Investigational agents that protect pancreatic islet β-cells from failure

Aston-Mourney, Kathryn, Proietto, Joseph and Andrikopoulos, Sofianos 2005, Investigational agents that protect pancreatic islet β-cells from failure, Expert opinion on investigational drugs, vol. 14, no. 10, pp. 1241-1250, doi: 10.1517/13543784.14.10.1241.

Attached Files
Name Description MIMEType Size Downloads

Title Investigational agents that protect pancreatic islet β-cells from failure
Author(s) Aston-Mourney, KathrynORCID iD for Aston-Mourney, Kathryn
Proietto, Joseph
Andrikopoulos, Sofianos
Journal name Expert opinion on investigational drugs
Volume number 14
Issue number 10
Start page 1241
End page 1250
Total pages 10
Publisher Informa Healthcare
Place of publication England, London
Publication date 2005-10
ISSN 1744-7658
Keyword(s) advanced glycation end-products
endoplasmic reticulum stress
islet dysfunction
oxidative stress
renin–angiotensin system
Summary Type 2 diabetes is associated with insulin resistance and reduced insulin secretion, which results in hyperglycaemia. This can then lead to diabetic complications such as retinopathy, neuropathy, nephropathy and cardiovascular disease. Although insulin resistance may be present earlier in the progression of the disease, it is now generally accepted that it is the deterioration in insulin-secretory function that leads to hyperglycaemia. This reduction in insulin secretion in Type 2 diabetes is due to both islet β-cell dysfunction and death. Therefore, interventions that maintain the normal function and protect the pancreatic islet β-cells from death are crucial in the treatment of Type 2 diabetes so that plasma glucose levels may be maintained within the normal range. Recently, a number of compounds have been shown to protect β-cells from failure. This review examines the evidence that the existing therapies for Type 2 diabetes that were developed to lower plasma glucose (metformin) or improve insulin sensitivity (thiazolidinediones) may also have islet-protective function. Newer emerging therapeutic agents that are designed to increase the levels of glucagon-like peptide-1 not only stimulate insulin secretion but also appear to increase islet β-cell mass. Evidence will also be presented that the future of drug therapy designed to prevent β-cell failure should target the formation of advanced glycation end products and alleviate oxidative and endoplasmic reticulum stress.
Language eng
DOI 10.1517/13543784.14.10.1241
Field of Research 119999 Medical and Health Sciences not elsewhere classified
Socio Economic Objective 970111 Expanding Knowledge in the Medical and Health Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
Copyright notice ©2005, Ashley Publications Ltd.
Persistent URL

Document type: Journal Article
Collections: Faculty of Health
School of Medicine
Connect to link resolver
Unless expressly stated otherwise, the copyright for items in DRO is owned by the author, with all rights reserved.

Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 5 times in TR Web of Science
Scopus Citation Count Cited 9 times in Scopus
Google Scholar Search Google Scholar
Access Statistics: 480 Abstract Views, 1 File Downloads  -  Detailed Statistics
Created: Thu, 30 Aug 2012, 09:32:59 EST

Every reasonable effort has been made to ensure that permission has been obtained for items included in DRO. If you believe that your rights have been infringed by this repository, please contact