Open AccessDPP‐4 inhibition and islet function
Author(s) -
Ahrén Bo
Publication year - 2012
Publication title -
journal of diabetes investigation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.089
H-Index - 50
eISSN - 2040-1124
pISSN - 2040-1116
DOI - 10.1111/j.2040-1124.2011.00184.x
Subject(s) - medicine , incretin , islet , type 2 diabetes , hypoglycemia , diabetes mellitus , endocrinology , glucagon like peptide 1 , dipeptidyl peptidase 4 , dipeptidyl peptidase , glucagon , secretion , stimulation , insulin , biochemistry , biology , enzyme
During recent years, dipeptidyl peptidase‐4 (DPP‐4) inhibition has been included in the clinical management of type 2 diabetes, both as monotherapy and as add‐on to several other therapies. DPP‐4 inhibition prevents the inactivation of the incretin hormones, glucose‐dependent insulinotropic polypeptide (GIP) and glucagon‐like peptide‐1 (GLP‐1). This results in stimulation of insulin secretion and inhibition of glucagon secretion, and there is also a potential β‐cell preservation effect, as judged from rodent studies; that is, it might target the key islet dysfunction in the disease. In type 2 diabetes. This reduces 24‐h glucose levels and reduces HbA 1c by ≈ 0.8–1.1% from baseline levels of 7.7–8.5%. DPP‐4 inhibition is safe, with a very low risk for adverse events including hypoglycemia, and it prevents weight gain. The present review summarizes the studies on the influence of DPP‐4 inhibition on islet function. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2011.00184.x, 2012)