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<b>Introduction: </b>This study employed combined transcriptomics and metabolomics analyses as well as experimental verification methods to comprehensively elucidate the molecular mechanism of ginsenoside Rb1 in preventing and treating dyslipidemia.<b>Methods: </b>First, we established a rat model of hyperlipidemia using male SPF-grade SD rats and performed a comprehensive analysis using metabolomics and transcriptomics. Based on the rats in the control group, the two experimental groups were fed a high-fat diet, and the Rb1 group was administered ginsenoside Rb1 intragastrically. Experimental methods such as lipid assay, hematoxylin-eosin (HE) staining and oil red O staining, ELISA, qRT-PCR, and Western blotting were used to verify the identified target genes by combined analysis of transcriptomics and metabolomics.<b>Results: </b>Metabolomics analysis revealed that 14 different metabolites were altered after administration of Rb1. These metabolites were associated with various metabolic pathways, such as glycosylphosphatidylinositol (GPI) anchor biosynthesis and sphingolipids, arachidonic acid,α-linolenic acid, etc. By integrating the transcriptomics and metabolomics data, we identified 55 genes, including glucose kinase (GCK) and phosphoglycerate mutase 1 (PGAM1), which are involved in metabolic pathways related to glycolysis, regulation of glycolytic processes, and carbohydrate phosphorylation. The results of this study indicate that compared to the model group, the content of regulatory enzymes and main products (mainly GCK) of the glycolytic pathway significantly decreased after administration of Rb1, and the key enzyme ACC for fatty acid synthesis also significantly decreased.<b>Conclusion: </b>This suggests that Rb1 may affect fatty acid synthesis through the glycolytic pathway, thereby influencing dyslipidemia.