Gut microbiota

Background: Vitamin D is an endocrine secosteroid with recognized extra-skeletal functions, including modulation of immune responses, epithelial barrier integrity, antimicrobial peptide expression, and inflammatory signaling. In parallel, the intestinal microbiota is increasingly recognized as a metabolic and immunological interface relevant to obesity, diabetes, inflammatory bowel disease, and systemic health. This review evaluates the evidence linking vitamin D status or supplementation to the composition and diversity of the human gut microbiota. Methods: A systematic narrative review was conducted using PubMed, ScienceDirect, and Google Scholar for studies published from 2010 to 2025. Human interventional and observational studies, systematic reviews, and mechanistic reports addressing vitamin D status or supplementation and gut microbiota outcomes were considered. The search and selection process was summarized using a PRISMA-style flow diagram. Findings were synthesized qualitatively because of substantial heterogeneity in populations, vitamin D regimens, microbiome sequencing methods, and reported endpoints. Results: Seventy-four records were identified; after duplicate removal and screening, 25 full-text reports were assessed and 11 evidence sources were retained for detailed synthesis. Higher serum 25-hydroxyvitamin D was generally associated with a more favorable microbiota profile, including greater microbial diversity and enrichment of taxa such as Bifidobacterium, Lactobacillus, Akkermansia, Bacteroides, and butyrate-associated organisms. Randomized supplementation studies showed biologically plausible but inconsistent effects on alpha diversity, beta diversity, and phylum-level changes, particularly the Bacteroidetes/Firmicutes balance. Conclusions: Current evidence supports a plausible vitamin D-gut microbiota axis, but causality remains unproven. Vitamin D supplementation should not yet be considered a targeted microbiota- modifying therapy outside correction of deficiency. Larger standardized randomized trials with integrated metabolomic, endocrine, and clinical endpoints are required.

Introduction: Dietary interventions are central to the management of obesity, insulin resistance, type 2 diabetes and related cardiometabolic disorders, yet clinical responses vary substantially between individuals exposed to apparently similar nutritional prescriptions. The gut microbiota may explain part of this variability because it transforms dietary substrates into bioactive metabolites and influences intestinal, immune and endocrine pathways. Methods: A narrative review informed by a structured literature search was conducted using PubMed, ScienceDirect and Google Scholar. Search terms combined concepts related to gut microbiota, intestinal microbiota, dietary intervention, nutrition, fiber, prebiotics, probiotics, metabolic response, obesity, insulin sensitivity and glycemic response. Forty records were initially identified, and 21 references were retained for qualitative synthesis after duplicate removal, screening and full-text eligibility assessment. Results: The reviewed literature indicates that baseline microbial diversity, community structure and functional capacity are associated with differential metabolic responses to calorie restriction, fiber-rich dietary patterns, probiotics, prebiotics and glycemia-oriented personalized nutrition. Key taxa and communities discussed in the evidence include Bacteroides, Prevotella, Akkermansia muciniphila, Bifidobacterium, Lactobacillus and Christensenella-associated communities. Mechanistic pathways include short-chain fatty acid generation, bile acid transformation, tryptophan-derived signaling, incretin-related pathways, epithelial barrier integrity and low-grade inflammation. Conclusion: The gut microbiota should be regarded as both a biomarker and a potential mediator of response to dietary interventions. Microbiota-informed nutrition is promising for precision diabetes and endocrinology care, but standardized prospective studies integrating microbiome profiling with robust metabolic outcomes remain necessary before routine clinical implementation.

Background: Obesity and type 2 diabetes mellitus (T2DM) are associated with chronic inflammation, immune dysfunction, and as a result increased risk of infections. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs) have emerged as key therapeutic agents with potential pleiotropic effects beyond glycemic control. Objective: This narrative review summarizes current evidence on the role of GLP-1 receptor agonists in modulating the immune–microbiome–infection axis and their potential impact on infection risk. Methods: A narrative review of recent experimental, clinical, and meta-analytic studies was performed focusing on immune regulation, inflammatory biomarkers, gut microbiota, and infectious outcomes. Results: GLP-1 RAs are associated with reduced systemic inflammation and oxidative stress, along with immunomodulatory effects including macrophage polarization and cytokine regulation. Emerging evidence suggests beneficial modulation of gut microbiota composition and improved intestinal barrier function. Studies have shown a reduction in infections, especially respiratory and systemic infections. Conclusion: GLP-1 receptor agonists may act as immunometabolic modulators linking metabolic health with immune and microbial homeostasis. Further mechanistic studies are required to clarify their role in infection susceptibility.