Central & peripheral glucagon-like peptide-1 receptor signaling differentially regulate addictive behaviors

2016 ◽  
Vol 161 ◽  
pp. 140-144 ◽  
Author(s):  
Sunil Sirohi ◽  
Jennifer D. Schurdak ◽  
Randy J. Seeley ◽  
Stephen C. Benoit ◽  
Jon F. Davis
Keyword(s):  
Addictive Behaviors ◽  
Receptor Signaling ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Differential Importance of Glucose-Dependent Insulinotropic Polypeptide vs Glucagon-Like Peptide 1 Receptor Signaling for Beta Cell Survival in Mice

2009 ◽  
Vol 137 (6) ◽  
pp. 2146-2157 ◽  
Author(s):  
Adriano Maida ◽  
Tanya Hansotia ◽  
Christine Longuet ◽  
Yutaka Seino ◽  
Daniel J. Drucker
Keyword(s):  
Beta Cell ◽  
Cell Survival ◽  
Receptor Signaling ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Glucagon-like peptide 1 receptor signaling attenuates respiratory syncytial virus–induced type 2 responses and immunopathology

2018 ◽  
Vol 142 (2) ◽  
pp. 683-687.e12 ◽  
Author(s):  
Melissa H. Bloodworth ◽  
Mark Rusznak ◽  
Connor C. Pfister ◽  
Jian Zhang ◽  
Lisa Bastarache ◽  
...  
Keyword(s):  
Respiratory Syncytial Virus ◽  
Receptor Signaling ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Syncytial Virus

Glucagon-like peptide 1 receptor signaling influences topography of islet cells in mice

2001 ◽  
Vol 438 (4) ◽  
pp. 382-387 ◽  
Author(s):  
Z. Ling ◽  
D. Wu ◽  
Y. Zambre ◽  
D. Flamez ◽  
D.J. Drucker ◽  
...  
Keyword(s):  
Islet Cells ◽  
Receptor Signaling ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Long-Acting Glucagon-Like Peptide-1 Receptor Agonists Suppress Voluntary Alcohol Intake in Male Wistar Rats

2020 ◽  
Vol 14 ◽  
Author(s):  
Vincent N. Marty ◽  
Mehdi Farokhnia ◽  
Joseph J. Munier ◽  
Yatendra Mulpuri ◽  
Lorenzo Leggio ◽  
...  
Keyword(s):  
Wistar Rats ◽  
Alcohol Intake ◽  
Ethanol Intake ◽  
Addictive Behaviors ◽  
Gut Hormone ◽  
Male Wistar Rats ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Long Acting ◽  
Alcohol Seeking

Alcohol use disorder (AUD) is a chronic relapsing condition characterized by compulsive alcohol-seeking behaviors, with serious detrimental health consequences. Despite high prevalence and societal burden, available approved medications to treat AUD are limited in number and efficacy, highlighting a critical need for more and novel pharmacotherapies. Glucagon-like peptide-1 (GLP-1) is a gut hormone and neuropeptide involved in the regulation of food intake and glucose metabolism via GLP-1 receptors (GLP-1Rs). GLP-1 analogs are approved for clinical use for diabetes and obesity. Recently, the GLP-1 system has been shown to play a role in the neurobiology of addictive behaviors, including alcohol seeking and consumption. Here we investigated the effects of different pharmacological manipulations of the GLP-1 system on escalated alcohol intake and preference in male Wistar rats exposed to intermittent access 2-bottle choice of 10% ethanol or water. Administration of AR231453 and APD668, two different agonists of G-protein receptor 119, whose activation increases GLP-1 release from intestinal L-cells, did not affect voluntary ethanol intake. By contrast, injections of either liraglutide or semaglutide, two long-acting GLP-1 analogs, potently decreased ethanol intake. These effects, however, were transient, lasting no longer than 48 h. Semaglutide, but not liraglutide, also reduced ethanol preference on the day of injection. As expected, both analogs induced a reduction in body weight. Co-administration of exendin 9-39, a GLP-1R antagonist, did not prevent liraglutide- or semaglutide-induced effects in this study. Injection of exendin 9-39 alone, or blockade of dipeptidyl peptidase-4, an enzyme responsible for GLP-1 degradation, via injection of sitagliptin, did not affect ethanol intake or preference. Our findings suggest that among medications targeting the GLP-1 system, GLP-1 analogs may represent novel and promising pharmacological tools for AUD treatment.

scholarly journals The food intake-suppressive effects of glucagon-like peptide-1 receptor signaling in the ventral tegmental area are mediated by AMPA/kainate receptors

2013 ◽  
Vol 305 (11) ◽  
pp. E1367-E1374 ◽  
Author(s):  
Elizabeth G. Mietlicki-Baase ◽  
Pavel I. Ortinski ◽  
Laura E. Rupprecht ◽  
Diana R. Olivos ◽  
Amber L. Alhadeff ◽  
...  
Keyword(s):  
Food Intake ◽  
Ventral Tegmental Area ◽  
Dopamine Neurons ◽  
Kainate Receptors ◽  
System Control ◽  
Receptor Signaling ◽  
Palatable Food ◽  
Glucagon Like Peptide ◽  
Ventral Tegmental ◽  
Glucagon Like Peptide 1

Glucagon-like peptide-1 receptor (GLP-1R) activation in the ventral tegmental area (VTA) is physiologically relevant for the control of palatable food intake. Here, we tested whether the food intake-suppressive effects of VTA GLP-1R activation are mediated by glutamatergic signaling within the VTA. Intra-VTA injections of the GLP-1R agonist exendin-4 (Ex-4) reduced palatable high-fat food intake in rats primarily by reducing meal size; these effects were mediated in part via glutamatergic AMPA/kainate but not NMDA receptor signaling. Additional behavioral data indicated that GLP-1R expressed specifically within the VTA can partially mediate the intake- and body weight-suppressive effects of systemically administered Ex-4, offering the intriguing possibility that this receptor population may be clinically relevant for food intake control. Intra-VTA Ex-4 rapidly increased tyrosine hydroxylase levels within the VTA, suggesting that GLP-1R activation modulates VTA dopaminergic signaling. Further evidence for this hypothesis was provided by electrophysiological data showing that Ex-4 increased the frequency of AMPA-mediated currents and reduced the paired/pulse ratio in VTA dopamine neurons. Together, these data provide novel mechanisms by which GLP-1R agonists in the mesolimbic reward system control for palatable food intake.

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