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The effects of glucagon‐like peptide‐1 on the beta cell
Author(s) -
Vilsbøll T.
Publication year - 2009
Publication title -
diabetes, obesity and metabolism
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.445
H-Index - 128
eISSN - 1463-1326
pISSN - 1462-8902
DOI - 10.1111/j.1463-1326.2009.01073.x
Subject(s) - beta (programming language) , beta cell , glucagon , peptide , chemistry , medicine , microbiology and biotechnology , endocrinology , biology , biochemistry , computer science , insulin , hormone , islet , programming language
Type 2 diabetes is a progressive disease characterized by insulin resistance and impaired beta‐cell function. Treatments that prevent further beta‐cell decline are therefore essential for the management of type 2 diabetes. Glucagon‐like peptide‐1 (GLP‐1) is an incretin hormone that is known to stimulate glucose‐dependent insulin secretion. Furthermore, GLP‐1 appears to have multiple positive effects on beta cells. However, GLP‐1 is rapidly degraded by dipeptidyl peptidase‐4 (DPP‐4), which limits the clinical relevance of GLP‐1 for the treatment of type 2 diabetes. Two main classes of GLP‐1‐based therapies have now been developed: DPP‐4 inhibitors and GLP‐1 receptor agonists. Liraglutide and exenatide are examples of GLP‐1 receptor agonists that have been developed to mimic the insulinotropic characteristics of endogenous GLP‐1. Both have demonstrated improved beta‐cell function in patients with type 2 diabetes, as assessed by homoeostasis model assessment‐B analysis and proinsulin : insulin ratio. Additionally, liraglutide and exenatide are able to enhance first‐ and second‐phase insulin secretion and are able to restore beta‐cell sensitivity to glucose. Preclinical studies have shown that both liraglutide and exenatide treatment can increase beta‐cell mass, stimulate beta‐cell proliferation, increase beta‐cell neogenesis and inhibit beta‐cell apoptosis. Clinical studies are needed to confirm these findings in humans. Replication of these data in humans could have important clinical implications for the treatment of type 2 diabetes.