Om Kolthoum SALLEM

Background: Eating disorders and disordered eating behaviors are increasingly recognized among medical trainees, but data in young physicians remain limited. Screening in this population is clinically relevant because eating disorder risk may coexist with anxiety, depressive symptoms, weight-control behaviors, and occupational stress. Objective: To estimate the prevalence of a positive SCOFF-F screen for eating disorder risk among interns and residents at a Tunisian university hospital and to describe associated sociodemographic, psychological, and weight-control factors. Methods: This cross-sectional descriptive and analytical study was conducted at Fattouma Bourguiba University Hospital, Monastir, during the 2022-2023 academic year. Interns and residents completed an anonymous self-administered questionnaire assessing sociodemographic characteristics, clinical history, substance use, body mass index, weight-control behaviors, gastrointestinal symptoms, the French SCOFF questionnaire, and the Hospital Anxiety and Depression Scale. Categorical variables were summarized as counts and percentages. Exploratory comparisons used the chi-square test or Fisher exact test when appropriate. Results: Of 55 returned questionnaires, 50 were analyzable. The mean age was 26 years, 28 participants (56%) were women, and 33 (66%) were residents. Twelve participants (24%) screened positive for eating disorder risk. Underweight, overweight, and obesity were observed in 12%, 16%, and 2% of participants, respectively. Anxiety symptoms were common, and depressive symptoms were present in approximately one quarter of participants. In exploratory analyses based on the available tabulated counts, SCOFF positivity was associated with anxiety category, depression category, dieting, and exercise used as a weight-control behavior, whereas sex and training status were not statistically significant. Conclusion: One in four young physicians screened positive for eating disorder risk in this single-center cohort. The findings support systematic awareness, early screening, and institutional wellness strategies targeting disordered eating, psychological distress, and potentially harmful weight-control behaviors among medical trainees.

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.

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: 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.