Journal
PHARMACOTHERAPY
Volume 26, Issue 3, Pages 360-374Publisher
WILEY
DOI: 10.1592/phco.26.3.360
Keywords
incretin mimetic; dipeptidyl peptidase-IV inhibitors; DPP-IV inhibitors; type 2 diabetes mellitus; glucose-dependent insulinotropic polypeptide; GIP; glucagon-like peptide-1; GLP-1; exenatide; AC2993; liraglutide; NN2211; vildagliptin; LAF237; sitagliptin; MK-0431
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The emergence of the glucoregulatory hormones glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide has expanded our understanding of glucose homeostasis. In particular, the glucoregulatory actions of the incretin hormone GLP-1 include enhancement of glucose-dependent insulin secretion, suppression of inappropriately elevated glucagon secretion, slowing of gastric emptying, and reduction of food intake. Two approaches have been developed to overcome rapid degradation of GLP-1. One is the use of agents that mimic the enhancement of glucose-dependent insulin secretion, and potentially other antihyperglycemic actions of incretins, and the other is the use of dipeptidyl peptidase-IV inhibitors, which reduce the inactivation of GLP-1, increasing the concentration of endogenous GLP-1. The development of incretin mimetics and dipeptidyl peptidase-IV inhibitors opens the door to a new generation of antihyperglycemic agents to treat several otherwise unaddressed pathophysiologic defects of type 2 diabetes mellitus. We review the physiology of glucose homeostasis, emphasizing the role of GLP-1, the pathophysiology of type 2 diabetes mellitus, the clinical shortcomings of current therapies, and the potential of new therapies-including the newly approved incretin mimetic exenatide-that elicit actions similar to those of GLP-1.
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