Suzuki et al. [39] found that AGEs accumulate in osteoblasts with age and induce apoptosis via ER stress by activating glucose-regulated protein, inositol-requiring protein-1α (IRE1α), C-Jun n-terminal kinase, etc. These findings have demonstrated that these pathways were associated with bone metabolism in T2DM, which can provide potential directions for the study of the molecular mechanism of T2DM complicated by osteoporosis. This evidence concerns the gene ERN1 and type 2 diabetes mellitus.