As a
metabolic disease,
fatty liver hemorrhagic syndrome (
FLHS) has become the major factor responsible for the noninfectious cause of mortality in laying hens, which lead to huge economic losses to poultry industry. However, the pathogenesis of
FLHS remains unclear. The aim of present study was to identify novel liver metabolites associated with
FLHS. Twenty healthy Chinese commercial Jing Fen laying hens aged 90 d were used in present study. After acclimatization for 2 wk, the hens were divided into 2 treatments (n = 10): control group (normal diet) and
FLHS group (high-energy
low-protein diet). The experiment lasted for 48 d, and the laying hens were killed for blood and liver sampling at the end of the experiment. Blood biochemical indicators and liver pathological changes were examined. Meanwhile, the changes in liver metabolic profile were investigated with the application of metabolomics approach. Significant increased levels of
alanine aminotransferase,
aspartate aminotransferase,
low density lipoprotein, total
cholesterol and
triglycerides, decreased
high density lipoprotein (P < 0.01), and hepatic steatosis were observed in hens of
FLHS group, which suggested
FLHS was successfully established in this study. Distinct changes in metabolite patterns in liver between control and
FLHS group were observed by partial least-squares discriminant analysis. In total, 42 liver metabolites including
tyrosine,
glutathione,
carnitine,
linoleic acid,
uric acid,
arachidonic acid (ARA),
lactate and
lysophosphatidylcholine (14: 0) were identified and considered to be related with pathogenesis of
FLHS. Pathway analysis revealed that these metabolites were mainly involved in
amino acid metabolism,
fatty acid metabolism, ARA metabolism,
glucose metabolism and
glycerophospholipid metabolism. Furthermore, targeted metabolomics found that ARA metabolites such as
prostaglandins and
hydroxyeicosatetraenoic acids were significantly increased in
FLHS group (P < 0.05). In conclusion, our data showed that liver metabolites and ARA metabolism were linked to the pathophysiology of
FLHS, which provided a basis for understanding the pathogenesis of
FLHS in laying hens.