Abstract
Clostridium butyricum (C. butyricum) can attenuate oxidative stress, inflammation, and hepatic fatty deposition in poultry, however, the underlying mechanisms for this in Pekin ducks remain unclear. This study evaluated these hepatoprotective effects and the underlying mechanisms in a corticosterone (CORT)-induced liver injury model in Pekin ducks fed a C. butyricum intervention diet. A total of 500 Pekin ducks were randomly divided into five groups: one group (CON group) was only provided with a basal diet, three groups were provided a basal diet with 200 mg/kg (LCB group), 400 mg/kg (MCB group), or 600 mg/kg (HCB group) C. butyricum, respectively, and one group was provided a basal diet with 150 mg/kg aureomycin (ANT group) for 42 d. At 37 days-old, all ducks received daily intraperitoneal injections of CORT for five days to establish a liver injury model. C. butyricum intervention alleviated liver injury by decreasing the liver organ indices, hepatic steatosis and hepatocyte necrosis, and improving liver function, antioxidant capacity, and inflammatory factors. Hepatic RNA-seq revealed 365 differentially expressed genes (DEGs) between the MCB and CON groups, with 229 up- and 136 down-regulated DEGs in the MCB group. Between the MCB and ANT groups, 407 DEGs were identified, including 299 up- and 108 down-regulated genes in MCB group. Some DEGs in the MCB group related to oxidative stress and inflammatory responses such as Sod3, Tlr2a/b, and Il10, which were up-regulated, while Apoa1, Cyp7a1, Acsl1/5, Fasn, Ppar-γ, and Scd, which are involved in lipid metabolism, were down-regulated, indicating that these genes were responsive to dietary C. butyricum for the alleviation of corticosterone-induced hepatic injury. Toll-like receptor signaling, PI3K-Akt signaling pathway, cytokine-cytokine receptor interaction, peroxisome proliferator-activated receptor (PPAR) signaling pathway, adipocytokine and glycerophospholipid metabolism signaling pathway were significantly enriched in the MCB group. These findings indicate that C. butyricum intervention can protect Pekin ducks from corticosterone-induced liver injury by the modulation of immunoregulatory- and lipid metabolism-related genes and pathways.
Highlights
The timid nature of Pekin ducks makes them stressed
These genes were demonstrated to decrease gluconeogenesis and increase fatty acid β-oxidation, fatty acid transportation and cholesterol metabolism [51,52,53]. These results indicated that C. butyricum supplementation in MCB group can modulate hepatic lipid metabolism-related genes in Pekin ducks to alleviate the hepatic steatosis induced by CORT
According to the Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, we found that the peroxisome proliferator-activated receptor (PPAR) signaling pathway, which is associated with lipid metabolism regulation [54], was activated in the C. butyricum-treated group in Pekin ducks, indicating that providing C. butyricum to Pekin ducks can regulate the expression of lipid metabolism-related genes through activation of the PPAR signaling pathway
Summary
The timid nature of Pekin ducks makes them stressed. Reared ducks are constantly exposed to various adverse influences, such as noise, crowding, handling, transport, high temperature, and immune challenges, which leads to chronic stress [1,2]. Stress in poultry can activate the hypothalamic pituitary adrenal axis, resulting in increased corticosterone (CORT). The serum CORT level is considered a reliable stress indicator in poultry [4]. Numerous publications have demonstrated that a CORT challenge can reliably induce physiological stress in rodents and birds [5,6]. A CORT challenge can lead to decreased body weight, and can influence lipid metabolism and immune system responses [7,8,9]
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