Background: Diabetes is a chronic metabolic disease characterized by hypergyclemia due to insulin deficiency (type 1 diabetes) or insulin insensitivity/resistance (type 2 diabetes). The significant metabolic changes that occur in diabetes also affect the skeleton and cause bone loss and/or altered bone matrix and strength, thereby increasing the risk of fracture. Hyperglycemia can alter cellular metabolic processes through the formation of advanced glycation end products (AGEs), which caused dysregulation of various cytokines as the underlying mechanism in the decrease of bone density. This study aimed to see the bone loss caused by hyperglycemia in rats, using cortical bone thickness as a parameter. Methods: This study was an analytical experimental study, which was conducted in a laboratory. The sample of this study was Wistar rat (Rattus norvegicus). Diabetes in the rats were induced using streptozotocin. The diabetic rats were then sacrificed 11 days later, and the left femur bone was obtanied. The bone was decalcified for 1 week, then prepared for histological slides. Cortical bone thickness was measured microscopically using Optilab Image Raster software at 10 different axis points, and then averaged. Results: The mean of cortical bone thickness were 32.43 Â± 2.65 Î¼m in the control (non diabetic) rats, and 26.64 Â± 2.89 Î¼m in streptozotocin-induced diabetic rats (p < 0.001). The diabetic rats had lower mean of cortical bone thickness than control by 5.79 Î¼m. Conclusion: Cortical bone thickness in the diabetic rats were lower by 18% compared to control 11 days after induction of streptozotocin.