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Therapeutic potential for GIP receptor agonists and antagonists

Irwin, Nigel and Flatt, Peter (2009) Therapeutic potential for GIP receptor agonists and antagonists. BEST PRACTICE AND RESEARCH CLINICAL ENDOCRINOLOGY AND METABOLISM, 23 (4). pp. 499-512. [Journal article]

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DOI: 10.1016/j.beem.2009.03.001


Glucose-dependent insulinotropic polypeptide (GIP or gastric inhibitory polypeptide) is a 42-amino-acid hormone, secreted from the enteroendocrine K cells, which has insulin-releasing and extrapancreatic glucoregulatory actions. However, the unfavourable pharmacokinetic profile and the weak biological effects of native GIP limit its effectiveness for the treatment of type 2 diabetes. To overcome this, longer-acting GIP agonists exhibiting enzymatic stability and enhanced bioactivity have been generated and successfully tested in animal models of diabetes. Thus,GIP receptor agonists offer one of the newest classes of potential antidiabetic drug. GIP is also known to play a role in lipid metabolism and fat deposition. Accordingly, both genetic and chemical ablation of GIP signalling in mice with obesity-diabetes can protect against, or even reverse many of the obesity-associated metabolic disturbances. Strong parallels exist with the beneficial metabolic effects of Roux-en-Y gastric bypass in obese, insulin-resistant humans that surgically ablates GIP-secreting K cells. The purpose of this article is to highlight the therapeutic potential of GIP-based therapeutics in the treatment of type 2 diabetes and obesity. (C) 2009 Elsevier Ltd. All rights reserved.

Item Type:Journal article
Faculties and Schools:Faculty of Life and Health Sciences > School of Biomedical Sciences
Faculty of Life and Health Sciences > School of Pharmacy and Pharmaceutical Science
Faculty of Life and Health Sciences
Research Institutes and Groups:Biomedical Sciences Research Institute
Biomedical Sciences Research Institute > Diabetes
ID Code:2884
Deposited By: Professor Peter Flatt
Deposited On:17 Dec 2009 09:28
Last Modified:19 Nov 2012 15:50

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