McIntosh Christopher H S, Demuth Hans-Ulrich, Pospisilik J Andrew, Pederson Raymond
Department of Physiology, Faculty of Medicine, University of British Columbia, 2146 Health Sciences Mall, Vancouver, British Columbia, Canada V6T 1Z3.
Regul Pept. 2005 Jun 15;128(2):159-65. doi: 10.1016/j.regpep.2004.06.001.
A number of new approaches to diabetes therapy are currently undergoing clinical trials, including those involving stimulation of the pancreatic beta-cell with the gut-derived insulinotropic hormones (incretins), GIP and GLP-1. The current review focuses on an approach based on the inhibition of dipeptidyl peptidase IV (DP IV), the major enzyme responsible for degrading the incretins in vivo. The rationale for this approach was that blockade of incretin degradation would increase their physiological actions, including the stimulation of insulin secretion and inhibition of gastric emptying. It is now clear that both GIP and GLP-1 also have powerful effects on beta-cell differentation, mitogenesis and survival. By potentiating these pleiotropic actions of the incretins, DP IV inhibition can therefore preserve beta-cell mass and improve secretory function in diabetics.
目前，多种新型糖尿病治疗方法正在进行临床试验，其中包括使用肠道源性促胰岛素激素（肠促胰岛素）GIP和GLP - 1刺激胰腺β细胞的方法。本综述重点关注基于抑制二肽基肽酶IV（DP IV）的一种方法，DP IV是体内负责降解肠促胰岛素的主要酶。这种方法的理论依据是，阻断肠促胰岛素的降解会增强其生理作用，包括刺激胰岛素分泌和抑制胃排空。现在已经明确，GIP和GLP - 1对β细胞分化、有丝分裂和存活也具有强大作用。因此，通过增强肠促胰岛素的这些多效性作用，抑制DP IV可以保留糖尿病患者的β细胞数量并改善分泌功能。
