Endocrine Abstracts

The incidence of diabetes, a disease characterized by high blood glucose levels, is increasing worldwide. Besides the well-known complications of diabetes including cardiovascular disease, retinopathy, nephropathy, and neuropathy, also bone fragility has recently been recognized as a complication of diabetes. In fact, type 1 diabetes is associated with a 6-fold increase in hip fractures with a marked loss of bone mineral density, while type 2 diabetes is associated with a 1.5-fold increase of hip fractures even in the presence of a higher bone mineral density. In both cases, diabetic bone disease is characterized by a low bone turnover and an increased incorporation of advanced glycation end-products into the collagenous matrix, rendering it stiff and inflexible. Moreover, bone vascularization is reduced in diabetic animals; in particular the number of pro-osteogenic H-type vessels is diminished. Experimental evidence shows that elevated ROS production, senescence, and suppressed Wnt signaling contribute to diabetic bone disease. Suppressed Wnt signaling also stimulates the differentiation of adipocytes in the bone marrow, which contribute to an inflammatory, pro-osteoclastogenic milieu. Finally, several miRNAs are differentially expressed any may contribute to diabetic bone disease.