Tauroursodeoxycholic acid (TUDCA) protects against soybean meal-induced hepatopancreatic steatosis and intestinal inflammation in grass carp (Ctenopharyngodon idellus).

This study evaluated the potential for tauroursodeoxycholic acid (TUDCA) to ameliorate the negative effects associated with high soybean meal (SBM) diets in the grass carp (Ctenopharyngodon idellus). Grass carp (initial weight 25.42 ± 0.16 g) were fed one of four diets for 8 weeks: a control diet (fish meal [FM]-based), Control+TUDCA (0.5 g/kg), a high SBM diet (100SBM, completely replacing FM), or 100SBM + TUDCA. The 100SBM diet reduced growth performance and feed efficiency. However, TUDCA supplementation did not reverse these growth deficits. The 100SBM diet induced hepatopancreatic lipid accumulation, which was attenuated by TUDCA. Regarding hepatic lipid metabolism, the SBM diet significantly increased apolipoprotein E gene expression, while TUDCA supplementation decreased acetyl-CoA carboxylase gene expression. Hepatic farnesoid X receptor (FXR) signaling and endoplasmic reticulum stress (ERS)-related gene expression remained unaltered across all dietary treatments. Histological analysis revealed that the 100SBM diet reduced intestinal villus height and muscle thickness while increasing capillary width. TUDCA ameliorated SBM-induced muscular atrophy and capillary dilation in the foregut and midgut. Furthermore, the 100SBM diet elevated inflammatory cytokine concentrations (interleukin-6, tumor necrosis factor-α, and interleukin-1β) in the foregut and midgut, an effect mitigated by TUDCA. Intestinal FXR and ERS pathways displayed segment-specific modulation by TUDCA, with significant activation in the midgut and hindgut, respectively. Overall, although it lacked significant growth-promoting effects, TUDCA protected against SBM-induced hepatopancreatic lipid accumulation and intestinal inflammation, partially through the modulation of intestinal ERS and FXR signaling pathways.