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Glucagon‐like peptide‐1 in type 2 diabetes: the β‐cell and beyond
Author(s) -
Nauck Michael A.
Publication year - 2008
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.1463-1326.2008.00919.x
Subject(s) - incretin , type 2 diabetes , medicine , disease , diabetes mellitus , glucagon like peptide 1 , cell , cell metabolism , weight loss , exenatide , intensive care medicine , bioinformatics , endocrinology , metabolism , obesity , biology , biochemistry
Many traditional treatments for type 2 diabetes fail to achieve and maintain effective glycaemic control, witnessed by a progressive decline in β‐cell functionality and a corresponding rise in blood glucose levels over time. The routine loss of 50% of β‐cell function at diagnosis lends new urgency that both diagnosis and treatment initiation take place as early as possible in the course of the disease, before β‐cell decline proceeds too far. This review describes the role of the β‐cell and glucagon‐like peptide‐1 (GLP‐1) in both normal metabolism and type 2 diabetes, highlights available and anticipated therapies and explores the prospect that certain incretin‐derived therapies, which seek to harness the therapeutic potential of native GLP‐1, may offer more than glycaemic control alone: they may also facilitate weight loss, improve the cardiovascular profile and, ideally, treat the β‐cell in such a way as to modify the natural history of the disease itself.