Diabetic osteoporosis (DOP) is a diabetic complication associated with a significant disability rate. Liraglutide, a glucagon-like peptide-1 receptoragonist, is a promising and innovative drug for type 2 diabetes mellitus (T2DM), with potential therapeuticimplications for bone disorders. Thisinvestigation examined the impact of liraglutide on osteoporosis in rats with T2DM and studied the influence of vitamin D receptor Bsm1polymorphism on liraglutide-induced outcomes. Thirty rats were divided into control, T2DM induced by a combination of a high-fat diet and25 mg/kg streptozotocin, and T2DM-liraglutide (T2DM treated with 0.4 mg/kg/day liraglutide) groups. After 8 weeks of liraglutide treatment,femurs and blood samples were obtained from all rats for subsequent investigations. Diabetes induced a remarkable rise in the serum levelsof receptor activator of nuclear factor kappa B ligand (RANKL) and C-telopeptide of type Icollagen (CTX-1) associated with a remarkabledecline in osteocalcin and osteoprotegerin (OPG). Impaired bone architecture was also demonstrated by light andscanning electronmicroscopic study. The immune expression of OPG was down-regulated, while RANKL was up-regulated. Interestingly, the administration ofliraglutide ameliorated the previous changes induced by diabetes mellitus. In conclusion,liraglutide can prevent DOP, mostly due toliraglutide’s ability to increase bone growth, while inhibiting bone resorption.