Microbiota dysbiosis and gut-brain axis interactions in short bowel syndrome: A rat model study

Short bowel syndrome (SBS), resulting from extensive intestinal resection, disrupts gut microbiota composition and may impact gut-brain axis (GBA) signaling. This study investigates microbiota alterations and GBA-associated biomarkers in a rat model of SBS.

SBS was induced in rats through small intestine resection (SB group), while controls underwent sham surgery. Fecal, serum, and brain tissue were collected 21 days post-surgery. Gut microbiota composition was analyzed via 16S-rRNA sequencing, and alpha and beta diversity were assessed. Differentially abundant taxa were identified using edgeR and LEfSe analysis. Serum and brain biomarkers, including cortisol, serotonin, and GABA, were quantified using ELISA.

SBS led to significant microbiota shifts, with increased Enterococcus, Clostridium, Alistipes, and Odoribacter, and reduced Romboutsia, Schaedlerella, and Turicibacter. While alpha diversity showed no significant differences, beta diversity analysis revealed distinct microbial profiles (PERMANOVA, P < 0.01). Differential abundance analysis identified Enterococcus, Drancourtella, Citrobacter, and Neglectibacter as significantly enriched in SB group (FDR <0.05). LEfSe confirmed microbial compositional shifts. Serum cortisol was higher in SB group (69.95 ± 39.04 vs. 42.84 ± 21.79 ng/mL, P = 0.17), while serum serotonin remained unchanged. Brain serotonin was significantly lower in SB group (1.22 ± 0.24 vs. 1.81 ± 0.38 ng/g, P < 0.01), whereas brain GABA showed no significant difference.

SBS induces gut microbiota dysbiosis, characterized by shifts in microbial composition and enrichment of opportunistic taxa. The reduction in brain serotonin suggests potential GBA dysfunction. These findings highlight microbiota alterations in SBS pathology and the need for microbiota-targeted interventions.