Diabetes mellitus type I and type II are associated with an increased prevalence of fractures. While in type I diabetes (T1D) bone mass is severely reduced, type II diabetes (T2D) is characterized by a high bone mineral density. However, decreased bone quality properties have been identified in T2D, which may decrease bone strength in T2D. Diabetes commonly leads to suppressed osteoblast function. As the Wnt signaling pathway is one of the key regulators of osteoblast function, several studies have investigated the regulation of Wnt signaling in bone in diabetes. The expression of several Wnt ligands, including Wnt1, Wnt5a, Wnt10b are decreased in bone tissue of diabetic animals. At the same time, the skeletal expression of sclerostin and Dickkopf-1 (Dkk1) are highly increased. Blocking sclerostin has been shown to be efficacious in reversing diabetes-induced bone loss in rat and mouse models. Thus, the Wnt pathway appears to be an ideal target to improve bone mass in diabetic bone disease, however, must be further validated in humans.