Investigation of endothelial nitric oxide (NO) signalling in response to the incretin hormone glucose-dependent insulinotropic polypeptide (GIP)

Pj Savage,Ap Harvey,E Robinson,Dj Grieve

doi:10.1186/1753-6561-6-s4-o38

Pj Savage, Ap Harvey + Show 2 more

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https://doi.org/10.1186/1753-6561-6-s4-o38

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Journal: BMC Proceedings	Publication Date: Jul 1, 2012
Citations: 1	License type: CC BY 2.0

Affiliation: Queen's University Belfast

Abstract

The incretin hormone, GIP, is responsible for augmenting postprandial insulin release and regulation of β-cell mass. The advent of newly-developed GIP analogues, which have been demonstrated to restore glycaemic control in animal models of type 2 diabetes mellitus (T2DM), suggest that GIP-based therapies may now realise their long-held promise for the treatment of T2DM. Interestingly, we have recently shown that GIP may also exert vasodilatory actions which appear to be mediated via endothelium-dependent NO production. This may be particularly relevant to T2DM as over 60 % of associated mortality is attributable to cardiovascular disease related to dysregulation of endothelial NO homeostasis. An improved understanding of the mechanisms underlying GIP's recently-described vascular actions is clearly important. The aim of this study was therefore to dissect the precise mechanisms involved in GIP-mediated endothelial NO signalling.

Highlights

The incretin hormone, glucose-dependent insulinotropic polypeptide (GIP), is responsible for augmenting postprandial insulin release and regulation of b-cell mass
We have recently shown that GIP may exert vasodilatory actions which appear to be mediated via endothelium-dependent nitric oxide (NO) production
This may be relevant to type 2 diabetes mellitus (T2DM) as over 60 % of associated mortality is attributable to cardiovascular disease related to dysregulation of endothelial NO homeostasis

Summary

Introduction

The incretin hormone, GIP, is responsible for augmenting postprandial insulin release and regulation of b-cell mass. We have recently shown that GIP may exert vasodilatory actions which appear to be mediated via endothelium-dependent NO production. This may be relevant to T2DM as over 60 % of associated mortality is attributable to cardiovascular disease related to dysregulation of endothelial NO homeostasis. An improved understanding of the mechanisms underlying GIP’s recently-described vascular actions is clearly important. The aim of this study was to dissect the precise mechanisms involved in GIP-mediated endothelial NO signalling

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Conclusion