Incretin plays an import role in postprandial insulin secretion. Glucagon-like peptide-1 (GLP-1) and gastric inhibitory polypeptide have well been known to have properties of incretin effect. Patients with type 2 diabetes are noted to be with lost or severely impaired incretin effect. Therefore, the patients also have decresed post-prandial insulin secretion. The major cause of impaired incretin effect in patients with type 2 diabetes is decrease in GLP-1 secretion. GLP-1 also has some effects on promotion of β cell growth and differentiation, decreasing β cell apoptosis, and glucagon suppression effect. In addition, some beneficial extrapancreatic effects, such as decreasing food intake by acting on central nervous system and direct action on cardiovascular system are also noted. Due to its glucose-dependent insulin secretion effect, the risk of hypoglycemia is low. The incretins are rapidly inactivated by dipeptidyl peptidase IV (DPP VI). Recently, two different approaches are developed to retard DPP VI action. One is to use GLP-1 receptor agonists that are resistant to degradation by DPP VI. These GLP-1 mimetics include exenatide and liraglutide. Another approach is to inhibit the activity of DPP VI so that half-life of endogenously released GLP-1 can be prolonged. These DPP VI inhibitors include sitagliptin and vildagliptin. The beneficial effects of these preparations on clinical parameters in patients with type 2 diabetes mellitus have recently been reported in some evidence-based studies.
|Number of pages||6|
|Journal||Journal of Internal Medicine of Taiwan|
|Publication status||Published - 2007 Aug 1|
All Science Journal Classification (ASJC) codes
- Internal Medicine