Glucagon-like peptide-1 (GLP-1) is a 30-amino acid peptide hormone primarily expressed in the intestine and hypothalamus. Recent studies have highlighted its role in lipid metabolism, including inhibiting fat synthesis, promoting fat differentiation, enhancing cholesterol metabolism, and promoting adipose browning. GLP-1 plays a crucial role in metabolic diseases such as obesity, nonalcoholic fatty liver disease (NAFLD), and atherosclerosis. This article reviews the recent research progress on GLP-1's effects on lipid metabolism. GLP-1 increases ABCA1 mRNA and apo AI, mediating intracellular cholesterol efflux. It induces FNDC5 expression in β-cells via CREB, promoting WAT to BAT conversion. GLP-1 oxidizes fatty acids and reduces their influx into hepatocytes, inhibiting NAFLD. GLP-1R/GIPR dual agonists improve lipid metabolism more effectively than GLP-1RAs. GLP-1 modulates lipid metabolism in the liver by reducing fat synthesis, lipolysis, and cholesterol metabolism. It increases ABCA1 and ABCG1 expression, promoting cholesterol efflux. GLP-1 also modulates fat synthesis and differentiation, and promotes fat browning through FNDC5 induction. In clinical applications, GLP-1 and GLP-1RAs have shown potential in treating obesity, NAFLD, and atherosclerosis. GLP-/GIP dual agonists, which activate both GLP-1 and GIP receptors, have demonstrated significant lipid-regulating effects and weight loss potential. Overall, GLP-1 and its analogs offer promising therapeutic targets for metabolic disorders, with dual agonists showing greater potential in improving lipid metabolism.Glucagon-like peptide-1 (GLP-1) is a 30-amino acid peptide hormone primarily expressed in the intestine and hypothalamus. Recent studies have highlighted its role in lipid metabolism, including inhibiting fat synthesis, promoting fat differentiation, enhancing cholesterol metabolism, and promoting adipose browning. GLP-1 plays a crucial role in metabolic diseases such as obesity, nonalcoholic fatty liver disease (NAFLD), and atherosclerosis. This article reviews the recent research progress on GLP-1's effects on lipid metabolism. GLP-1 increases ABCA1 mRNA and apo AI, mediating intracellular cholesterol efflux. It induces FNDC5 expression in β-cells via CREB, promoting WAT to BAT conversion. GLP-1 oxidizes fatty acids and reduces their influx into hepatocytes, inhibiting NAFLD. GLP-1R/GIPR dual agonists improve lipid metabolism more effectively than GLP-1RAs. GLP-1 modulates lipid metabolism in the liver by reducing fat synthesis, lipolysis, and cholesterol metabolism. It increases ABCA1 and ABCG1 expression, promoting cholesterol efflux. GLP-1 also modulates fat synthesis and differentiation, and promotes fat browning through FNDC5 induction. In clinical applications, GLP-1 and GLP-1RAs have shown potential in treating obesity, NAFLD, and atherosclerosis. GLP-/GIP dual agonists, which activate both GLP-1 and GIP receptors, have demonstrated significant lipid-regulating effects and weight loss potential. Overall, GLP-1 and its analogs offer promising therapeutic targets for metabolic disorders, with dual agonists showing greater potential in improving lipid metabolism.