Hyperlipidemia (HL) maintains a complex bidirectional relationship with the gut microbiota. The gut microbiota and its metabolic products deeply participate in the regulation of host lipid metabolism, making them a highly promising target for intervention in HL. This article systematically reviews the role of the gut microbiota in the pathogenesis and progression of HL, and compares the microbial composition, metabolic products, and their effects on lipid metabolism across animal models such as rats, mice, golden hamsters, and pigs. Research indicates that a high-fat diet generally leads to an increased ratio of Firmicutes to Bacteroidetes, reduced microbial diversity, decreased short-chain fatty acid production, imbalanced bile acid (BAs) metabolism, and elevated levels of trimethylamine N-oxide (TMAO) and lipopolysaccharides (LPS), thereby exacerbating dyslipidemia and inflammation through signaling pathways such as the farnesoid X receptor (FXR), Takeda G protein-coupled receptor 5 (TGR5), and lipoprotein lipase (LPL). Based on the integration of multi-omics approaches, this study provides a theoretical basis for the precise regulation of gut microbiota and the development of novel interventions, promoting translational research in the prevention and treatment of hyperlipidemia.