BACKGROUND: Alcoholic liver disease (ALD), an important cause of acute or chronic liver injury, results from binge drinking or long-term alcohol consumption. To date, there is no well-established mouse model with a comprehensive metabolic profile that mimics ALD in humans. This study aimed to explore the differential metabolic pathways and related differential metabolites in the liver of an ALD mouse model.

MATERIAL AND METHODS: A C57BL/6J mouse model of ALD was induced by alcohol feeding for 10 days plus binge alcohol feeding. The metabolomic profiles in the liver of the ALD mouse model was detected through ultra-high-pressure liquid chromatography-quadrupole time-of-flight tandem mass spectrometry (UHPLC/Q-TOF-MS).

RESULTS: A total 35 metabolites were significantly altered during the development of ALD. These metabolites were correlated to multiple metabolic pathways, including purine metabolism, the pentose phosphate pathway, cysteine and methionine metabolism, D-glutamine and D-glutamate metabolism, pyrimidine metabolism, and vitamin B6 metabolism.

CONCLUSIONS: The findings of the present study reveal potential biomarkers of ALD, and provide further insights into the pathogenesis of ALD.

Keywords: lipid metabolism disorders, Liver Diseases, Alcoholic, Metabolomics, Alcohol Drinking, Chromatography, Liquid, Ethanol, Liver, Metabolic Networks and Pathways, Metabolome, tandem mass spectrometry