Search Results (2,391)

Background/Objectives: Histologic remission has emerged as a key treatment target in inflammatory bowel disease (IBD), but routine assessment requires repeated endoscopy and biopsies. Blood-based indices reflecting inflammation, nutritional status and atherogenic risk are inexpensive and widely available, yet their integrated contribution to histologic activity remains unclear. This study addresses this gap by simultaneously analyzing a broad panel of 44 variables—including nutritional status indicators, CBC-derived inflammation indices, and atherogenic lipid indices—in IBD patients. Methods: In this retrospective study, 100 patients with IBD (50 Crohn’s disease [CD], 50 ulcerative colitis [UC]) without additional comorbidities and with concomitant histologic assessment were analyzed. Histologic activity was coded as active vs. remission. At the time of biopsy, the complete blood count, biochemistry and lipid profile were used to calculate immuno-nutritional indices (CONUT score, prognostic nutritional index), inflammatory indices (neutrophil-to-platelet ratio, platelet-to-lymphocyte ratio, lymphocyte-to-monocyte ratio [LMR], systemic immune-inflammation index, systemic immune-inflammation index, systemic inflammation response index [SIRI], aggregate index of systemic inflammation, C-reactive protein to albumin ratio) and atherogenic indices (atherogenic index of plasma [AIP], triglyceride-to-HDL cholesterol ratio). Variable selection was performed separately for CD and UC using least absolute shrinkage and selection operator (LASSO) regression and sparse partial least squares discriminant analysis (sPLS-DA). Independently associated predictors were then entered into multivariable logistic regression models, and their discriminative performance was evaluated using ROC analysis with bootstrap-derived 95% confidence intervals. Results: LASSO analysis identified a broadly similar systemic profile associated with histologic activity in CD and UC, dominated by the CONUT score, SIRI, AIP, LMR and red blood cell parameters, whereas demographic features and most routine biochemical markers were shrunk towards zero. Cross-validated AUCs for the LASSO models were 0.93 in CD and 0.87 in UC. sPLS-DA confirmed this pattern: CONUT, SIRI and AIP consistently showed the highest variable importance in projection scores and loadings on the first latent component. In multivariable regression, the CONUT score, SIRI and AIP remained independent predictors of histologic activity in CD, while hematocrit, CONUT score, SIRI and AIP were independently associated with histologic activity in UC. In ROC analysis, AUCs for CONUT, SIRI and AIP were 0.81, 0.89 and 0.87 in UC, and 0.72, 0.82 and 0.83 in CD, respectively. Conclusions: Histologic activity in IBD is characterized by a coupled systemic profile in which immuno-nutritional compromise (captured by CONUT) forms the core signal, supplemented by systemic inflammation (SIRI) and atherogenic dyslipidemia (AIP). These readily available blood-based indices may help to approximate histologic disease activity in clinical practice. However, considering that comorbid diseases may affect these indices, the strict exclusion criteria applied in this study may limit the generalizability of the findings among patients with IBD. Consequently, further validation in larger prospective cohorts is warranted. Full article

Phenolamides in bee pollen exhibit notable bioactivities, such as antioxidant, anti-inflammatory, and antimicrobial effects. Ulcerative colitis (UC) is a prevalent intestinal disorder, while the potential effects of phenolamides on UC remain unclear. This study aims to investigate the effects and mechanisms of phenolamide extract (PAE) from apricot bee pollen on dextran sulfate sodium (DSS)-induced UC in mice. Firstly, we analyzed the main compounds of PAE. Mice were treated with PAE (100, 200, and 400 mg/kg bw) both during the 7 days preceding 2.5% DSS induction and throughout the induction period (7 days). The results show that the primary compounds of PAE were isomers of tri-p-coumaroyl spermidine (97.78 ± 2.76%). A biochemical analysis showed that PAE decreased the levels of pro-inflammatory cytokines and increased the activities of antioxidant enzymes. Regarding the gut microbiota, PAE reduced the Bacillota/Bacteroidota ratio. Additionally, PAE elevated beneficial bacteria, including norank_f_Muribaculaceae, norank_o_Clostridia_UCG-014, and Lachnospiraceae_NK4A136_group, while reducing harmful bacteria, including Escherichia-Shigella, Clostridium, and Romboutsia. A quantitative analysis of short-chain fatty acids (SCFAs) demonstrated that PAE intervention promotes the biosynthesis of SCFAs in UC mice. This study first demonstrates that PAE attenuates DSS-induced colitis by modulating gut microbiota and SCFAs, suggesting its potential as a functional dietary supplement for colitis. Full article

Background/Objectives: Acute severe ulcerative colitis (ASUC) affects up to one quarter of patients with ulcerative colitis and carries a substantial risk of colectomy. Early recognition of the need for escalation beyond intravenous (IV) corticosteroids is essential, yet most indices—such as the Oxford criteria—require reassessment on day 3, delaying rescue therapy. The ASUC score, based on admission albumin, C-reactive protein (CRP), endoscopic severity (Ulcerative Colitis Endoscopic Index of Severity, UCEIS), and pre-admission steroid use, was recently proposed to predict early escalation at admission. This study aimed to externally validate the ASUC score and compare its performance with established indices. Methods: We performed a single-center retrospective validation study including consecutive ASUC admissions (2015–2024). The primary outcome was escalation beyond IV steroids, defined as medical rescue therapy with infliximab or ciclosporin and/or colectomy during the index hospitalization. As a sensitivity analysis providing a more specific estimate of IV corticosteroid non-response, we repeated analyses restricting the outcome to medical rescue therapy alone. The model performance was assessed for discrimination (AUC and bootstrap-corrected 2000 resamples), calibration (intercept, slope, and Brier score), and clinical utility (decision-curve analysis). Comparator indices included Albumin-CRP-Endoscopy score (ACE), Admission Model for Acute Severe Colitis (ADMIT-ASC), Oxford Day 3, Lindgren, and Edinburgh. Predefined subgroup analyses (exploratory and underpowered) evaluated infection and biologic exposure. Results: Ninety-one admissions were included overall. The primary validation was performed in the infection-free cohort (n = 77), and infected cases (n = 14) were analyzed separately. In the infection-free cohort, 17/77 (22.1%) required escalation beyond IV steroids during the index hospitalization (medical rescue therapy and/or colectomy), and 5/91 (5.5%) underwent colectomy within 90 days. The ASUC score showed excellent discrimination (Area under the receiver-operating characteristic curve [AUC] 0.89, 95% Confidence Interval [CI] 0.81–0.95), good calibration (intercept 0.26, slope 1.29), and net clinical benefit across 30–50% thresholds. In the rescue-only sensitivity analysis, discrimination remained high (AUC 0.86, 95% CI 0.77–0.94). At a cut-off of ≥2, sensitivity 94% and specificity 78% outperformed other indices (AUC 0.62–0.83). Exploratory subgroup analyses were imprecise due to small sample sizes; discrimination was lower in the infected-only subgroup (AUC 0.71), and estimates in biologic-experienced patients were unstable because of severe imbalance. Conclusions: The ASUC score accurately identified patients likely to require escalation beyond IV steroids on the day of admission, outperforming or matching established day-3 indices. Its simplicity and reliability support its integration into early ASUC management to expedite rescue therapy and potentially improve outcomes. Full article

Maclekarpine E is a minor alkaloid from Macleaya species with reported in vitro anti-inflammatory activity, but its in vivo metabolism remains unexplored. This study investigated the metabolic fate of maclekarpine E in rats and evaluated the potential pharmacological relevance of its metabolites. Maclekarpine E was orally administered to male Sprague-Dawley rats (250 mg/kg). Plasma, urine and feces were collected and analyzed by UPLC-Q-TOF-MS/MS. CYP phenotyping was performed using recombinant human enzymes. Molecular docking against ABCG2 and ABCC2 was conducted to assess potential interactions of all fecal compounds with these efflux transporters. Network pharmacology was employed to predict potential anti-ulcerative colitis-related targets of the metabolites, generating hypotheses for future experimental validation. Nineteen phase I metabolites were identified. Biotransformations included ring-opening, demethylation and oxidation. All 19 metabolites were detected in feces, nine in plasma and two in urine. No phase II conjugates were observed. CYP2C19 was the only significantly active isoform under the tested conditions, mediating approximately 16.5% substrate depletion (p < 0.05). All 20 fecal compounds bound ABCG2 (ΔG < −5.0 kcal/mol); 19 bound ABCC2. Network pharmacology yielded 57 overlapping targets with ulcerative colitis, enriched in PI3K-Akt and MAPK pathways. This study provides the first comprehensive metabolic profile of maclekarpine E in rats. The compound undergoes CYP2C19-mediated oxidation and is predominantly excreted into feces. Its fecal metabolites are potential ABCG2/ABCC2 substrates and may target UC-associated pathways based on network pharmacology predictions, warranting further experimental validation. Full article

Background: Inflammatory bowel disease (IBD), comprising Crohn’s disease (CD) and ulcerative colitis (UC), has been associated with elevated cardiovascular risks. However, the impact of IBD on outcomes following percutaneous coronary intervention (PCI) remains underexplored. We aimed to evaluate the clinical and procedural outcomes of PCI in patients with concurrent IBD. Methods: This study utilized the National Readmission Database from 2016 to 2020 to evaluate outcomes such as all-cause mortality and post-PCI complications, including various cardiovascular and gastrointestinal (GI) complications in IBD patients undergoing PCI. Patients with concurrent IBD and PCI were compared to non-IBD controls via multivariable logistic regression. Results: On propensity-score-matching analysis, IBD patients undergoing PCI had a higher prevalence of GI complications, including acute liver failure (Odds ratio (OR) 1.48, 95% confidence interval (CI) 1.13–1.93, p = 0.004), mesenteric ischemia (OR 5.34, 95% CI 1.56–18.40, p = 0.007), and need for blood transfusion (OR 1.74, 95% CI 1.46–2.08, p < 0.001). There was also a higher rate of cardiac complications (OR 1.31, 95% CI 1.05–1.64, p = 0.017). No significant difference in all-cause mortality (OR 0.86, 95% CI 0.72–1.04, p = 0.113) was observed. Conclusions: IBD patients undergoing PCI face increased GI and cardiovascular complications without a significant mortality difference. These findings highlight the complex interplay between systemic inflammation, vascular integrity, and procedural outcomes in IBD patients. Full article

Abnormal intestinal mucosal immunity plays a crucial role in ulcerative colitis (UC). Autotaxin (ATX) can promote T cell migration and was reported to have a regulatory effect on Th17 cells, while sphingosine-1-phosphate (S1P) and its receptors (S1PRs) modulate Th17/Treg balance and inflammation, with S1PR modulators approved for UC. ATX can catalyze sphingosylphosphorylcholine (SPC) to produce S1P; however, the relationship between ATX and S1P/S1PRs in UC is unclear. Understanding the role of ATX-S1P/S1PRs in intestinal immunity can provide new treatment strategies for intestinal inflammatory diseases. Both UC patients and DSS-induced colitic mice showed significantly increased levels of ATX and S1P compared with healthy controls. ATX inhibitor PF8380 treatment led to reduced levels of S1P/S1PRs in colitic mice. Consistent with this, the S1PR antagonist etrasimod was able to alleviate ATX-induced intestinal inflammation, as well as partially restore ATX-induced Th17/Treg imbalance in MLNs and the spleen. In HT-29 and Raw246.7 cells, ATX treatment led to enhanced expression of S1P/S1PRs, with S1PR1 being the most significant. Furthermore, S1PR1 mediates the effect of ATX on Th17/Treg cell differentiation and function in vivo. Therefore, ATX affects the differentiation and function of Th17/Treg cells through S1P/S1PR1 signaling, increased ATX expression leading to Th17/Treg cell imbalance, intestinal mucosal immune dysfunction, and exacerbating intestinal inflammation. Full article

Almond gum is a resource-rich natural polysaccharide; however, its high viscosity and low solubility severely limit industrial applications in separation, purification, and functional development. This study aimed to overcome these bottlenecks by optimizing an ethylenediaminetetraacetic acid (EDTA) preparation process and evaluating its protective efficacy against colitis. Using response surface methodology, optimal conditions were identified (1% EDTA, 3 h reaction, 10 h extraction), resulting in a modified polysaccharide (EAGP) with significantly reduced viscosity (from 640.8 to 238.7 mPa·s). SEM-EDX confirmed that EDTA efficiently removed cross-linking metal ions (K, Ca, Mg), creating a porous structure that facilitates purification. The purified fraction, EAGP-W1, was characterized as an arabinogalactan primarily composed of galactose (40.51%) and arabinose (38.38%). In vivo experiments demonstrated that EAGP-W1 significantly alleviated DSS-induced colitis, reducing colonic shortening and histopathological damage (p < 0.05). Mechanistically, EAGP-W1 reshaped the gut microbiota by downregulating pro-inflammatory genera and upregulating probiotics (p < 0.05). This shift promoted the production of short-chain fatty acids (SCFAs) (p < 0.05), thereby repairing the intestinal barrier and suppressing inflammation. Overall, this study establishes an efficient EDTA-based strategy for almond gum processing and elucidates its anti-inflammatory mechanism through the “microbiota–metabolite–barrier” axis, providing a theoretical basis for its development as a high-value functional food for gut health. Full article

Diet is a major modifiable determinant of gastrointestinal (GI) health, influencing disease risk and progression through coordinated effects on the gut microbiome, immune regulation, epithelial barrier integrity, oxidative balance, and epigenetic mechanisms. This narrative review synthesizes epidemiological, mechanistic, and clinical evidence from the past decade to examine bidirectional relationships between dietary patterns and seven common GI disorders: celiac disease, irritable bowel syndrome (IBS), Crohn’s disease, ulcerative colitis, Helicobacter pylori-associated gastritis, peptic ulcer disease, and lactose intolerance. Western dietary patterns, characterized by high intake of ultra-processed foods and saturated fats and low fiber consumption, are consistently associated with microbial dysbiosis, impaired barrier function, and enhanced inflammatory signaling. In contrast, Mediterranean and plant-forward dietary patterns show protective associations across multiple GI conditions. Mechanistically, diet influences GI pathophysiology largely through microbiome-derived metabolites, particularly short-chain fatty acids, which regulate epithelial homeostasis, immune tolerance, and inflammatory pathways. Condition-specific dietary strategies remain clinically important. Gluten exclusion is essential in celiac disease, low- fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAP) approaches provide evidence-based symptom control in IBS, and exclusive enteral nutrition or targeted exclusion diets support remission induction in Crohn’s disease. Selected probiotics and emerging postbiotics may provide adjunctive benefits in specific contexts. Despite growing evidence, dietary research remains limited by methodological heterogeneity and interindividual variability. Precision nutrition approaches integrating microbiome profiling and artificial intelligence represent a promising translational direction. Overall, dietary patterns—rather than isolated nutrients—form the foundation of GI dietary therapy. Full article

Background/Objectives: Chronic diseases, such as inflammatory bowel disease (IBD), influence patients’ sexuality. Therefore, the aim of this study was to analyze the sexual functioning (SF) of patients with IBD. Methods: We perform a prospective survey study on male and female individuals with IBD using an anonymous questionnaire including 60 inquiries concerning patients’ intimate relationships and SF. The following statistical tests were used: chi-square test of independence, Spearman’s rank correlation coefficient, and Wilcoxon and Mann–Whitney U tests. A significance level of p = 0.05 was assumed as statistically significant. Results: There were 110 respondents with IBD (41% with Crohn’s disease and 57% with ulcerative colitis): 52 women (47%) and 58 men (53%), with a mean age of between 31 and 40 (45%). In 34% of respondents, the assessment of satisfaction with sex after diagnosis decreased, and the difference was statistically significant (p = 0.007). Statistically significant correlations were found between IBD clinical activity and the impact of the disease on sexual desire (p < 0.001), the need for sex after diagnosis (p < 0.001), satisfaction with sex after diagnosis (p = 0.003), the average frequency of intercourse (p = 0.004), the average duration of intercourse after diagnosis (p = 0.001), feeling guilty in the sexual sphere due to the disease (p = 0.006), assessment of one’s attractiveness since diagnosis (p = 0.032), and change in the partner’s erotic perception after diagnosis (p < 0.001). The more aggressive the course of the disease, the more negative the impact on patients’ sexuality. Conclusions: The diagnosis of IBD has a negative impact on patients’ SF—disease flare leads to a decrease in sexual needs, worse experiences and negative body image. Full article

Background/Objectives: Ulcerative Colitis (UC) is a chronic inflammatory disease of the colon that profoundly impacts human health. Conventional pharmacological treatments are associated with serious adverse reactions and toxic side effects. Consequently, the development of natural plant-derived biological agents for UC treatment is an urgent imperative. Methods: Utilising a Dextran Sulfate Sodium (DSS)-induced ulcerative colitis mouse model, with mice receiving low, medium, and high doses of water extract of Tibetan Fritillaria cirrhosa D. Don extract (FCD), alongside a group receiving 5-aminosalicylic acid. The Disease Activity Index (DAI) was calculated, colon length was measured, histological scores were assessed, and histopathological alterations were evaluated. Inflammatory factor were determined by ELISA; mRNA and protein expression in colonic tissue was analysed by RT-qPCR and Western blotting; intestinal barrier-related proteins were examined by immunofluorescence and immunohistochemistry; and gut microbiota composition was assessed by 16S rRNA sequencing. Results: Research has confirmed that FCD alleviates symptoms of DSS-induced colitis in mice, specifically manifested by a slower rate of weight loss, reduced colon shortening, and decreased disease activity index. It has been demonstrated that the process under investigation exerts a beneficial effect on intestinal injury by means of a number of mechanisms. These include increased goblet-cell production, elevated IL-10 levels, and reduced levels of TNF-α, IL-1β, and IL-6. Furthermore, immunofluorescence detection, immunohistochemical analysis, and RT-qPCR results indicate that FCD maintains the integrity of the intestinal mucosal barrier by enhancing the expression of Zonula occludens-1 (ZO-1), occludin, and claudin-1 proteins and their corresponding mRNAs, in addition, FCD can regulate the gut microbiota and promote its diversity. Conclusions: Research indicates that FCD may exert therapeutic effects on ulcerative colitis (UC) by regulating intestinal barrier integrity and modulating the gut microbiota. These findings reinforce the idea that FCD could be used as a natural therapy to improve UC. Full article

Background/Objectives: Ejiao, a macromolecular protein complex derived from donkey hide, is a traditional Chinese medicine with clinically demonstrated efficacy against ulcerative colitis (UC). Due to its large molecular size and poor absorbability, its therapeutic effects are presumed to depend on gut microbiota. We hypothesized that specific gut bacteria capable of degrading Ejiao might also mediate its biological functions. Methods: To test this hypothesis, a systematic investigation was conducted by integrating culturomics, proteomics, metabolomics, 16S rRNA gene amplicon high-throughput sequencing, and animal disease models. Results: A total of 134 human gut bacterial strains capable of utilizing Ejiao as a nutrient source were isolated. Among them, Ligilactobacillus salivarius D3-8 exhibited the strongest growth in Ejiao-based medium. Genomic analysis identified 63 protease/peptidase genes, and peptidomic profiling confirmed its degradation activity, which released 50 novel peptides. Notably, administration of L. salivarius D3-8 alone significantly alleviated dextran sodium sulfate (DSS)-induced colitis, concurrently increasing the abundance of beneficial bacterium Dubosiella newyorkensis and elevating the anti-inflammatory metabolite indole-3-carbinol via upregulated tryptophan metabolism. Conclusions: Our findings identify L. salivarius D3-8 as both a dedicated Ejiao-degrader and a protective probiotic against colitis. This work provides direct evidence that gut bacteria can utilize Ejiao and proposes a potential novel mechanistic framework in which the biological effects of Ejiao may be mediated through its interaction with specific, functionally potent degraders such as L. salivarius D3-8. Full article

Background/Objectives: Epigenetic factors are increasingly recognized to contribute to the pathogenesis of intestinal diseases, yet the precise mechanisms through which these factors influence ulcerative colitis (UC) remain poorly understood. Methods: Transcriptome profiles pertaining to UC and genes associated with epigenetic factors (EFRGs) were retrieved from publicly accessible datasets. Candidate genes were ascertained through the intersection of differentially expressed genes (DEGs) and EFRGs. Key genes were screened through machine learning algorithms and validated via the Artificial Neural Network (ANN) model. Enrichment analysis and immune infiltration assays were conducted to elucidate the underlying mechanisms of these genes. The hub gene, CBX4 (Chromobox homolog 4), was validated through immunohistochemical analysis of both healthy controls and patients with UC, and the correlation was evaluated using UC-related clinical parameters. Additionally, CBX4 expression was knocked down in dextran sulphate sodium (DSS)-treated mice to examine its regulatory function. Unlike conventional broad-spectrum biomarker screens, this study specifically integrated epigenetic factor-related genes (EFRGs) with machine learning and experimental validation using both clinical samples and animal models. Results: SMARCB1, JAK2, CBX4, and PPARGC1A were identified as key genes, with SMARCB1, JAK2, and CBX4 being upregulated in the UC group, while PPARGC1A was significantly downregulated. The ANN model exhibited excellent diagnostic performance. Enrichment analysis revealed that the key genes were associated with pathways such as the “chemokine signaling pathway”. Immune cell infiltration analysis results revealed marked differences in the abundances of 13 immune cell types between the UC and control groups, and there were notable associations between immune cell infiltration and key genes. Notably, CBX4 expression was elevated in both DSS-treated mice and patients with UC, showing positive correlations with clinical indicators of UC. Further in vivo experiments revealed that silencing CBX4 alleviated DSS-induced colon damage and inflammation. Conclusions: This study identifies four EFRG-related key genes (SMARCB1, JAK2, CBX4, PPARGC1A) in UC, suggesting that CBX4 may play a significant role as an epigenetic regulator. CBX4 is upregulated in UC intestinal tissues, and its knockdown mitigates DSS-induced colitis. These findings provide critical theoretical support for developing targeted therapies for UC. Full article

Background/Objectives: Dietary intake of fruits and vegetables (FVs) has been inversely associated with a lower risk of ulcerative colitis. Using a pig model, we evaluated the effect of FV supplementation on dextran sulfate sodium (DSS)-induced colitis. Methods: Six-week-old pigs were fed a grower diet (negative control), grower diet + 4% DSS (positive control), half-FV diet + DSS, or full-FV diet + DSS. FV levels matched half or full daily recommendations from the Dietary Guidelines for Americans (DGA). Clinical signs were monitored; proximal colon contents (PCs) and mucosa (PCM) were analyzed for metagenome, transcriptome and histopathology. Results: Full-FV pigs showed no diarrhea, less fecal occult blood (FOB), crypt hyperplasia, but no changes in gene expression or microbiome diversity (p < 0.05). Half-FV pigs had increased FOB, differentially expressed genes (DEGs) linked to tissue remodeling, crypt/goblet cell hyperplasia and two cases of diarrhea (p < 0.05). DSS controls showed reduced immune-related DEGs, altered microbiome, PCM erosion, FOB, and persistent diarrhea in one pig (p < 0.05). Conclusions: A three-week full-FV diet conferred protection against DSS-induced colitis, with a dose-dependent protection of intestinal tissue and gut metagenome under inflammatory challenge. Full article

The escalating global burden of Ulcerative Colitis (UC) underscores the urgent need for novel therapeutic strategies. Although dietary modulation is known to influence UC progression, the specific molecular mediators remain largely undefined. Recently, the G protein coupled receptor 35 (GPR35) has emerged as a promising target for maintaining gut homeostasis and promoting intestinal epithelium repair. Yet, whether the therapeutic benefits of dietary polyphenols are mediated through the direct activation of GPR35 remains unexplored. Here, the NanoLuc Binary Technology (NanoBiT) assay was first used to identify the potential GPR35 agonist from a library of 30 natural polyphenolic compounds. We discovered Ellagic acid (EA), a natural polyphenol abundant in fruits and nuts, as the potent GPR35 agonist owing to its most potent agonistic effect. The dose-dependent effect was further confirmed by both NanoBiT and Bret assay. Then, the binding site of the ligand-receptor complex was predicted via molecular docking, and key interactions were validated by site-directed mutagenesis. The results indicated the key binding site of the complex was Gln93, Arg100, Arg151, Phe163 and Ser262. And the conformation of the complex was verified stable by the molecular dynamics simulation. The bioactivity of EA was then evaluated in vivo. And the in vivo experiment indicated that EA alleviated the symptoms of UC. In addition, complementary in vitro assays, including a wound healing (scratch) assay and an SRB proliferation assay, were employed to investigate its effect on intestinal epithelial repair. The in vitro experiment demonstrated that EA enhanced the migration and proliferation of human colonic epithelial cells, an effect that was specifically abolished by the GPR35 antagonist CID2745687, indicating the key role GPR35 played in the intestinal repair. Collectively, our study demonstrates that the natural polyphenolic compound EA promotes epithelial healing and ameliorates colitis by acting as a GPR35 agonist. Full article

Background: Malnutrition and suboptimal diet quality are common, yet under-recognized, in inflammatory bowel disease (IBD) and are associated with worse clinical outcomes and lower quality of life. Digital tools may facilitate continuous, personalized nutritional support, but evidence in IBD remains limited. The aim of this study was to evaluate the impact of a nutritional intervention based on a mobile application (Nootric^®) on nutritional status, diet quality, and malnutrition risk in patients with IBD undergoing stable follow-up. Methods: We conducted a prospective longitudinal cohort study without a control group including 151 adult patients with Crohn’s disease or ulcerative colitis under stable follow-up in a tertiary IBD unit. Participants used a structured digital nutritional support program through the Nootric^® app for 24 weeks, supervised by dietitians and the IBD team. Clinical activity, biochemical markers (C-reactive protein, fecal calprotectin), nutritional biomarkers (albumin, prealbumin, micronutrients), body mass index (BMI), malnutrition risk (self-administered Malnutrition Universal Screening Tool, MUST), and diet quality (PREDIMED and an expanded “Nootric score”) were assessed at baseline, 12 weeks, and 24 weeks. Analyses focused on patients with adequate adherence. Results: Of the 151 included IBD patients, 110 maintained stable app use. Mean albumin increased from 4.38 to 4.49 g/dL at 24 weeks (p = 0.003), and prealbumin from 24.9 to 26.1 mg/dL (p = 0.047), despite the absence of overt protein–calorie malnutrition at baseline. Patients with obesity achieved a mean weight loss of approximately 6% of baseline body weight. Diet quality improved significantly, with higher Nootric score and a positive correlation between app use intensity and increased score. Malnutrition risk according to the MUST scale improved in more adherent patients, while clinical and biochemical disease activity remained stable overall. Conclusions: A mobile app-based nutritional program supervised by dietitians was feasible, well accepted, and associated with improved nutritional markers, diet quality, and malnutrition risk, supporting its role as a complementary component of IBD care. Full article