An Update on the Effect of Incretin-Based Therapies on β-Cell Function and Mass.
- Author:
Suk CHON
1
;
Jean François GAUTIER
Author Information
- Publication Type:Review
- Keywords: Diabetes mellitus; Dipeptidyl peptidase-4 inhibitor; Glucagon-like peptide-1 receptor agonist; Incretins; Insulin-secreting
- MeSH: Animals; Blood Glucose; Diabetes Mellitus; Diabetes Mellitus, Type 2; Humans; Hypoglycemic Agents; Incretins; Insulin Resistance; Korea; Treatment Outcome
- From:Diabetes & Metabolism Journal 2016;40(2):99-114
- CountryRepublic of Korea
- Language:English
- Abstract: Type 2 diabetes mellitus (T2DM) is a multifactorial disease with a complex and progressive pathogenesis. The two primary mechanisms of T2DM pathogenesis are pancreatic β-cell dysfunction and insulin resistance. Pancreatic β-cell dysfunction is recognized to be a prerequisite for the development of T2DM. Therapeutic modalities that improve β-cell function are considered critical to T2DM management; however, blood glucose control remains a challenge for many patients due to suboptimal treatment efficacy and the progressive nature of T2DM. Incretin-based therapies are now the most frequently prescribed antidiabetic drugs in Korea. Incretin-based therapies are a favorable class of drugs due to their ability to reduce blood glucose by targeting the incretin hormone system and, most notably, their potential to improve pancreatic β-cell function. This review outlines the current understanding of the incretin hormone system in T2DM and summarizes recent updates on the effect of incretin-based therapies on β-cell function and β-cell mass in animals and humans.
