The incretin hormones glucagon‐like‐peptide‐1 (GLP‐1) and glucose‐dependent insulinotropic polypeptide (GIP) are released from the intestine following oral ingestion of nutrients. Incretins promote insulin secretion, while GLP‐1 also inhibits glucagon release and gastric emptying, minimizing postprandial glucose excursions. The incretins share similar effects on the pancreatic β cell; however, there are a number of differences in extrapancreatic actions. Type 2 diabetes (T2DM) is associated with abnormal incretin physiology, and although treatment with GIP is ineffective, GLP‐1 effects are preserved. The current incretin‐based approaches to T2DM include the GLP‐1 agonists that are resistant to the serine protease dipeptidylpeptidase‐4 (DPP4), which normally rapidly degrades the incretins, and DPP4 inhibitors (DPP4i). Incretin‐based treatments have provoked much interest due to use‐associated weight loss (GLP‐1 agonists), minimal hypoglycemia, and potential for positive effects on pancreatic β cell biology and the cardiovascular system. However, the long‐term safety of these agents has yet to be established. This review outlines the current understanding of incretin biology, available data pertaining to incretin‐based treatment in T2DM, and differences between GLP‐1 and DPP4i therapy.