Background and Objectives: Metabolic dysfunction-associated steatotic liver disease (MASLD) is now widely acknowledged as belonging to the broader category of metabolic disorders, being closely associated with obesity, insulin resistance, and chronic systemic inflammation. Recent evidence indicates that in MASLD, alterations in the gut–liver axis—particularly increased intestinal permeability may serve as a crucial mechanistic link between metabolic dysfunction and hepatic steatosis. Zonulin, a physiological modulator of intestinal tight junctions, has been suggested as an indicator of compromised barrier integrity; however, its specific role in MASLD remains to be fully elucidated. Materials and Methods: We conducted a prospective observational study including 52 adult patients diagnosed with MASLD. Hepatic steatosis was evaluated using the SteatoTest (FibroMax panel), while fecal zonulin levels were measured by ELISA at baseline. Clinical, anthropometric, and metabolic parameters were assessed. We used ROC curve analysis to explore zonulin’s predictive value for moderate-to-severe steatosis (≥S2). Results: Elevated fecal zonulin (>107 ng/mL) occurred in 26.9% of participants. In a binary logistic model with SteatoTest ≥ S2 as outcome, zonulin was independently associated with clinically significant steatosis (OR per 1 ng/mL = 1.017; 95% CI 1.002–1.032; p = 0.029). Discrimination for ≥S2 was AUC = 0.680 (95% CI 0.535–0.825; p = 0.015). The Youden-optimal cut-off was 57.0 ng/mL (sensitivity 68.2%, specificity 63.3%) versus 40.9%/83.3% at the manufacturer’s 107 ng/mL threshold. Conclusions: Fecal zonulin shows modest discriminatory ability for steatosis and is best used as an adjunct to non-invasive assessment; cohort-specific calibration (57.0 ng/mL) outperformed the generic 107 ng/mL threshold.

Gastric cancer (GC) is the fifth most common malignancy worldwide, with 968,784 new cases reported in 2022. Since 1975, when stomach cancer was the most common cancer, its incidence has declined in many regions. This decline can be attributed to improved food preservation and recognition of Helicobacter pylori (H. pylori) as a group 1 carcinogen in intestinal-type GC. The aim of this review was to summarize current strategies for primary and secondary prevention of GC, with an emphasis on H. pylori management, dietary factors, novel biomarkers, and screening approaches relevant in Europe. Papers from large databases, namely Web of Science, Scopus, and PubMed/MEDLINE, were selected (reviews, guidelines, and peer-reviewed studies) from about the last 1–5 years. The research was conducted using the keywords gastric cancer, prevention, primary prevention, secondary prevention, and endoscopy guidelines on prevention of gastric cancer. Primary prevention of GC is directed at screening for H. pylori and dietary changes. Secondary prevention is supported by traditional tumor markers, pepsinogen-based serological biopsy, newer blood-based markers, and major technological progress in endoscopy. High-definition endoscopy, magnification, virtual chromoendoscopy, and artificial intelligence have improved the detection of preneoplastic lesions and early cancer, while advanced therapeutic techniques such as endoscopic mucosal resection and endoscopic submucosal dissection permit organ-sparing treatment. Large projects, including GISTAR, EUROHELICAN, TOGAS, and EUCanScreen, are expected to clarify optimal screening strategies. Although GC incidence has declined, it remains a common and significant malignancy. Understanding the facets of primary and secondary prevention of GC will lead to a reduction in the burden of this disease.

Background: Short-chain fatty acids (SCFAs) are produced by the colon microbiome and bind to specific G-protein coupled receptors GPR 41 and GPR 43. Leptin and glucagon-like peptide 1 (GLP-1) are produced mainly in the intestinal lumen as a result of SCFAs binding to their receptors at this level. Inflammatory bowel diseases (IBD) such as Crohn’s disease (CD) and ulcerative colitis (UC), and their major complication, colorectal cancer (CRC), can disturb the dynamics of the colonic microenvironment thus influencing SCFAs production and effects. Our study aimed to investigate serum levels of SCFAs and SCFAs-mediated production of circulating leptin, GLP-1, and Nesfatin-1 in patients with IBD and CRC. Methods: A total of 88 subjects (29 with CRC, 29 with IBD, and 30 controls) were included in this pilot study. Serum SCFAs, leptin, Nesfatin-1, and GLP-1 levels were analyzed. Results: Nesfatin-1 levels were significantly higher in CRC patients (p < 0.05) compared to IBD and controls. Leptin levels were positively correlated with Nesfatin-1 levels in CRC, IBD, and control groups (CRC: R² = 0.6585, p < 0.01; IBD: R² = 0.2984, p < 0.01; Control: R² = 0.2087, p < 0.05). Serum SCFAs levels were negatively correlated with GLP-1 levels in CRC and IBD (CRC: R² = 0.3324, p < 0.01; IBD: R² = 0.1756, p < 0.05) and negatively correlated with Nesfatin-1 levels in CRC (R² = 0.2375, p < 0.05). Conclusions: These findings suggest that alterations in gut microenvironment may influence systemic metabolic regulators involved in appetite control and inflammation, potentially influencing IBD and CRC pathogenesis. This is the first study to evaluate the relationships between Nesfatin-1, leptin, GLP-1, and SCFAs in CRC and IBD patients; further research is needed to clarify their mechanistic links and therapeutic potential.

Background: Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as part of the broader spectrum of metabolic disorders, with links to obesity, insulin resistance, and systemic inflammation. Emerging evidence points to a role of the gut–liver axis, particularly intestinal permeability, in its pathogenesis. Zonulin—a regulator of tight junctions—has been proposed as a marker of impaired barrier function, but its relevance in MASLD remains unclear. Methods: We conducted a prospective observational study including 52 adult patients diagnosed with MASLD. Hepatic steatosis was evaluated using the SteatoTest (FibroMax panel), while fecal zonulin levels were measured by ELISA at baseline. Clinical, anthropometric, and metabolic parameters were assessed. We used ROC curve analysis to explore zonulin’s predictive value for moderate-to-severe steatosis (≥S2). Results: Fecal zonulin levels above 107 ng/mL were found in 26.9% of participants. This group showed a higher frequency of moderate-to-severe steatosis (78.6%) compared to those with lower zonulin levels (55.3%), although the correlation with SteatoTest was weak (r = 0.19, p > 0.05). No significant associations were found between zonulin and liver fibrosis, insulin resistance (HOMA-IR), or the BARD score. The AUC for detecting steatosis ≥ S2 was 0.68. Conclusions: Although limited as a standalone diagnostic tool, fecal zonulin may reflect underlying gut barrier dysfunction in MASLD and show moderate association with hepatic steatosis. Its role as a complementary biomarker in non-invasive stratification frameworks warrants further study, especially in larger cohorts with control groups.

Background: Short-chain fatty acids (SCFAs) support mucosal integrity and reduce inflammation, while nesfatin-1 is a neuropeptide with antiapoptotic, anti-inflammatory, antioxidant, and anorexigenic actions. Their roles in inflammatory bowel disease (IBD) and links to quality of life (QoL) are unclear. Methods: We conducted a cross-sectional study including adults with Crohn’s disease (CD), ulcerative colitis (UC), and healthy controls (HC). Serum total short-chain fatty acids and nesfatin-1 were measured using enzyme-linked immunosorbent assays (ELISA). Quality of life was assessed using the Inflammatory Bowel Disease Questionnaire (IBDQ). Group comparisons and correlation analyses were performed using non-parametric statistical methods. Results: Serum total SCFA concentrations did not differ significantly between patients with CD, UC, and HC (p = 0.29). Nesfatin-1 levels showed between-group variability, with lower values in CD compared with healthy controls, while patients with UC showed intermediate and variable levels (p = 0.064). An inverse correlation between SCFAs and nesfatin-1 was observed in UC and in the combined IBD cohort, but not in CD. Quality of life was comparably impaired in CD and UC. No statistically significant associations were observed between serum SCFAs or nesfatin-1 and IBDQ scores. Conclusions: In this pilot exploratory study, circulating SCFAs and nesfatin-1 showed distinct patterns across IBD subtypes, with evidence of subtype-specific associations between these biomarkers. However, no relationship with quality of life was demonstrated. Larger longitudinal studies are required to confirm these findings and clarify their clinical relevance.

Introduction Eosinophils contribute to inflammatory bowel disease (IBD) pathogenesis by infiltrating the intestinal mucosa and releasing pro-inflammatory mediators, including eosinophilic cationic protein (ECP). Although biomarkers like C-reactive protein and fecal calprotectin commonly assess IBD activity, the clinical utility of eosinophil-derived markers like ECP is unclear. Our aims were to compare serum ECP across ulcerative colitis (UC), Crohn’s disease, and healthy controls, with the prespecified primary contrast UC vs. controls. Our secondary objectives were to examine associations between ECP and disease activity (CDAI, MAYO scores) and quality of life, and explanatory objectives were to assess correlations with white blood cells and neutrophil and eosinophil counts and explore UC-control discrimination. Methods We conducted an observational study including 50 IBD patients (20 Crohn’s disease patients, 30 UC patients) and 32 healthy controls. Clinical data recorded included disease duration, Crohn’s Disease Activity Index (CDAI), Mayo score for UC, and quality of life (IBDQ questionnaire). Serum ECP (enzyme immunoassay), eosinophil counts, and routine blood tests were measured. Statistical analysis employed Kruskal-Wallis with Dunn’s post-hoc tests, Mann-Whitney U tests, and Spearman’s correlation. Ethical approval and informed consent were obtained. Results Median serum ECP differed significantly among controls, Crohn’s, and UC patients (16,807 (13,007-24,314) pg/mL vs 18,496 (12,261-28,231) vs 24,224 (17,335-32,997); p=0.03). UC patients had significantly higher ECP than controls (p=0.008), while the increase in Crohn’s disease was not significant (p=0.418). ECP was higher in UC compared to Crohn’s disease, though this difference did not reach statistical significance (p=0.128). No significant differences emerged between Crohn’s disease and UC in total leukocyte count, eosinophil count, disease duration, or Inflammatory Bowel Disease Questionnaire (IBDQ) scores (all p>0.1). Serum ECP positively correlated with total leukocyte (r=0.279, p=0.049) and neutrophil counts (r=0.298, p=0.036) across IBD patients. No significant correlations existed between ECP and patient age, disease duration, CDAI, Mayo score, IBDQ, or eosinophil count (all p>0.1). Conclusion In this cross-sectional cohort, serum ECP was higher in UC vs controls and showed only modest associations with leukocytosis, while not tracking CDAI, partial Mayo, or IBDQ. These findings are hypothesis-generating and consistent with eosinophil involvement; they do not demonstrate mechanism or clinical utility and require prospective validation.