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Increased circulating sclerostin and accumulation of advanced glycation end‐products (AGEs) are two potential mechanisms underlying low bone turnover and increased fracture risk in type 2 diabetes (T2D). Whether the expression of the sclerostin‐encoding SOST gene is altered in T2D, and whether it is associated with AGEs accumulation or regulation of other bone formation‐related genes is unknown. We hypothesized that AGEs accumulate and SOST gene expression is upregulated in bones from subjects with T2D, leading to downregulation of bone forming genes (RUNX2 and osteocalcin) and impaired bone microarchitecture and strength. We obtained bone tissue from femoral heads of 19 T2D postmenopausal women (mean glycated hemoglobin [HbA1c] 6.5%) and 73 age‐ and BMI‐comparable nondiabetic women undergoing hip replacement surgery. Despite similar bone mineral density (BMD …