Background: Nonalcoholic fatty liver disease (NAFLD) is a widespread health issue and regarded as the most prevalent condition affecting the liver worldwide. Liraglutide, a glucagon-like peptide-1 receptor agonist, is a promising and innovative drug. Our study aimed to investigate the protective role of liraglutide in experimentally induced NAFLD in the rat model. Methods: Forty healthy adult male albino rats were used, they were assigned to 3 main groups: Group I (Control group) which was subdivided into two equal subgroups, Group II (High-fat diet group) which rats were given a fatty diet for 12 weeks and Group III (High-fat diet +liraglutide group) in which rats were fed with high fatty diet in the same way as group II in concomitant with liraglutide that was injected subcutaneously daily (0.2 mg/kg) for 12 weeks. Blood samples and liver tissues were collected and assayed for biochemical, histological, and immunohistochemical studies. Results: The high-fat diet group exhibited a significant increase in body mass index, abdominal circumference, serum ALT, AST, and serum lipid profile levels. Additionally, hepatic destructive changes were observed such as hepatocellular vacuolation, apoptosis, and congested blood vessels, along with a significant increase in the area percentage of collagen fibers, caspase 3 immunoreactions, and the number of GFAP immunoreactivity of hepatic stellate cells. These distortions were confirmed by ultrastructural assessment. In contrast, the high-fat diet +liraglutide group exhibited normal BMI, AC, ALT, AST, and lipid profiles with preservation of the liver histoarchitecture. Conclusion: NAFLD significantly affects hepatic cytoarchitecture and biochemical parameters, leading to apoptosis and fibrosis. Liraglutide administration with a high-fat diet can protect the liver from these changes.