Taurochenodeoxycholic acid promotes abdominal fat deposition by modulating the crosstalk between bile acid metabolism and intestinal microbiota in broilers.

BACKGROUND: The role of bile acids in modulating the gut microbiota and their impact on host metabolism has garnered significant attention. Taurochenodeoxycholic acid (TCDCA) is the predominant bile acid within the chicken bile acid pool and is closely related to metabolic disorders. The current study aims to investigate the potential effects of TCDCA on abdominal fat deposition in broilers. From 14 to 28 days of age, the broilers in the CON group received an oral administration of 1 mL of saline, while those in the treatment groups were administered 1 mL of a solution containing 0.05 g, 0.10 g, or 0.20 g of TCDCA. RESULTS: The results showed that TCDCA treatments from 14 to 28 d had no significant effects on BW, ADFI, ADG and FCR in broilers at the age of 28 days of age. However, the abdominal fat percentage in the 0.20 g TCDCA group significantly increased, accompanied by higher TBA and HDL-c levels, as well as a reduction in apolipoprotein B levels in serum. In addition, serum triglyceride levels tended to be higher in the 0.20 g TCDCA group (P = 0.098). The 0.20 g TCDCA treatment increased the gene expressions of SREBP-1, C/EBP-α, and ELOVL6, while decreasing the mRNA abundance of ATGL and CPT-1 in the abdominal fat. Serum levels of TCDCA, TDCA, and THDCA were significantly higher after 0.20 g TCDCA administration, while TCA levels were significantly lower, as determined by the targeted bile acid metabolomics analysis. Conversely, hepatic mRNA levels of CYP7A1, CYP27A1, BAAT, and BSEP were increased in the 0.20 g TCDCA group. The oral administration of 0.20 g TCDCA also upregulated the expression of FXR, VDR, and FGF19 in abdominal fat. The 16S rRNA analysis of cecal microbiota revealed that a decrease in the Shannon and Simpson indexes in the 0.20 g TCDCA group, and an increase in the Firmicutes/Bacteroidetes ratio. LEfSe analysis revealed that the predominant bacteria in the CON group were Streptococcus and Oscillospira at the genus level, while Lactobacillus, Parabacteroides, Anaeroplasma, and Helicobacter were identified as the dominant genera in the 0.20 g TCDCA group. Functional predictions for the gut microbiota exhibited that lipid metabolism, replication and repair pathway were enhanced in the 0.20 g TCDCA group. Correlation analysis demonstrated that the abundance of Lactobacillus was positively correlated with serum levels of TCDCA, THDCA, and TDCA, while the abundance of Streptococcus and Oscillospira showed a positive correlation with serum TCA levels. CONCLUSION: Overall, this study elucidates that the intervention of 0.20 g TCDCA may promote abdominal fat deposition by activating bile acid receptors in abdominal fat, and concurrent alterations in both the intestinal microbial community and bile acid profile.