Studies have indicated that sarcopenia and a decrease in BMD in T2DM patients may share pathological mechanisms such as insulin resistance, chronic inflammation, and oxidative stress: insulin resistance inhibits muscle protein synthesis and interferes with the function of osteoblasts; hyperglycemia induces the accumulation of advanced glycation end products (AGEs), which damages the microstructures of muscle and bone; persistent low-grade inflammation [such as an increase in interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α)] accelerates muscle breakdown and bone resorption (4, 5). This evidence concerns the gene IL6 and Insulin resistance.