3 transcript levels; however, these changes did not remain significant after FDR correction. These findings identify CR as a promising source of bioactive compounds associated with the preservation of epithelial barrier integrity, possibly through the modulation of selected inflammatory and barrier-related pathways. The lack of a direct relationship between glucosinolate abundance and biological activity suggests that the observed effects may depend on the overall phytochemical complexity of the extracts, including both sulfur-containing compounds and polyphenols. Full article

Childhood obesity now affects more than 160 million children and adolescents worldwide, and over the same period ultra-processed foods have come to dominate the early-life diet. This review sets out a single argument: that the effect of ultra-processed foods on childhood obesity is better read developmentally, and that the digestive tract is the organ through which much of that effect is transmitted. Exposure begins before birth and continues through the first 1000 days and complementary feeding, the period in which the gut microbiota assembles and the intestinal barrier matures. We show how ultra-processed foods perturb these two systems in particular: a low-fibre, additive-rich, energy-dense diet reshapes microbial community structure and depletes short-chain fatty acid production, while emulsifiers and other additives thin the mucus layer and raise intestinal permeability, admitting microbial products that sustain low-grade inflammation. We trace how these gut-level changes feed forward into altered appetite regulation, adipocyte biology and, ultimately, excess adiposity, and we situate the other proposed mechanisms (matrix disruption, hyperpalatability, accelerated eating rate, endocrine-disrupting additives and central reward signalling) around this digestive core, marking at each step where the evidence is paediatric and where it rests on adult or animal data. The epidemiological literature is appraised by study design, and the constraints on causal inference are stated plainly: NOVA misclassification, residual confounding, reverse causation, dietary misreporting and the scarcity of paediatric trials. The practical implication is that prevention framed around early-life gut health, rather than around cumulative adult-style exposure, is where intervention is most plausibly effective. We are explicit throughout that most of the mechanistic evidence derives from animal or adult studies and that a causal role for ultra-processed foods in childhood adiposity, though biologically plausible, is not yet established in paediatric populations; the developmental reading we advance is the most coherent interpretation of an associational evidence base, not a demonstrated causal chain. Full article

Type 2 diabetes mellitus (T2DM) is a metabolic disorder characterized by insufficient insulin production and diminished insulin receptor sensitivity. Prediabetes, which often precedes T2DM, involves elevated blood glucose levels that do not yet meet T2DM diagnostic criteria. Research has shown that complications linked to T2DM often begin during this prediabetic phase. In this study, we examined changes in intestinal barrier integrity during prediabetes by measuring biomarkers associated with intestinal permeability. With ethical approval, samples were collected from King Edward Hospital and Albert Luthuli Central Hospital in Durban and categorized into type 2 diabetes (T2D), prediabetes (PD), and non-prediabetes (NPD) groups. Blood levels of neutrophils and HbA1c were measured and analyzed, followed by serum zonulin and plasma levels of markers, including IFABP, sCD14, TNF-α, IL-6, glucose, insulin, and pancreatic lipase, which were measured and analyzed. The results showed significantly higher levels of these markers in the PD group compared to the NPD group, with further elevations in the T2D group. These findings align with existing research suggesting an association between increased intestinal permeability and the development of prediabetes. Altogether, these results indicate that prediabetes is a transitional phase marked by metabolic and intestinal permeability changes, though less severe than in T2DM. This underscores the need for additional research to cover a wider range of metabolic health, oxidative stress, inflammation, and vascular function markers, as such comprehensive assessments could provide deeper insight into underlying physiological processes. Full article

Multifunctional histamine H₃ receptor (H₃R) ligands with cholinesterase inhibitory activity are being explored as potential Alzheimer’s disease therapeutics, but their interactions with biological membranes and associated ADME properties require parallel evaluation. Here, six structurally related alkoxyamine H₃R ligands were characterized using an HPLC-based biomimetic workflow centered on immobilized artificial membrane (IAM) chromatography to assess phospholipid affinity, estimate passive blood–brain barrier permeability and human intestinal absorption. IAM measurements were complemented by HSA/AGP plasma protein binding, biomimetic distribution descriptors, plasma stability, chromatographic lipophilicity at pH 7.4 and solubility in JP1 (pH 1.2), JP2 (pH 6.8), and phosphate buffer (pH 7.4). The IAM models classified all six ligands as CNS-positive and predicted high intestinal absorption, while CHI_IAM values indicated strong membrane affinity. After 24 h, 77.5–89.5% and 62.2–80.5% parent compound remained in human and rat plasma, respectively. Solubility remained measurable across all three media. Integrated consideration of membrane-related ADME properties and previously reported pharmacology prioritized compounds (6), (5) and (2). Compound (6) showed the strongest overall potency–developability balance, although the biomimetic membrane predictions require confirmation in direct permeability, transporter, and in vivo pharmacokinetic studies. Full article

Background: Alzheimer’s disease (AD) and Parkinson’s disease (PD) are major neurodegenerative disorders for which disease-modifying therapies are limited. Increasingly, evidence suggests that diet influences neurodegenerative risk through interactions among the gut microbiome, immune system, and brain. The Mediterranean diet (MD) is associated with improved cognitive health, but the mechanisms underlying its potential neuroprotective effects remain incompletely understood. Objective: In this narrative review, evidence on microbiome-mediated mechanisms linking MD adherence to neuroprotection was synthesized, and how Mediterranean dietary components influence microbial ecology, metabolites, immune regulation, and neuroinflammation relevant to cognitive aging, AD, and PD was evaluated. Methods: Evidence from experimental, observational, and clinical studies was reviewed, focusing on microbial metabolites, intestinal barrier integrity, immune regulation, and inflammatory pathways. Discussion: Mediterranean dietary components, including fiber, polyphenols, whole grains, legumes, nuts, extra-virgin olive oil, and omega-3 fatty acids, may promote beneficial microbial communities and metabolite production. Short-chain fatty acids, secondary bile acids, indole derivatives, and phenolic metabolites may strengthen the intestinal and blood–brain barriers, regulate immune responses, and suppress neuroinflammation. Conversely, dysbiosis may increase intestinal permeability, lipopolysaccharide translocation, systemic inflammation, and microglial activation. However, evidence remains heterogeneous and largely observational or experimental. Conclusions: The MD may promote neuroprotection through interconnected diet–microbiome–immune pathways. Longitudinal and intervention studies integrating microbiome, metabolomic, inflammatory, neuroimaging, and cognitive measures are needed to establish causality and advance precision nutrition strategies to prevent neurodegenerative disease. Full article

Chronic kidney disease (CKD) is associated with intestinal dysbiosis, barrier dysfunction, uremic toxin accumulation, and systemic inflammation. This narrative review critically evaluates the gut–kidney axis, focusing on the distinction between NLRP3 [Nucleotide-binding Oligomerization Domain (NOD)-like receptor pyrin domain-containing protein 3] inflammasome priming and direct activation. It also examines the diagnostic and prognostic relevance of related biomarkers. Preclinical studies, clinical investigations, systematic reviews, meta-analyses, and relevant clinical trials within the past decade were considered. CKD-associated barrier dysfunction increases exposure to lipopolysaccharides and gut-derived metabolites. Lipopolysaccharide (LPS)-mediated TLR4/NF-κB (Toll-like receptor 4/nuclear factor kappa B) signaling provides well-supported inflammasome priming. Indoxyl sulfate acts predominantly as a priming stimulus, although its effects vary among cell types. Direct NLRP3 activation by p-cresyl sulfate has not been demonstrated. Trimethylamine N-oxide has the strongest experimental evidence for inflammasome activation. Candidate biomarkers include these metabolites, microbial profiles, intestinal permeability markers, and inflammasome-related mediators. However, their interpretation is limited by dependence on renal clearance, assay heterogeneity, absent standardized thresholds, and uncertain added value beyond estimated glomerular filtration rate and urinary albumin-to-creatinine ratio. Interventional studies remain small and predominantly use surrogate endpoints. The gut–toxin–inflammasome axis is mechanistically plausible, but evidence for priming is substantially stronger than that for direct activation. Its biomarkers remain research tools and require assay harmonization, prospective validation, and demonstration of independent clinical value before routine implementation. Full article

The intestinal barrier (IB) is a critical interface that maintains internal homeostasis. Its functional compromise—termed intestinal hyperpermeability—permits luminal antigens such as lipopolysaccharide to enter the circulation, triggering metabolic endotoxemia and low-grade systemic inflammation that underpin both intestinal and extra-intestinal diseases. This narrative review was based on a comprehensive literature search of PubMed, Web of Science, and Scopus databases up to July 2026, using keywords related to exercise, intestinal barrier, tight junction proteins, inflammation, oxidative stress, gut microbiota, and short-chain fatty acids. The synthesis indicates that regular moderate-intensity continuous training (30–60 min/session, 3–5 sessions/week) enhances barrier integrity through upregulation of tight junction proteins, suppression of TLR4/NF-κB-driven inflammation, activation of Nrf2-mediated antioxidant defenses, and beneficial remodeling of gut microbiota composition and short-chain fatty acid production. Exercise also induces peripheral–gut crosstalk mediated by myokines and vagal cholinergic signaling. The relationship between exercise volume and barrier function follows a J-shaped dose–response curve, with moderate exercise conferring protection while excessive high-intensity or prolonged exercise transiently increases permeability via splanchnic hypoperfusion and hypoxia-induced epithelial stress. Exercise shows preliminary therapeutic potential as an adjunctive intervention in inflammatory bowel disease, irritable bowel syndrome, and metabolic-associated fatty liver disease, with systemic benefits extending through the gut–liver and gut–brain axes. However, clinical translation remains limited by small sample sizes, short follow-up periods, and heterogeneous protocols. Future research should prioritize large-scale randomized controlled trials, precision exercise prescriptions, and synergistic exercise–probiotic co-interventions to establish definitive clinical guidelines. Full article

Background: Childhood undernutrition is associated with intestinal barrier dysfunction, gut dysbiosis, and increased susceptibility to gastrointestinal complications. This review examines whether plant-derived protein hydrolysates and bioactive peptides can influence gut barrier integrity, inflammatory signaling, oxidative stress, nutrient absorption, and microbiota composition. Methods: A scoping review of evidence published from 2010 and 2026 was conducted following a structured, multi-database search and screening process. Studies were assigned to defined evidence categories according to whether the intervention was an identified peptide sequence, a peptide fraction, a whole hydrolysate, an intact protein, or a complex food matrix. Results: Plant-derived protein hydrolysates, peptide fractions, and identified peptides were reported to increase occludin, claudin-1, and ZO-1 expression and reduce epithelial permeability in colitis models and in human-derived intestinal monolayers. Several interventions inhibited NF-κB and MAPK signaling, reducing TNF-α, IL-6, and IL-1β. Selected interventions lowered intestinal malondialdehyde and raised superoxide dismutase, glutathione peroxidase, and total antioxidant capacity; three studies demonstrated Keap1–Nrf2–ARE pathway activation directly. Microbiota effects were compositional, with increased short-chain fatty acid production, higher abundances of Lactobacillus and Bifidobacterium, and reduced pathobionts. Evidence for nutrient absorption was weaker: no included study measured PEPT1 expression, transport activity, or peptide flux following hydrolysate administration, and most sequences reviewed exceeded the di- and tripeptide substrate limit of that transporter. Conclusions: No included study administered a plant-derived peptide in a model of undernutrition, and none assessed clinically diagnosed SIBO. Mechanistic evidence suggests plausible benefits for gut barrier integrity, redox balance, inflammation, and microbiota composition, but controlled trials in undernourished children are required before clinical claims can be made. Full article