dysbiosis

Background: Obesity is a chronic endocrine-metabolic disease characterized by excess adiposity, metabolic inflammation and a high burden of cardiometabolic complications. The gut microbiota has emerged as a biologically plausible determinant of obesity because it regulates energy harvest, gut barrier integrity, immune signaling, bile acid metabolism and appetite-related neuroendocrine pathways. Methods: A structured literature search was conducted in PubMed/MEDLINE, ScienceDirect and Google Scholar for publications from 2000 to 2024 using English and French terms related to obesity, gut microbiota, dysbiosis, inflammation, probiotics, prebiotics, fecal microbiota transplantation, microbiota-targeted therapy and energy metabolism. Systematic reviews, meta- analyses, randomized trials, observational studies and mechanistic investigations were eligible when they addressed microbiota composition, obesity-related mechanisms or microbiome-based therapeutic strategies. Results: Seventy-two records were initially identified. After duplicate removal, 40 records were screened and 26 full-text publications were retained for qualitative synthesis. Obesity was frequently associated with reduced microbial richness, altered Firmicutes and Bacteroidetes profiles, enrichment of inflammatory taxa and depletion of potentially beneficial organisms such as Akkermansia muciniphila, Bifidobacterium and Faecalibacterium prausnitzii. The principal mechanisms involve short-chain fatty acid signaling, bile acid transformation, metabolic endotoxemia, low-grade inflammation, altered intestinal permeability, adipose-tissue dysfunction and gut-brain axis dysregulation. Dietary strategies, probiotics, prebiotics, next-generation probiotics and fecal microbiota transplantation show therapeutic potential, although clinical efficacy remains heterogeneous. Conclusion: The gut microbiota is not merely an associated biomarker of obesity but a dynamic metabolic interface that may influence disease expression and therapeutic response. Microbiome- targeted approaches are promising for future precision obesity care, but routine clinical implementation requires standardized, adequately powered and mechanistically informed human trials.

Introduction: Type 2 diabetes is a complex endocrine-metabolic disorder in which insulin resistance, beta-cell dysfunction, chronic low-grade inflammation and environmental exposures interact. The gut microbiota has emerged as a biologically plausible determinant of this process because it regulates nutrient fermentation, microbial metabolite production, gut barrier integrity, immune tone and endocrine-metabolic signalling. Methods: A structured review of the literature was conducted using PubMed/MEDLINE, ScienceDirect and Google Scholar. English and French publications were screened using terms related to gut microbiota, type 2 diabetes, dysbiosis, insulin resistance, inflammation, probiotics, prebiotics, microbiota-targeted therapy and fecal microbiota transplantation. Forty-two records were identified, and 32 references were retained for qualitative synthesis after screening and full-text eligibility assessment. Results: The evidence consistently indicates that type 2 diabetes is associated with dysbiosis, reduced microbial diversity, depletion of butyrate-producing or metabolically favorable taxa and enrichment of opportunistic or pro-inflammatory communities. Recurrent mechanisms include intestinal barrier dysfunction, lipopolysaccharide-mediated metabolic endotoxemia, impaired short-chain fatty acid signalling, bile acid dysregulation, excessive imidazole propionate, branched-chain amino acid metabolism, altered incretin responses and immune-metabolic activation. Microbiota-targeted interventions, including fermented foods, probiotics, prebiotics, synbiotics, resistant starch and fecal microbiota transplantation, show promise but remain clinically heterogeneous. Conclusion: The gut microbiota is best understood as a dynamic metabolic interface rather than a passive marker of type 2 diabetes. Microbiome-informed strategies may enrich future precision endocrinology, but standardised human trials integrating taxonomic, functional and clinical endpoints are required before routine implementation.