Therefore, using a non-insulin-dependent streptozotocin (STZ) DM animal model that develops insensate neuropathy, the purpose of this investigation was to examine in parallel the development of DSPN and DM-associated changes in cardiac structure and function, as well as potential mechanisms, such as autonomic dysfunction, evaluated by changes in urinary and myocardial NE content and myocardial neuronal markers. The gene discussed is INS; the disease is neuropathy.