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Physical activity is a cornerstone in the treatment of obesity and metabolic syndrome (MetS). Given the leading physical activity barrier of time commitment and safety concerns about vigorous exercise in high-risk groups, this study aimed to investigate the effects of two extremely time-efficient training protocols (< 30 min time effort per week), either performed as high- (HIIT) or moderate-intensity interval training (MIIT) over 12 weeks, in obese MetS patients. In total, 117 patients (49.8 ± 13.6 years, BMI: 38.2 ± 6.2 kg/m 2 ) were randomized to HIIT (n = 40), MIIT (n = 37) or an inactive control group (n = 40). All groups received nutritional counseling to support weight loss. Maximal oxygen uptake (VO 2max ), MetS severity (MetS z-score), body composition and quality of life (QoL) were assessed pre-and post-intervention. All groups significantly reduced body weight (~ 3%) but only the exercise groups improved VO 2max , MetS z-score and QoL. VO 2max (HIIT: + 3.1 mL/kg/min, p  < 0.001; MIIT: + 1.2 mL/kg/min, p  < 0.05) and MetS z-score (HIIT: − 1.8 units, p  < 0.001; MIIT: − 1.2 units, p  < 0.01) improved in an exercise intensity-dependent manner. In conclusion, extremely low-volume interval training, even when done at moderate intensity, is sufficiently effective to improve cardiometabolic health in obese MetS patients. These findings underpin the crucial role of exercise in the treatment of obesity and MetS.

The ex vivo generation of gastrointestinal organoids from crypt stem cells opens up the possibility of new research approaches investigating gastrointestinal diseases. We used this technology to study differences between healthy controls and patients with celiac disease (CD). We noticed distinct dissimilarities in the phenotypes of organoids between our study groups and found considerable variations in their gene expression. Extracellular matrix genes involved in epithelial-mesenchymal transition are expressed most differently. In addition, we demonstrated epigenetic modifications that might be responsible for the different organoid gene expression thus accounting for a deranged crypt/villus axis development in CD. The organoids have proven valuable to demonstrate fundamental differences in duodenal derived organoids between healthy controls and patients with CD and thus are a suitable tool to gain new insights in pathogenesis of CD.

Food allergy (FA) affects approximately 3 to 4% of the adult population in westernized countries. Suspected FA is even more prevalent and requires extensive diagnostic work-up. Within this study, we evaluated whether assessment of the integrity of the epithelial barrier by confocal laser endomicroscopy (CLE) during colonoscopy can be used as a screening tool to identify patients with FA. 60 patients with suspected FA were prospectively included. Serology with total and food-specific IgE, anti-tissue transglutaminase, skin prick testing, food intolerance tests, food intake registration and assessment of clinical complaints were performed. During colonocopy, standardized CLE was performed in the terminal ileum and at two colorectal sites. Analysis of CLE images included functional (i.e. presence of epithelial barrier dysfunction) and quantitative parameters of intestinal architecture. 27 of 60 patients (45%) were diagnosed with FA. Barrier dysfunction was analyzed on 65.837 ileal and on 93.251 colonic images. 96% of patients with FA exhibited functional and structural barrier defects while barrier dysfunction was found in only 33% of patients without FA ( p  < 0.0001). Visualizing barrier dysfunction with CLE for in vivo diagnosis of FA had a sensitivity and specificity of 96% and 67%, respectively, with a positive and negative prediction of 70% and 96%, respectively. Parameters intrinsic to the crypt architecture including crypt diameter, intercrypt distance, crypt lumen diameter and colonic vasculature were not different between patients with and without FA. CLE-based imaging of the intestinal barrier during colonoscopy might help in stratifying patients with suspected FA for further diagnostic work-up.

The use of antibodies against tumour necrosis factor (TNF) has markedly improved the treatment of Crohn's disease, but only certain patients respond to therapy. Here, Raja Atreya and colleagues have developed an approach using topical fluorescent antibodies to TNF and confocal laser endomicroscopy to evaluate the expression of transmembrane TNF (mTNF) in the intestinal mucosa of patients with active Crohn's disease in order to identify patients likely to respond to subsequent treatment with the anti-TNF therapy, adalimumab. As antibodies to tumor necrosis factor (TNF) suppress immune responses in Crohn's disease by binding to membrane-bound TNF (mTNF), we created a fluorescent antibody for molecular mTNF imaging in this disease. Topical antibody administration in 25 patients with Crohn's disease led to detection of intestinal mTNF + immune cells during confocal laser endomicroscopy. Patients with high numbers of mTNF + cells showed significantly higher short-term response rates (92%) at week 12 upon subsequent anti-TNF therapy as compared to patients with low amounts of mTNF + cells (15%). This clinical response in the former patients was sustained over a follow-up period of 1 year and was associated with mucosal healing observed in follow-up endoscopy. These data indicate that molecular imaging with fluorescent antibodies has the potential to predict therapeutic responses to biological treatment and can be used for personalized medicine in Crohn's disease and autoimmune or inflammatory disorders.

Background: Cancer-related cachexia is primarily characterized by systemic inflammation and progressive muscle wasting, which is why a high-protein diet (from 1.2 to 1.5 g/kg/day) is commonly recommended. However, concerns remain that an excessive supply of amino acids could promote tumor growth due to the metabolic flexibility of cancer cells, thereby favoring proliferation and survival. Systematic evidence addressing these concerns under controlled conditions for various types of cancer cells remains limited and inconclusive. Methods: We investigated the short-term effects of all 20 amino acids at both moderate (2×) and high (10×) concentrations to evaluate three key oncological endpoints in four human cancer cell lines: MDA-MB-231 (breast), HT29 (colorectal), PC3 (prostate), and PANC-1 (pancreatic). Cell proliferation was assessed by BrdU incorporation, metabolic activity by WST-1 assay, and apoptosis signaling by caspase-3/7 activity measurement. Results: Amino acid supplementation was not associated with a significant change in proliferation at either concentration across all four cell lines studied. Metabolic activity showed only minor variations throughout, with PC3 cells exhibiting slightly greater variability, although this did not reach statistical significance. Caspase-3/7 activity remained largely unchanged under all conditions; however, high-concentration lysine induced an approximately 2.5-fold increase in PANC1 cells, which was not statistically significant. Conclusions: These findings suggest that short-term exposure to individual amino acids, even at supraphysiological conditions, does not acutely enhance proliferative activity in the cancer cell lines studied, supporting the rationale for adequate protein and amino acid intake in patients with cancer cachexia.

Prolonged intermittent fasting is associated with metabolic and immune adaptation; however, the extent to which transcriptional immune responses translate into systemic inflammatory changes, and how these processes relate to autophagy, senescence-associated signaling, and inflammasome regulation, remains incompletely understood. This study represents a secondary integrative analysis of a previously characterized cohort of healthy young men undergoing Ramadan fasting. Longitudinal data across four time points (T1-T4) were re-analyzed, integrating targeted mRNA profiling of autophagy-, senescence-, and inflammasome-related genes with circulating cytokines and clinical parameters. Baseline-stratified regression and exploratory clustering were applied to assess inter-individual variability. Fasting was associated with modest reductions in body weight (-1.78 ± 1.44 kg, FDR < 0.001) and BMI (-0.56 ± 0.47 kg/m , FDR < 0.001), without hemodynamic instability. Autophagy-related transcripts (ULK1, ATG5) were upregulated, while senescence markers showed divergent regulation (p53↑, p21↓). Inflammasome-related genes (NLRP3, IL1B) increased at the transcriptional level; however, circulating IL-1β and IL-6 remained stable and TNFα decreased (FDR < 0.001), indicating dissociation between transcriptional priming and systemic cytokine output. ΔNLRP3 was inversely associated with baseline expression (β = -1.88, R = 0.31, = 0.0056), suggesting baseline-dependent transcriptional responsiveness. Responses followed a continuous spectrum rather than discrete subtypes. Prolonged intermittent fasting is associated with coordinated immunometabolic remodeling characterized by transcriptional changes in autophagy-, senescence-, and inflammasome-related pathways, without systemic inflammatory escalation. Inflammasome-related responses appear baseline-dependent, suggesting graded immunological responsiveness rather than a uniform activation. These findings are hypothesis-generating and support the interpretation of fasting as a graded immunometabolic modulator rather than a uniform pro-inflammatory stimulus within the limitations of a secondary exploratory analysis.

Background/Objectives: Although discrepancies between bioelectrical impedance analysis (BIA) devices are well documented, their clinical relevance in vulnerable populations remains unclear. This study aims to assess the impact of device choice on muscle mass classification criteria in patients with cancer or obesity and to identify modifiers of device variability. Methods: BIA data from 224 adults (85 with cancer, 139 with obesity) measured with two segmental multi-frequency devices (seca mBCA 515 and InBody 970) were analyzed. Device differences were assessed using the Wilcoxon signed-rank test and agreement analyses. Differences in classification of body composition cut-offs cited in the GLIM criteria for malnutrition and the ESPEN and EASO criteria for sarcopenic obesity were evaluated using McNemar’s test. The impact of disease type, sex, and age on device differences was examined through multivariable models. Results: Significant device differences were found for all parameters (all p ≤ 0.005). Discrepancies were largest for skeletal muscle mass (kg and %), with effect sizes r > 0.8 and poor agreement (Lin’s CCC < 0.90). A significant impact of device choice on muscle mass classification was observed for both cancer and obesity patients (p < 0.001), with seca classifying more patients as having low fat-free mass (50% vs. 20%) and as having a body composition consistent with sarcopenic obesity (90% vs. 50%) than InBody. Discrepancies were more pronounced in cancer patients and females. Conclusions: Muscle mass assessment by BIA is highly dependent on device choice, potentially leading to clinically relevant discrepancies in classification when rigid cut-offs are applied. An individualized interpretation of BIA data and further validation of prediction equations in disease-specific subpopulations is warranted.

Background/Objectives: Nutritional therapy is an essential part of oncologic care, yet patients with brain tumors—especially those with glioblastoma—remain underserved by disease-specific dietary guidelines. This cross-sectional study compares energy and macronutrient intake, as well as body composition, between brain tumor patients, including a glioblastoma subgroup, and patients with gastrointestinal (GI) cancer. Methods: A total of 95 brain tumor patients and 109 GI cancer patients completed standardized three-day estimated food records and underwent bioelectrical impedance analysis and hand-grip strength measurements. Anthropometric parameters, as well as energy and macronutrient intake, were compared between groups. Results: Energy intake was lower in brain tumor patients compared with GI cancer patients (22.8 kcal/kg/day vs. 31.2 kcal/kg/day), as were protein (1.01 g/kg/day vs. 1.34 g/kg/day) and carbohydrates (182.8 g/day vs. 246.8 g/day; all p < 0.01). Despite the lower intake, brain tumor patients exhibited higher BMI scores, body fat percentages, and visceral fat levels (p < 0.05), while fat-free mass and skeletal muscle mass were comparable between groups. The phase angle was higher in brain tumor patients (p = 0.002), whereas the ECW/TBW ratio was lower (p = 0.003). In the glioblastoma subgroup, protein intake did not differ significantly compared with the GI cancer group. However, carbohydrate intake (190.9 g/day vs. 246.8 g/day; p = 0.01), as well as energy intake (25.7 kcal/kg/day vs. 31.2 kcal/kg/day; p = 0.05), remained significantly lower. Conclusions: Brain tumor patients were found to have energy intake levels below ESPEN recommendations for cancer patients (25–30 kcal/kg/day), and their protein intake was at the lower ESPEN threshold (1.0 g/kg/day), coupled with increased adipose tissue. The observed caloric deficit was accompanied by reduced carbohydrate intake, particularly in the glioblastoma subgroup. These findings highlight the need for individualized nutritional approaches in neuro-oncology. Until disease-specific recommendations are available, general dietary guidelines such as those by ESPEN offer a pragmatic interim orientation.

Background/Objectives: Nutritional medicine remains underrepresented in medical education despite its relevance across specialties. Online learning offers a resource-efficient option to address this gap, yet evidence on the effectiveness and acceptability of online learning modules (OLMs) is limited. Methods: In this exploratory randomized controlled single post-test trial, medical students were assigned to either an OLM or an in-person lecture (IPL) on nutritional medicine (n = 91, no a priori sample size calculation performed). After course completion, students took a knowledge test and completed a questionnaire on their learning experience. Group differences were analyzed using permutation Welch t-tests, Wilcoxon–Mann–Whitney tests, or Fisher’s exact tests, depending on variable characteristics, with α = 0.05. Results: OLM students achieved significantly higher test scores than IPL students (mean difference: 2.4 points on a 0–40 scale), resulting in differences in grade classification (p < 0.05). OLM was further rated more favorably regarding content delivery, overall course evaluation, and exam preparation (all p < 0.05), while self-reported attention, concentration, and involvement did not differ between groups. Flexibility, time savings, and convenience were the most frequently reported advantages of OLM over IPL. Conclusions: This study suggests that OLM in nutritional medicine may be associated with higher test performance and more favorable student evaluations compared to IPL. These findings highlight the potential of online learning as a scalable, resource-efficient approach that may help address persistent gaps in nutritional medicine education. Building on this evidence, future work should examine how such modules can be optimally integrated into medical curricula to complement existing teaching structures.

Gut microbiota are permanent residents of humans with the highest concentrations being found in human colon. Humans get the first contact with bacteria at delivery, and microbiota are subject of permanent change during the life. The individual microbiota pattern is highly variable and varying environmental conditions, e.g., diets, antigen exposure, infections, or medication, as well as genetics, age, or hygiene factors, strongly influence the bacterial community. A fine interaction between the host and microbiota determines the outcome of health or disease. The gut immune system is constantly challenged to distinguish between commensal non-invasive bacteria and potential pathogens. Goblet cells produce mucins that prevent most gut bacteria from penetrating through intestinal epithelial barrier, and Paneth cells are the main supplier of anti-microbial defensins. Gut epithelial and immune cells recognize bacteria via surface markers and they initiate an adequate immune answer. A dysbiosis is noticed in several diseases, but the crucial role in pathogenesis has to be proven. Prebiotics or probiotics are discussed as valuable tools to preserve or restore a healthy gut community.