Premium
The pleiotropic cardiovascular effects of dipeptidyl peptidase‐4 inhibitors
Author(s) -
Avogaro Angelo,
Fadini Gian Paolo
Publication year - 2018
Publication title -
british journal of clinical pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.216
H-Index - 146
eISSN - 1365-2125
pISSN - 0306-5251
DOI - 10.1111/bcp.13611
Subject(s) - incretin , dipeptidyl peptidase , dipeptidyl peptidase 4 , endocrinology , medicine , glucose homeostasis , liraglutide , diabetes mellitus , hormone , type 2 diabetes , neprilysin , glucagon like peptide 1 , exenatide , insulin , homeostasis , chemistry , insulin resistance , biochemistry , enzyme
Patients with Type 2 diabetes have an excess risk for cardiovascular disease. One of the several approaches, included in the guidelines for the management of Type 2 diabetes, is based on dipeptidyl peptidase 4 (DPP‐4; also termed CD26) inhibitors, also called gliptins. Gliptins inhibit the degradation of glucagon‐like peptide‐1 (GLP‐1): this effect is associated with increased circulating insulin‐to‐glucagon ratio, and a consequent reduction of HbA1c. In addition to incretin hormones, there are several proteins that may be affected by DPP‐4 and its inhibition: among these some are relevant for the cardiovascular system homeostasis such as SDF‐1α and its receptor CXCR4, brain natriuretic peptides, neuropeptide Y and peptide YY. In this review, we will discuss the pathophysiological relevance of gliptin pleiotropism and its translational potential.