Impact of fraction size on the efficacy of xylo-oligosaccharides in broiler chicken diets.

The role of claudins in the physiology and pathology of the digestive system.

Molecular insights into physiological impact of micro- and nano-plastics on the digestive system and gut-brain axis.

Polyester microfiber accumulation and toxicological effects on freshwater fish Labeo rohita.

Robust detection in faeces and in vivo quantification of bacteriophages infecting enterotoxigenic Escherichia coli by quantitative PCR.

The utilization of a magneto-fluorescence sequential labeling strategy for the visualization and tracking of intestinal translocation of oral microbiota.

Heavy metals, gastrointestinal polymer-related materials, and gut microbiome in an Indo-Pacific bottlenose dolphin (Tursiops aduncus) recovered from a fisheries bycatch-related event in the East China Sea.

Microplastics in two fish species from Prydz Bay and King George Island: Occurrence, characteristics and risk assessment.

Contribution of macrophages and naive T cells during infection with E. coli in presence of exogenous cytokines on the autophagy-apoptosis pathway.

Targeted and quantitatively modeled biologic delivery via dual-functional probiotic yeast in inflammatory bowel disease.

Cancer trends among young adults in Russian Federation: An analysis of population-based cancer registry data.

On-Chip modeling of drug-gut interactions in Oral drug delivery.

Glepaglutide is a long-acting glucagon-like peptide 2 (GLP-2) analog under development for the treatment of short bowel syndrome (SBS). Glepaglutide enhances intestinal absorption, which may hypothetically lead to changes in the intestinal microbiota, mainly by slowing gastrointestinal transit time. This study evaluated whether glepaglutide affects bacterial load and composition of the intestinal microbiota in SBS patients enrolled in a phase 3b trial assessing its 24-week efficacy on intestinal wet weight and energy absorption. In this single-center, open-label, EASE SBS-4 phase 3b study, 10 patients with SBS (8 of the 10 with intestinal failure and 8 of the 10 without colon-in-continuity) were treated with glepaglutide 10 mg by subcutaneous injection once weekly for 24 weeks. While the primary trial findings demonstrated increased intestinal wet weight and energy absorption assessed by metabolic balance studies, this study investigated whether these adaptations were associated with changes in bacterial load and composition of the intestinal microbiota. Samples were obtained from either stool or ostomy effluent at baseline and after 24 weeks of treatment with glepaglutide. Bacterial load was quantified using a spike-in approach, and microbiota composition was assessed by V3V4 16S rRNA gene sequencing. No major changes in bacterial load or microbiota composition were observed following glepaglutide treatment. Bacterial load showed distinct differences between patients with and without a colon-in-continuity; in patients without a colon, most samples had values below 109 cells per gram, whereas those with a colon-in-continuity had bacterial loads within the physiological range observed in healthy individuals, ranging from 1010 to 1011 cells per gram feces. Microbiota composition also differed markedly by intestinal anatomy: patients without a colon-in-continuity had higher abundances of genera mainly associated with the upper gastrointestinal tract, such as Streptococcus, while those with a colon-in-continuity exhibited greater abundance of genera more commonly found in the lower gastrointestinal tract, including Bifidobacterium. Treatment with the GLP-2 analog glepaglutide increased intestinal wet weight and energy absorption without altering the intestinal bacterial microbiota in the majority of the SBS patients participating in this study. Differences in bacterial load and composition were influenced by intestinal anatomy. gov no: NCT04991311; ClincalTrialsRegister.eu EudraCT no: 2020-005194-27.

The interplay between gut microbiota metabolites and host body: Implications in health and disease

Oral gut-restricted therapies are being explored as a drug delivery strategy for inflammatory bowel disease (IBD), with the aim of achieving therapeutic effects within the intestinal mucosa while minimizing systemic exposure. Advances in molecular engineering and formulation technologies have enabled the development of orally administered agents intentionally designed to act locally within the gastrointestinal tract. This narrative review examines the biological, pharmacokinetic, and formulation principles underlying oral gut-restricted drug delivery in IBD, including an analysis of discontinued clinical development programs in ulcerative colitis and Crohn's disease. Across locally acting antibodies, peptides, and small molecules, the analysis of these programs reveals recurring factors contributing to discontinuation. These include limited or absent clinical efficacy despite evidence of mucosal target engagement, challenges in achieving consistent and adequate intestinal exposure, constraints related to formulation or delivery technologies, and trial-related factors such as high placebo response rates. In several cases, manufacturing variability or strategic considerations also influenced development outcomes. The review of the current clinical trial pipeline suggests an evolution in development strategies relative to earlier programs, with increasing emphasis on the confirmation of local tissue drug levels, incorporation of mucosal pharmacodynamic readouts, and selection of endpoints aligned with localized mechanisms of action, including endoscopic and histologic outcomes. These elements appear critical for interpreting early phase efficacy signals for agents designed to have minimal systemic activity. Effective translation requires alignment between mechanism of action, intestinal drug delivery, tissue-level pharmacodynamics, and clinical trial design. Incorporating these lessons may improve the likelihood of success for future oral gut-restricted therapies in IBD.

Influence of hypoxic conditions on Trichosporon asahii virulence in a Galleria mellonella infection model.

Therapeutic peptides and proteins: Status and developments in drug delivery.

Microencapsulation of probiotics using crosslinked lotus seed starch and alginate: protection and structural evolution during digestion.

Therapeutic effect of polydatin graphene hydrogel on intestinal injury.

Microplastics (MPs), a pervasive environmental pollutant, present a significant and growing threat to human health. Metabolomics has emerged as a powerful tool for deciphering pollutant toxicity by sensitively detecting metabolic perturbations. This review outlines metabolomic methodologies and their application in environmental toxicology. Meanwhile, evidence of the multisystem toxic effects of MPs revealed by metabolomics is synthesized, and progress in integrating metabolomic data with multiomics to elucidate underlying mechanisms is summarized. Results indicate that MPs induce systemic toxicity through organ-specific metabolic disruptions. In the intestinal tract, MPs compromise barrier integrity, induce amino acid and lipid metabolic reprogramming, and cause microbial dysbiosis, impacting distal organs via the gut-organ axes. Upon entering the nervous system, they disrupt neurotransmitter metabolism and impair cognitive function. Concurrently, MPs impair reproductive function by altering testicular phospholipid metabolism, reducing sperm quality, and disrupting placental lysine and glucose homeostasis, restricting fetal growth. Furthermore, MPs inhibit central energy metabolism pathways, including glycolysis and the tricarboxylic acid cycle across diverse species, resulting in impaired growth and development. Future research should leverage spatial metabolomics, causal validation techniques, and advanced computational algorithms to systematically map MP-induced metabolic disruptions, establish definitive mechanistic links, and reconstruct toxicity networks. Our study provides scientific basis for further clarifying the MP toxicity and identifying molecular targets of metabolic reprogramming to develop interventions that mitigate the health risks of MPs.