The mechanisms of insulin resistance can be proposed in three ways: (1) impairing osteoblast function via hyperglycemia-induced oxidative stress and AGE accumulation, reducing osteocalcin synthesis; (2) triggering compensatory osteoblast proliferation (elevating BALP) to counter increased apoptosis; and (3) suppressing osteoclast activity through adipokine dysregulation (e.g., elevated adiponectin), lowering β-CrossLaps. The gene discussed is BGLAP; the disease is Hyperglycemia.