Effect of dietary chenodeoxycholic acid on fat deposition and intestinal health in Wenchang chickens.

Chenodeoxycholic acid (CDCA), an endogenous agonist of the farnesoid X receptor, is involved in lipid homeostasis and intestinal barrier regulation. This study examined how dietary CDCA alleviates high-energy diet (HED)-induced metabolic disorders in Wenchang chickens and determined the optimal supplemental dose. A total of 525 Wenchang hens were randomly assigned to five groups: Con (basal diet), HED, and HED supplemented with 50, 100, or 200 mg/kg CDCA (≥ 98% purity). The experiment spanned 42 days. Compared with the control group, HED significantly increased abdominal fat percentage, serum LDL-C, and GLU levels (P < 0.05), reduced jejunal villus height by 35.05% and increased crypt depth by 35.44%, downregulated tight junction protein expression, activated the TLR-4/NF-κB pathway, and elevated serum LPS, DAO, and d-lactate levels (P < 0.05). The 50 and 100 mg/kg doses showed lesser effects, while 200 mg/kg was identified as the most effective dose. Compared to the HED group, 200 mg/kg CDCA supplementation significantly decreased abdominal fat by 41.7%, LDL-C by 40.53%, and GLU by 18.77% (P < 0.05). It enhanced lipolytic gene expression, suppressed adipogenic gene expression (P < 0.05), improved intestinal morphology (villus height increased by 36.60%, VH/CD by 53.79%), inhibited the TLR-4/NF-κB inflammatory pathway, and reduced harmful bacteria like Desulfovibrio, Helicobacter, and Bilophila (P < 0.05). Although the CDCA-supplemented groups had significantly less intramuscular fat content than the HED group, more than the control group (P < 0.05). In summary, dietary supplementation with 200 mg/kg CDCA effectively alleviates HED-induced lipogenesis and intestinal damage in female Wenchang chicken through regulation of lipid metabolism genes, restoration of intestinal barrier function, inhibition of the TLR-4/NF-κB inflammatory pathway, and modulation of gut microbiota composition, making it the ideal dose.