Irwin, Nigel, Green, BD, Gault, Victor, Harriot, P, O'Harte, Finbarr and Flatt, Peter (2006) Stable agonist of glucose-dependent insulinotropic polypeptide (GIP) restores pancreatic beta cell glucose responsiveness but not glucose intolerance in aging mice. EXPERIMENTAL GERONTOLOGY, 41 (2). pp. 151-156. [Journal article]
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Glucose tolerance progressively declines with age whilst the onset of type two diabetes increases dramatically. Glucose-dependent insulinotropic polypeptide (GIP) potentiates glucose-induced insulin secretion. The present study was designed to assess the insulinotropic effects of a potent long-acting GIP receptor agonist, N-AcGIP(LysPAL(37)), in aging mice. In older mice, body weights, basal plasma glucose and insulin concentrations were significantly higher than in young mice (P < 0.05 to P < 0.001). Intraperitoneal injection of glucose alone (18 mmol/kg body weight) revealed a significantly lower (P < 0.05) insulin response in older mice, which was accompanied by impaired glucose tolerance (P < 0.05). Normal glucose-mediated insulin secretion was restored in N-AcGIP(LysPAL37) treated older mice. However the glycaemic excursion remained significantly, impaired in older mice (P < 0.05), suggestive of impaired insulin action. Native GIP had a similar overall effect in younger and older mice. These data indicate that N-AcGIP(LysPAL(37)) is able to counter the age-related deterioration of pancreatic beta cell glucose sensitivity and insulin secretion. (c) 2005 Elsevier Inc. 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
|Deposited By:||Professor Peter Flatt|
|Deposited On:||18 Dec 2009 09:47|
|Last Modified:||19 Nov 2012 16:17|
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