A fragility fracture is a serious complication in patients with diabetes mellitus as a result of hyperglycaemia, insulin resistance and the production of AGEs (advanced glycation end-products). In their paper published in the Biochemical Journal, Bartolomé et al. identified a role for autophagy in the differentiation, function and survival of osteoblastic cells in a high-glucose environment, and they also demonstrated that osteoblastic cell survival was limited by chemical and genetic inhibition of autophagy. These novel findings show the possibility of investigating a therapeutic strategy of maintaining autophagy in osteoblasts to lead to the prevention of diabetes-related osteopaenia. Autophagy is one of the common functions for maintaining cellular health, and the regulation of autophagy that is perturbed by diabetes mellitus may induce improvement of cellular functions not only for diabetes-related osteopaenia, but also for other systemic complications. However, systemic activation of autophagy may not always induce beneficial effects for non-targeted healthy cells, and autophagy should be controlled at a proper level at each disease stage in each target organ.