The gut microbiota, dominated by bacteria from the Firmicutes, Bacteroidetes, Proteobacteria, and Actinobacteria phyla, plays an essential role in fermenting indigestible carbohydrates, regulating metabolism, synthesizing vitamins, and maintaining immune functions and intestinal barrier integrity. Dysbiosis is associated with obesity development. Shifts in the ratio of Firmicutes to Bacteroidetes, particularly an increase in Firmicutes, may promote enhanced energy storage, appetite dysregulation, and increased inflammatory processes linked to insulin resistance and other metabolic disorders. The purpose of this literature review is to summarize the current state of knowledge on the relationship between the development and treatment of obesity and overweight and the gut microbiota. Current evidence suggests that probiotics, prebiotics, synbiotics, and fecal microbiota transplantation (FMT) can influence gut microbiota composition and metabolic parameters, including body weight and BMI. The most promising effects are observed with probiotic supplementation, particularly when combined with prebiotics, although efficacy depends on strain type, dose, and duration. Despite encouraging preclinical findings, FMT has shown limited and inconsistent results in human studies. Diet and physical activity are key modulators of the gut microbiota. Fiber, plant proteins, and omega-3 fatty acids support beneficial bacteria, while diets low in fiber and high in saturated fats promote dysbiosis. Aerobic exercise increases microbial diversity and supports growth of favorable bacterial strains. While microbiota changes do not always lead to immediate weight loss, modulating gut microbiota represents an important aspect of obesity prevention and treatment strategies. Further research is necessary to better understand the mechanisms and therapeutic potential of these interventions.

Recent studies increasingly highlight the complex interaction between gut microbiota and mental health, drawing attention to the role of the microbiota–gut–brain axis (MGBA) in the pathophysiology of mental and neurodevelopmental disorders. Changes in the composition of the gut microbiota—dysbiosis—are associated with conditions such as depression, schizophrenia, bipolar disorder (BD), autism spectrum disorders (ASD), attention deficit hyperactivity disorder (ADHD), and neurodegenerative diseases such as Parkinson’s and Alzheimer’s. These microbial imbalances can affect brain function through a variety of mechanisms, including activation of the immune system, alteration of intestinal permeability, modulation of the digestive and central nervous systems, and changes in the production of neuroactive metabolites such as short-chain fatty acids, serotonin, and tryptophan derivatives. The aim of this paper is to review the current state of knowledge on therapeutic strategies targeting the gut microbiome—including probiotics, prebiotics, synbiotics, personalized dietary interventions, and fecal microbiota transplantation (FMT)—which are becoming promising adjuncts or alternatives to conventional psychopharmacology, offering a forward-looking and individualized approach to mental health treatment. Understanding the bidirectional and multifactorial nature of MGBA may pave the way for new, integrative treatment paradigms in psychiatry and neurology, requiring further research and exploration of their scope of application.

Cyclosporine is a selective calcineurin inhibitor used, among other areas, in pediatric gastroenterology as rescue therapy in the treatment of severe ulcerative colitis (ASUC—acute severe ulcerative colitis) in children. The introduction of systemic glucocorticosteroids (GCSs) has significantly reduced mortality in ASUC. However, it should be emphasized that long-term use of these drugs is limited due to the high risk of adverse effects observed during therapy and their limited efficacy. The role of cyclosporine as a second-line therapy is referred to as a ‘rescue therapy,’ which aims to alleviate the symptoms of ASUC, often avoiding life-threatening complications (including toxic megacolon) and postponing the need for urgent colectomy. If colectomy is necessary, this provides time to better prepare the patient nutritionally and psychologically for surgery and to await the effect of slower-acting thiopurine preparations or other chronic treatments; their effectiveness in achieving long-term clinical and endoscopic remission is limited. New therapeutic approaches include cyclosporine as an inducer, which acts as a bridge to new forms of therapy, such as biological drugs, which are used as maintenance preparations in patients. In pediatric patients, there is limited research in the literature on new strategies for the use of cyclosporine. The aim of this review is to assess current evidence on cyclosporine as induction or rescue therapy in pediatric ASUC and explore future integration with biologic and biosimilar strategies, emphasizing its evolving role as a bridging agent toward biologics and novel targeted therapies.

Aim: This review aims to explore the pathophysiological mechanisms by which SARS-- CoV-2 affects lipid metabolism and the metabolome in patients with Type 2 Diabetes Mellitus (T2DM). It compares these alterations with those observed in non-diabetic individuals and proposes strategies to mitigate potential long-term metabolic complications. Methods: A narrative review was conducted using PubMed, Scopus, and Google Scholar to identify studies published between 2004 and 2025 concerning adult T2DM patients during or after COVID-19 infection. The analysis focused on lipid profiles, including total cholesterol, high-density lipoprotein (HDL), low-density lipoprotein (LDL), and triglycerides, along with hemoglobin A1C levels and COVID-19 severity. Search terms included: (Post-COVID-19) AND (Diabetes Mellitus Type 2), ((Post-COVID-19) AND (Diabetes Mellitus Type 2)) AND (Lipid Profile), ((- COVID-19) AND (Lipid Profile)) AND (Diabetes Mellitus Type 2), (Post-COVID-19) AND (Lipid Metabolism), (COVID-19) AND (Lipid Metabolism), (Post-COVID-19) AND (Metabolome), (COVID-19) AND (Metabolome). Results: Post-COVID-19, patients with T2DM exhibit persistent disturbances in lipid metabolism and broader metabolic pathways. SARS-CoV-2 infection amplifies metabolic dysregulation, leading to decreased levels of total cholesterol, HDL, and LDL, while triglyceride levels remain variable. Mechanistically, the virus disrupts lipid homeostasis by upregulating genes such as CD36 and peroxisome proliferator-activated receptor gamma (PPAR-γ) and by altering amino acid metabolism, particularly within the tryptophan-kynurenine and glutamine pathways. Discussion: Enhanced oxidative stress and lipid peroxidation contribute to systemic inflammation and endothelial dysfunction. Furthermore, glycemic control worsens due to increased insulin resistance and pancreatic interactions involving angiotensin-converting enzyme 2 (ACE2). Conclusion: COVID-19 significantly alters lipid metabolism and the metabolomic profile in individuals with T2DM. Longitudinal studies are warranted to clarify the duration and clinical impact of these changes and to develop personalized therapeutic strategies for this high-risk population.

Background. Sedentary behavior is an independent determinant of metabolic health. Prolonged sitting is associated with insulin resistance, dyslipidemia, obesity, metabolic syndrome, and type 2 diabetes, even in physically active individuals. Aim. To synthesize evidence on the impact of sedentary behavior on metabolic health in adults, including epidemiological associations, mechanisms, and intervention effects. Material and methods. A systematic narrative review was conducted using PubMed and reference screening. Studies evaluating sedentary behavior and metabolic outcomes in adults were included. Due to heterogeneity, findings were synthesized thematically. Results. Higher sedentary time was consistently associated with adverse metabolic profiles, particularly impaired glucose metabolism and increased diabetes risk. Experimental studies show that interrupting sitting improves glucose and insulin responses. Mechanistic evidence supports links with reduced muscle activity and insulin sensitivity. Evidence for lipid profile and obesity is less consistent, and long-term intervention data remain limited. Conclusions. Sedentary behavior is a modifiable risk factor for metabolic dysfunction. Reducing and interrupting sitting should complement physical activity. Further studies should use standardized measures and clinically relevant endpoints.

Background: Transport exclusion and difficult access to educational institutions pose a significant problem for maintaining daily routines, sleep patterns and eating habits and are a potential cause of gastroenterological disorders. This study aims to demonstrate the possible associations between transport difficulties and selected gastrointestinal symptoms. Methods: A cross-sectional anonymous online survey was conducted among 650 students aged 15–20 years from urban and rural areas. Data on place of residence, commuting time, wake-up time, breakfast habits, and gastrointestinal symptoms were analyzed by chi-square tests, nonparametric methods, and correlation analyses. Results: The survey demonstrated the association between commutes to school and the occurrence of morning nausea, abdominal pain, and irregular meal patterns. Early wake-up times are also associated with the risk of symptoms. Transport-related factors, particularly long commuting times and early wake-up schedules, are associated with more irregular eating patterns and a higher prevalence of morning gastrointestinal symptoms in adolescents. Conclusions: Transport exclusion may represent an important, yet understudied, factor influencing adolescent health.