Alcoholic liver disease (ALD) is a mounting public health problem with significant medical, economic and social burdens.  Tartary buckwheat (F. tataricum (L.) Gaertn, bitter buckwheat) is a kind of healthy and nutritious food, which has been  demonstrated to protect against ALD, but the underlying mechanism has not fully studied. Herein, we aimed to elucidate  the beneficial effects of Tartary buckwheat extract (mainly composed of polyphenols including rutin, quercetin, kaempferol  and kaempferol-3-O-rutinoside) in terms of lipid metabolism with the aid of lipidomic analysis. In our study, we employed  C57BL/6J mice and Lieber-DeCarli alcohol liquid diet to construct an ALD model and found that Tartary buckwheat extract  was able to prevent ALD-induced histopathological lesions, liver injury and abnormal plasma lipid levels. These beneficial  effects might be attributed to the regulation of energy metabolism-related genes (SIRT1, LKB1 and AMPK), lipid synthesisrelated genes (ACC, SREBP1c and HMGR) and lipid oxidation-related genes (PPARα, CPT1 and CPT2). In addition, lipidomic  profiling and KEGG pathway analysis showed that glycerophospholipid metabolism contributed the most to elucidating the  regulatory mechanism of Tartary buckwheat extract. In specific, chronic ethanol intake reduced the level of phosphatidyl  cholines (PC) and increased the level of phosphatidyl ethanolamines (PE) in the liver, resulting in a decrease in the PC/PE  ratio, which could be all significantly restored by Tartary buckwheat extract intervention, indicating that the Tartary  buckwheat extract might regulate PC/PE homeostasis to exert its lipid-lowering effect. Overall, we demonstrated that  Tartary buckwheat extract could prevent ALD by modulating hepatic glycerophospholipid metabolism, providing the  theoretical basis for its further exploitation as medical plant or nutritional food.