Objective: The preventive effect of camel milk on acute alcoholic liver injury in mice was analyzed by detecting serum and liver indexes， and the mechanism of metabonomics was explored. Methods: 24 ICR male mice were randomly divided into normal control group (NC)， model group (ET) and camel milk group (ET+CM). The mouse model of acute liver injury was established by gavage of large dose (7.3 g/kg) of alcohol for a short time. The protective effect of camel milk on liver was reflected by measuring serum indexes (ALT， AST， SOD and GSH) and liver indexes (TG and TC). The mechanism of camel milk on liver protection was discussed based on metabonomics. Results: Camel milk significantly inhibited the levels of ALT and AST in serum and TG and TC in liver. Meanwhile， camel milk can increase the contents of SOD and GSH in serum by eliminating reactive oxygen free radicals. Through metabolome analysis， the differential metabolites in ET， NC groups and ET， ET+CM groups were mainly related to lipid metabolism， organic acid metabolism and organic oxygen compounds； 28 metabolites with significant differences were screened and identified in NC， ET and ET+CM groups. Alcohol could reduce the contents of acetylcholine， glycine， linoleic acid and phosphatidylcholine in liver； however， camel milk alleviated the above metabolites. KEGG enrichment analysis of different metabolites showed that they were involved in choline metabolism， glycerol phospholipid metabolism and ABC transporter. Conclusion: Camel milk could alleviate the disorder of lipid metabolism and increase antioxidant capacity induced by acute alcohol exposure， and effectively prevents alcoholic liver injury by regulating choline metabolism， glycerol phospholipid metabolism and ABC transporter in mice.