Topic overview

Start with the big picture

Type 1 diabetes mellitus results from autoimmune β-cell destruction and absolute insulin deficiency, making exogenous insulin the effective therapeutic target. Type 2 diabetes involves insulin resistance and β-cell dysfunction, with contributing defects in tissues such as skeletal muscle, liver, adipose tissue, pancreas, gut, kidney, and brain. These defects can impair glucose uptake, increase hepatic glucose output, alter insulin or glucagon secretion, and affect glucose absorption and reabsorption. The lesson links these mechanisms to drug targets, including metformin, TZDs, incretin-based therapies, SGLT-2 inhibitors, and agents that slow gastric emptying or carbohydrate absorption. Understanding the organ-specific connections helps explain why type 2 diabetes therapy addresses multiple pathways rather than a single defect.