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This Article Full Text Full Text (PDF) All Versions of this Article: 293/3/E697    most recent 00219.2007v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in Web of Science Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Web of Science (5) Citing Articles via Google Scholar Google Scholar Articles by Gauna, C. Articles by van der Lely, A. J. Search for Related Content PubMed PubMed Citation Articles by Gauna, C. Articles by van der Lely, A. J.

Unacylated ghrelin acts as a potent insulin secretagogue in glucose-stimulated conditions

¹Division of Endocrinology, Department of Internal Medicine, Erasmus Medical Centre, Rotterdam, The Netherlands; ²Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Turin, Turin, Italy; ³Postgraduate School of Molecular Medicine, Rotterdam, The Netherlands

Submitted 9 April 2007 ; accepted in final form 18 June 2007

Acylated and unacylated ghrelin (AG and UAG) are gut hormones that exert pleiotropic actions, including regulation of insulin secretion and glucose metabolism. In this study, we investigated whether AG and UAG differentially regulate portal and systemic insulin levels after a glucose load. We studied the effects of the administration of AG (30 nmol/kg), UAG (3 and 30 nmol/kg), the ghrelin receptor antagonist [D-Lys³]GHRP-6 (1 µmol/kg), or various combinations of these compounds on portal and systemic levels of glucose and insulin after an intravenous glucose tolerance test (IVGTT, D-glucose 1 g/kg) in anesthetized fasted Wistar rats. UAG administration potently and dose-dependently enhanced the rise of insulin concentration induced by IVGTT in the portal and, to a lesser extent, the systemic circulation. This UAG-induced effect was completely blocked by the coadministration of exogenous AG at equimolar concentrations. Similarly to UAG, [D-Lys³]GHRP-6, alone or in combination with AG and UAG, strongly enhanced the portal insulin response to IVGTT, whereas exogenous AG alone did not exert any further effect. Our data demonstrate that, in glucose-stimulated conditions, exogenous UAG acts as a potent insulin secretagogue, whereas endogenous AG exerts a maximal tonic inhibition on glucose-induced insulin release.

acylated ghrelin; insulin secretion; portal vein; rat

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