Understanding the pathophysiology of T2DM is important for understanding the targets and mechanisms of the different drugs and drug classes that are available to treat T2DM. As seen in Figure 3:[1]

• Sulfonylureas are used to increase the insulin response of the dysfunctional pancreatic β-cells;
• Incretin mimetics like glucagon-like peptide-1 receptor agonists (GLP-1 RAs) increase insulin secretion from the pancreas;
• Metformin addresses the hepatic glucose over-production defect and reduces the amount of gluconeogenesis that occurs.
• Thiazolidinediones (TZDs), also known as glitazones, have been used for decades to improve insulin resistance and increase insulin sensitivity at the level of the muscle;
• A relatively new class of medications, the sodium–glucose transporter-2 (SGLT-2) inhibitors decrease abnormal glucose resorption by the kidney.

Given this wide choice of therapies it is important that practitioners understand where the pathophysiologic defects of T2DM occur, because this will help to understand how and where the 11 classes of medications that are now available interact physiologically to treat this disease.
As an additional comment concerning the incretin effects, it is important to note that there are actually 3 classes of drugs that exert their effects on the gastrointestinal incretin hormones and stimulate a decrease in blood glucose levels: the GLP-1 RAs, the dipeptidyl peptidase-4 (DPP-4) inhibitors, and the amylin agonists; all these agents exert their effects on the incretin receptors in the gut. Kapustin J. J Nurse Pract. 2014; 00:00 – 00.