This review introduces a novel integrative framework linking gut dysbiosis, systemic inflammation, and cardiovascular risk in patients with inflammatory bowel disease (IBD). We highlight emerging biomarkers, including short-chain fatty acids (SCFAs), calprotectin, and zonulin, that reflect alterations in the gut microbiome and increased intestinal permeability, which contribute to cardiovascular pathology. Cardiovascular diseases (CVDs) remain the leading cause of morbidity and mortality worldwide, and recent evidence identifies IBD, encompassing ulcerative colitis (UC) and Crohn’s disease (CD), as a significant non-traditional risk factor for CVD. This review synthesizes current knowledge on how dysbiosis-driven inflammation in IBD patients exacerbates endothelial dysfunction, hypercoagulability, and atherosclerosis, even in the absence of traditional risk factors. Additionally, we discuss how commonly used IBD therapies may modulate cardiovascular risk. Understanding these multifactorial mechanisms and validating reliable biomarkers are essential for improving cardiovascular risk stratification and guiding targeted prevention strategies in this vulnerable population.

Artificial intelligence (AI) and machine learning (ML) are transforming the management of acute appendicitis by enhancing diagnostic accuracy, optimizing treatment strategies, and improving patient outcomes. This study reviews AI applications across all stages of appendicitis care, from triage to postoperative management, using sources from PubMed/MEDLINE, IEEE Xplore, arXiv, Web of Science, and Scopus, covering publications up to 14 February 2025. AI models have demonstrated potential in triage, enabling rapid differentiation of appendicitis from other causes of abdominal pain. In diagnostics, ML algorithms incorporating clinical, laboratory, imaging, and demographic data have improved accuracy and reduced uncertainty. These tools also predict disease severity, aiding decisions between conservative management and surgery. Radiomics further enhances diagnostic precision by analyzing imaging data. Intraoperatively, AI applications are emerging to support real-time decision-making, assess procedural steps, and improve surgical training. Postoperatively, ML models predict complications such as abscess formation and sepsis, facilitating early interventions and personalized recovery plans. This is the first comprehensive review to examine AI’s role across the entire appendicitis treatment process, including triage, diagnosis, severity prediction, intraoperative assistance, and postoperative prognosis. Despite its potential, challenges remain regarding data quality, model interpretability, ethical considerations, and clinical integration. Future efforts should focus on developing end-to-end AI-assisted workflows that enhance diagnosis, treatment, and patient outcomes while ensuring equitable access and clinician oversight.

Background/Objectives: GLP-1-based obesity pharmacotherapy has shifted clinical attention from the magnitude of weight loss to the quality of weight loss. This review evaluates whether body composition changes during treatment with GLP-1-based agents represent clinically meaningful muscle loss and identifies nutrition, supplementation, exercise, and monitoring strategies that may help preserve lean mass, function, bone health, and nutritional adequacy. Methods: A comprehensive narrative review was performed using focused searches of PubMed, publisher-hosted journal platforms, and reference lists of key primary studies and recent evidence syntheses through March and May 2026. Evidence was organized around body composition, muscle quality and function, dietary protein and micronutrient adequacy, exercise, supplementation, bioelectrical impedance analysis, imaging, and emerging biomarkers. Results: Semaglutide and tirzepatide preferentially reduce fat mass, including visceral and ectopic adiposity, while producing smaller but consistent reductions in lean mass or lean soft tissue. However, DXA-derived lean mass and BIA-derived fat-free mass are not equivalent to skeletal muscle, and lean tissue loss does not necessarily indicate impaired strength or physical performance. The most defensible supportive care model combines food-first nutritional counseling, adequate protein intake, structured resistance exercise, management of gastrointestinal adverse effects, and risk-based monitoring of micronutrient inadequacy. Protein supplementation and nutritionally complete meal replacements may be useful when intake is insufficient, whereas creatine, essential amino acids or leucine, beta-hydroxy-beta-methylbutyrate, fiber, probiotics, omega-3 fatty acids, and multi-ingredient products remain adjunctive options supported mainly by indirect or phenotype-specific evidence. Conclusions: Future GLP-1 trials and clinical care should move beyond body weight and total lean mass toward integrated assessment of muscle quantity, muscle quality, function, bone, and nutritional adequacy, and standardized BIA-based clinical monitoring where advanced imaging is not feasible.

Cardiometabolic diseases are increasingly recognized as disorders of chronic low-grade systemic inflammation and gut barrier dysfunction that mutually reinforce one another. Each condition amplifies the other through progressive injury to the intestinal epithelium. Compromise of the mucus layer, altered tight junction dynamics, dysbiosis, and impaired epithelial restitution promote intestinal permeability and enable the translocation of lipopolysaccharide and other microbial products into the circulation, thereby inducing metabolic endotoxemia. This gut derived inflammatory signal activates Toll like receptor 4, nuclear factor kappa B, and inflammasome associated pathways, linking barrier dysfunction to insulin resistance, hepatic steatosis, adipose tissue inflammation, endothelial activation, and vascular injury. Here, we examine the gut barrier as an immunometabolic interface and synthesize current evidence connecting its disruption to endotoxin driven cardiometabolic pathology. We further evaluate selected natural bioactive compounds, including curcumin, resveratrol, quercetin, epigallocatechin gallate, berberine, anthocyanins, omega 3 polyunsaturated fatty acids, and dietary polysaccharides, as gut targeted interventions capable of reinforcing junctional integrity, restoring mucus and microbial homeostasis, lowering endotoxin burden, and attenuating inflammatory signaling. Finally, we highlight the principal translational barriers that currently limit clinical implementation, including pharmacokinetic variability, microbiota dependent biotransformation, source standardization, and the lack of robust, standardized biomarkers of barrier restoration and metabolic endotoxemia.

Inflammatory bowel disease (IBD; Crohn’s disease and ulcerative colitis) arises from convergent dysfunction of the epithelial barrier, mucosal immunity, and gut microbiome on a background of genetic susceptibility and environmental exposures. Diet is among the most modifiable of these exposures, yet much of the diet–microbiome research in IBD remains descriptive and poorly aligned with the molecular pathways linking food to mucosal effects. This comprehensive review reframes the field around functional dysbiosis, in which altered microbial metabolic capacity (rather than taxonomic shifts alone) drives disease-relevant biology. We trace how dietary substrates and additives are converted by gut microbes into bioactive metabolites (short-chain fatty acids, secondary bile acids, tryptophan-derived indoles, sulfur compounds, and polyphenol-derived molecules) and map these to host receptors and signaling pathways governing barrier function, mucus and antimicrobial peptide production, and Treg/Th17 balance. Defined dietary therapies (exclusive enteral nutrition, the Crohn’s disease exclusion diet plus partial enteral nutrition, and Mediterranean-style patterns) are reinterpreted as interventions that reshape microbial metabolic output, and candidate biomarkers for microbiome-informed precision nutrition are evaluated. Microbiota-derived metabolites provide the molecular interface between diet and mucosal immunity in IBD; personalized dietary algorithms remain a research goal, not a validated clinical tool, and diet is best framed as adjunctive to pharmacotherapy and dietitian care.

Obesity is increasingly recognized as a disease of dysregulated intercellular communication rather than merely an energy imbalance. Extracellular vesicles (EVs), membrane-bound nanoparticles (30–1000 nm) released by nearly all cell types, act as central mediators of this pathological crosstalk. In obesity, hypertrophic adipocytes, pro-inflammatory macrophages, and dysfunctional endothelial cells secrete EVs carrying altered cargo, including pro-inflammatory miRNAs (e.g., miR-34a, miR-155), bioactive lipids, and stress proteins, which propagate systemic metabolic dysfunction. Adipose tissue-derived EVs impair hepatic fatty acid oxidation, promote steatohepatitis, suppress pancreatic beta-cell insulin secretion, induce skeletal muscle insulin resistance via PPARγ repression, and contribute to endothelial dysfunction and atherosclerosis. EV-mediated adipocyte–macrophage crosstalk reinforces chronic adipose inflammation. Circulating EVs also provide biomarkers: subpopulation ratios, miRNA signatures, and tissue factor-positive EVs reflect disease severity, predict cardiovascular risk, and monitor therapeutic responses, with machine learning enhancing diagnostic precision. Therapeutically, EVs from mesenchymal stem cells, Wharton’s jelly MSCs, adipose progenitors, and M2 macrophages reverse insulin resistance, hepatic steatosis, and adipose inflammation in preclinical models. Engineering strategies improve EV potency and tissue targeting, and Phase I trials confirm safety, though manufacturing and cost remain barriers. Preclinical and early clinical studies of MSC-EVs confirm a favorable safety profile, though manufacturing scalability and cost remain barriers to widespread clinical adoption. Overall, EVs represent both diagnostic tools and therapeutic vehicles in precision obesity medicine, offering a pathway from symptom management toward true disease remission.