Excessive abdominal fat deposition and fatty liver syndrome are important industrial problems of lipid metabolism disorder in poultry breeding. The liver is the main site of de novo fatty acid synthesis in poultry, which plays a vital function in nutrients metabolism, formation of bile acids and detoxication. Therefore, the mechanism analysis of lipid metabolism disorder will provide reference for the healthy development of poultry industry, but the disease model is necessary for pathogenesis research.

This experiment was conducted to evaluate the effect of dexamethasone-induced fatty liver in broilers, aiming to provide the reference for the construction of lipid metabolism disorder model in poultry.

Sixteen 35-day-old AA broilers with similar body weight were randomly divided into control group and dexamethasone group (DXM), with 8 replicates in each group. The birds in the DXM were injected subcutaneously with dexamethasone sodium phosphate (4.5 mg·kg^-1) for 7 days, and the birds in the control group were given the administration of normal saline injection. After 7 days, oil red O staining was used to analyze the histopathological changes of the liver, and serum biochemical and antioxidant indexes were detected. RT-PCR was applied to detect genes expression related to lipid metabolism and inflammatory response in the liver.

Compared with the control group, the liver index of broilers in the DXM was significantly increased (P<0.05). Oil red O sections showed a large number of red lipid droplets, and the contents of TG and TC in the liver were higher than those in the control group (P<0.05). Serum biochemical results showed that aspartate amino transferase (AST), total bilirubin (TBIL), uric acid (UA), total protein (TP), high density lipoprotein cholesterol (HDL-c), low density lipoprotein cholesterol (LDL-c), total cholesterol (TC) and triglyceride (TG) levels in the DXM were significantly higher than those in the control group (P<0.05), but there was no significant difference about alanine aminotransferase (ALT) and glucose (GLU) (P>0.05). Dexamethasone injection significantly increased genes expression about lipid synthesis, such as ACC, FAS, SCD1, PPARγ, ChREBP, SREBP-1c, IGF2 and GR in the liver (P<0.05), but ELOVL6 expression was not affected (P>0.05). In addition, genes expression about lipid catabolism such as CPT1, LPL and PPARα were deceased in DXM group (P<0.05). However, the expression of ATGL gene related to lipid hydrolysis, CETP and MTTP gene related to lipid transport were significantly higher in DXM group (P<0.05). On the other hand, DXM injection significantly increased the genes expression of MyD88, NFκB, IL-6, TNF-α in the liver of broilers (P<0.05). Antioxidant analysis showed that there was no significant change in the total antioxidant capacity of liver and serum (P>0.05), but the content of malondialdehyde in serum was significantly higher in DXM group (P<0.05).

Neck subcutaneous injection of DXM could cause lipid metabolism disorders in broilers, and lead to oxidative stress and liver inflammation, which was similar to the characteristics of fatty liver disease, indicating that this method could be used to establish the fatty liver model in broilers quickly.

Fatty liver syndrome (FLS) is a common nutritional metabolic disease in laying hens during the laying period, which includes a multi-stage pathogenesis process, such as “simple steatosis, steatohepatitis, liver fibrosis, and cirrhosis”, causing substantial economic losses in poultry industry. The construction of fatty liver model is the key to exploring the pathogenesis of FLS, screening nutritional regulation measures and subsequent disease prevention and evaluation. However, there are few studies on poultry hepatocyte steatosis models.

Chicken embryo liver (CEL) cells were used to establish a liver lipid deposition model by oleic acid induction, aiming to explore the induction time required for different stages of FLS.

CEL at the age of 18 embryo was used and when CEL cells grew to about 80%, and the medium containing 400 μmol·L^-1 oleic acid was replaced for treatment. After 24 h, 48 h and 72 h of culture, the cells were stained with oil red O, and the lipid content was measured. At the same time, the mRNA and protein levels of genes related to lipid metabolism, inflammation and fibrosis were analyzed.

Compared with the Control group, there were a large number of red lipid droplets in 24 h group, 48 h group and 72 h group, and the red color gradually deepened with the increase of induction time (P<0.05), indicating that fat droplets in cells were increased. Meanwhile, the content of TG and TC in the liver were higher than those in the Control group (P<0.05). RT-PCR analysis revealed a significant upregulation of ACC, FAS, ELOVL6, and SREBP gene expression related to lipid synthesis following 24 h of oleic acid induction (P<0.05), indicating that oleic acid lipid deposited on cells after 24 h of processing. ELISA results showed that the content of IL-6, IL-1β and TNF-α were not significantly changed in 24 h (P>0.05). However, an upward trend was observed in IL-6 level with prolonged induction durations (P=0.052). Notably, following 72 h of oleic acid treatment, the levels of IL-6 and IL-1β were significantly increased in Control group (P<0.05), which indicated that acid treatment after 48 h cells began to inflammation reaction and increased with the extension of induction time. In addition, compared with the Control group, the expression level of IL-6 protein in the 48 h group was significantly increased, which was consistent with the ELISA results, while the protein expression levels of COL1A1 and FIBRONECTIN were increased (P<0.05). On the contrary, the protein expression levels of IL-6, COL1A1 and FIBRONECTIN were significantly higher than those in the Control group at 72 h (P<0.05).

The early lipid deposition model of hepatocytes could be established by 400 μmol·L^-1 oleic acid induction for 24 h. In addition, inflammation and fibrosis would occurr after 48 h and 72 h induction, respectively.