Objective: This study aimed to develop an animal model that closely replicates the clinical features of necrotizing enterocolitis (NEC), thereby providing a supportive platform for ongoing NEC research.Methods: 36 two-week-old neonatal suckling rabbits were randomly assigned to three groups: normal group (Group A, n = 12), traditional group (Group B, n = 12), and modified group (Group C, n = 12). Daily monitoring of general condition, post-modeling survival rate, and survival time was conducted in neonatal rabbits. Histopathological assessment of intestinal morphology was performed using hematoxylin and eosin staining, with scoring conducted to evaluate modeling success. Serum concentrations of C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10), occludin, zonula occludens-1 (ZO-1), and zonulin were quantified using ELISA. Protein expression levels of occludin and ZO-1 in intestinal tissues were analyzed via Western blot.Results: Modified group exhibited significantly higher survival rates and prolonged survival time compared to traditional group (p < 0.05). Both model groups demonstrated elevated serum levels of CRP, TNF-α, IL-10, along with reduced concentrations of occluding, ZO-1 and zonulin when compared to normal group (p < 0.05). Similarly, intestinal expression levels of occludin and ZO-1 were significantly lower in both model groups relative to control (p < 0.05). However, no significant differences were observed between model groups in these parameters (p > 0.05).Conclusion: Our study successfully established a novel neonatal rabbit model of NEC with prolonged survival time by refining conventional modeling methodologies, thereby providing a new platform for investigating NEC pathogenesis and therapeutic interventions.

Background: Dietary factors related to fermentable oligosaccharides, disaccharides, monosaccharides and polyols (FODMAPs) and gut microbiota may influence gastroesophageal reflux disease (GERD), but causal evidence and clinical consistency remain uncertain. Objective: We tested whether FODMAP-related and GERD-relevant dietary traits influence GERD risk using Mendelian randomization (MR), and whether gut microbiota mediate these associations. Methods: We integrated UK Biobank dietary GWAS, MiBioGen microbiota GWAS, and FinnGen GERD summary statistics using inverse-variance weighted MR, multivariable MR, Benjamini-Hochberg false discovery rate (BH-FDR) correction, MR-Steiger filtering, and two-step mediation analysis. A 525 matched-pair retrospective case–control cohort provided clinical validation. Results: After BH-FDR correction, genetically predicted cheese, cereal, oily fish, fresh/dried fruit, and salad/raw vegetables were associated with lower GERD risk (ORs, 0.46–0.77), whereas tea and poultry were associated with higher risk (ORs, 1.28–2.14). Microbiota-wide and mediation signals did not survive FDR correction. The oily fish- Erysipelatoclostridium indirect effect was small and statistically imprecise (indirect effect, −0.015; 95% CI, −0.034 to 0.005), corresponding to a mediated proportion of 4.1% (95% CI, −1.2 to 9.5%); therefore, it was interpreted as an exploratory signal rather than evidence of a confirmed microbial pathway. Clinical data directionally supported the main dietary signals: tea, poultry, processed meat, and sweets were associated with higher GERD risk (ORs, 1.04–1.19), while cheese, cereal, fruit, and oily fish were protective (ORs, 0.80–0.94). Conclusion: Dietary associations with GERD were more robust than microbiota-associated signals. These findings suggest that oily fish-related dietary patterns may be associated with lower GERD risk, while exploratory analyses provide preliminary evidence that gut microbiota may contribute to these associations. Further studies are required to validate these potential biological pathways.