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Background: Atherosclerosis (AS) is a chronic progressive disease caused by lipometabolic disorder. However, the pathological characteristics and mechanism of AS have not been fully clarified. Through high-fat and high-cholesterol diet induction, Tibetan minipigs can be used as the AS model animals, as they have a very similar AS pathogenesis to humans. Methods: In this study, we built an AS model of Tibetan minipigs and identified the differential abundance metabolites in the development of AS based on untargeted metabolomics. Results: We found that sphingolipid metabolism and glucose oxidation were obviously higher in the AS group and phenylalanine metabolism was reduced in the AS group. Moreover, in the development of AS, gluconolactone was enriched in the late stage of AS whereas biopterin was enriched in the early stage of AS. Conclusions: Our research provides novel clues to investigate the metabolic mechanism of AS from the perspective of metabolomics.