This increased fracture risk in individuals with type 2 diabetes is primarily due to abnormal bone remodeling, characterized by elevated blood glucose levels, accumulation of advanced glycation end-products (AGEs), defects in terminal product processing, altered insulin levels or function, reduced insulin-like growth factor 1 (IGF-1) levels, oxidative stress, and increased proinflammatory cytokines. This evidence concerns the gene INS and type 2 diabetes mellitus.