Dawid Wachowiak

Inflammatory bowel diseases, such as Crohn’s disease and ulcerative colitis, are chronic inflammatory conditions of the gastrointestinal tract characterized by periods of active disease and remission. Their pathogenesis is multifactorial and involves genetic predisposition, immune response, environmental factors, and alterations in gut microbiota composition and function. Growing evidence suggests that gut microbiota-associated metabolites not only reflect disease activity but also participate in regulating the immune response and maintaining the integrity of the intestinal barrier. The most important groups of metabolites associated with inflammatory bowel diseases include short-chain fatty acids, bile acids, and tryptophan derivatives. Reduced fecal butyrate and acetate concentrations have been reported in inflammatory bowel diseases, although the diagnostic value of fecal short-chain fatty acids remains uncertain. Potential therapeutic approaches include short-chain fatty acid supplementation, particularly sodium butyrate, and dietary interventions aimed at increasing short-chain fatty acid concentrations; however, the clinical efficacy of short-chain fatty acid supplementation remains inconclusive, and evidence for dietary interventions is limited. In the future, the use of gut microbiota metabolites may be based on personalized strategies grounded in multiomic data, enabling precise modulation of the microbiota–metabolite–immune system axis.

Obesity, type 2 diabetes mellitus (T2DM) and steatohepatitis associated with metabolic dysfunction (MASLD) are on the rise and pose serious health challenges worldwide. In recent years, researchers have gained a better understanding of the important role of the gut microbiota in the development and progression of these diseases. Intestinal dysbiosis can contribute to the occurrence of increased intestinal permeability, inflammation and reduced numbers of commensal bacteria. In obesity, these changes contribute to chronic low-grade inflammation and deregulated metabolism. In MASLD, gut microbiota dysbiosis can promote liver fibrosis and impair bile acid metabolism, while in T2DM, they are associated with impaired glycemic control and insulin resistance. Regular physical activity has a positive effect on the composition of the gut microbiota, increasing its diversity, modulating its metabolic functions, strengthening the intestinal barrier and reducing inflammation. These findings suggest that exercise and microbiota-targeted interventions may play an important role in the prevention and treatment of metabolic diseases.