Diabetes Metab J.  2016 Apr;40(2):99-114. 10.4093/dmj.2016.40.2.99.

An Update on the Effect of Incretin-Based Therapies on β-Cell Function and Mass

Affiliations
  • 1Department of Endocrinology and Metabolism, Kyung Hee University School of Medicine, Seoul, Korea.
  • 2Department of Diabetes and Endocrinology, DHU FIRE, Lariboisière Hospital, University Paris-Diderot Paris-7, Paris, France. jean-francois.gautier@lrb.aphp.fr
  • 3Clinical Investigation Center, INSERM-CIC9504, Saint-Louis University Hospital, University Paris-Diderot Paris-7, Paris, France.
  • 4INSERM UMRS 1138, Cordeliers Research Center, University Pierre et Marie Curie Paris-6, Paris, France.

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.

Keyword

Diabetes mellitus; Dipeptidyl peptidase-4 inhibitor; Glucagon-like peptide-1 receptor agonist; Incretins; Insulin-secreting

MeSH Terms

Animals
Blood Glucose
Diabetes Mellitus
Diabetes Mellitus, Type 2
Humans
Hypoglycemic Agents
Incretins
Insulin Resistance
Korea
Treatment Outcome
Blood Glucose
Hypoglycemic Agents
Incretins

Figure

  • Fig. 1 β-Cell function and mass changes over the time course of type 2 diabetes mellitus and proposed mechanisms. ER, endoplasmic reticulum. Figure extracted from: Chon S, Riveline JP, Blondeau B, Gautier JF. Incretin-based therapy and pancreatic beta cells. Diabetes Metab 2014;40:411-22 [4]. Copyright ©2014. With permission of Elsevier Masson SAS.

  • Fig. 2 Effect of incretins and incretin based therapy on pancreatic β-cell in animal models. GIP, gastric inhibitory polypeptide; GLP-1, glucagon-like peptide-1; ER, endoplasmic reticulum. Figure extracted from: Chon S, Riveline JP, Blondeau B, Gautier JF. Incretin-based therapy and pancreatic beta cells. Diabetes Metab 2014;40:411-22 [4]. Copyright ©2014. With permission of Elsevier Masson SAS.


Cited by  2 articles

Assessment of Insulin Secretion and Insulin Resistance in Human
So Young Park, Jean-François Gautier, Suk Chon
Diabetes Metab J. 2021;45(5):641-654.    doi: 10.4093/dmj.2021.0220.

Incretin and Pancreatic β-Cell Function in Patients with Type 2 Diabetes
Chang Ho Ahn, Tae Jung Oh, Se Hee Min, Young Min Cho
Endocrinol Metab. 2023;38(1):1-9.    doi: 10.3803/EnM.2023.103.


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