Peripheral and Central GLP-1 Receptor Populations Mediate the Anorectic Effects of Peripherally Administered GLP-1 Receptor Agonists, Liraglutide and Exendin-4 (original) (raw)

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1Department of Psychology, School of Arts and Sciences (S.E.K., S.M.F., H.J.G.) and Department of Psychiatry, University of Pennsylvania, Philadelphia, Pennsylvania 19104;

*Address all correspondence and requests for reprints to: Scott E. Kanoski, Department of Psychology, University of Pennsylvania, Solomon Laboratories, 3720 Walnut Street, Philadelphia, Pennsylvania 19104.

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1Department of Psychology, School of Arts and Sciences (S.E.K., S.M.F., H.J.G.) and Department of Psychiatry, University of Pennsylvania, Philadelphia, Pennsylvania 19104;

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3Physiology and Behavior Group (M.A.), Institute of Animal Sciences, ETH Zurich, 8603 Schwerzenbach, Switzerland

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1Department of Psychology, School of Arts and Sciences (S.E.K., S.M.F., H.J.G.) and Department of Psychiatry, University of Pennsylvania, Philadelphia, Pennsylvania 19104;

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2School of Medicine (M.R.H.), University of Pennsylvania, Philadelphia, Pennsylvania 19104;

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Received:

15 February 2011

Published:

01 August 2011

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Scott E. Kanoski, Samantha M. Fortin, Myrtha Arnold, Harvey J. Grill, Matthew R. Hayes, Peripheral and Central GLP-1 Receptor Populations Mediate the Anorectic Effects of Peripherally Administered GLP-1 Receptor Agonists, Liraglutide and Exendin-4, Endocrinology, Volume 152, Issue 8, 1 August 2011, Pages 3103–3112, https://doi.org/10.1210/en.2011-0174
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The long-acting glucagon-like peptide-1 receptor (GLP-1R) agonists, exendin-4 and liraglutide, suppress food intake and body weight. The mediating site(s) of action for the anorectic effects produced by peripheral administration of these GLP-1R agonists are not known. Experiments addressed whether food intake suppression after ip delivery of exendin-4 and liraglutide is mediated exclusively by peripheral GLP-1R or also involves direct central nervous system (CNS) GLP-1R activation. Results showed that CNS delivery [third intracerebroventricular (3rd ICV)] of the GLP-1R antagonist exendin-(9–39) (100 μg), attenuated the intake suppression by ip liraglutide (10 μg) and exendin-4 (3 μg), particularly at 6 h and 24 h. Control experiments show that these findings appear to be based neither on the GLP-1R antagonist acting as a nonspecific competing orexigenic signal nor on blockade of peripheral GLP-1R via efflux of exendin-(9–39) to the periphery. To assess the contribution of GLP-1R expressed on subdiaphragmatic vagal afferents to the anorectic effects of liraglutide and exendin-4, food intake was compared in rats with complete subdiaphragmatic vagal deafferentation and surgical controls after ip delivery of the agonists. Both liraglutide and exendin-4 suppressed food intake at 3 h, 6 h, and 24 h for controls; for subdiaphragmatic vagal deafferentation rats higher doses of the GLP-1R agonists were needed for significant food intake suppression, which was observed at 6 h and 24 h after liraglutide and at 24 h after exendin-4. Conclusion: Food intake suppression after peripheral administration of exendin-4 and liraglutide is mediated by activation of GLP-1R expressed on vagal afferents as well as direct CNS GLP-1R activation.

Copyright © 2011 by The Endocrine Society

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