scholarly journals GLP-1 receptor signaling contributes to anorexigenic effect of centrally administered oxytocin in rats

2002 ◽  
Vol 283 (1) ◽  
pp. R99-R106 ◽  
Author(s):  
Linda Rinaman ◽  
Elizabeth E. Rothe
Keyword(s):  
Food Intake ◽  
Receptor Antagonist ◽  
Male Rats ◽  
Neural Systems ◽  
Neural Pathways ◽  
Receptor Signaling ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Access To Food ◽  
Anorexigenic Effect

The present study examined possible interactions between central glucagon-like peptide-1 (GLP-1) and oxytocin (OT) neural systems by determining whether blockade of GLP-1 receptors attenuates OT-induced anorexia and vice versa. Male rats were acclimated to daily 4-h food access. In the first experiment, rats were infused centrally with GLP-1 receptor antagonist or vehicle, followed by an anorexigenic dose of synthetic OT. Access to food began 20 min later. Cumulative food intake was measured every 30 min for 4 h. In the second experiment, rats were infused with OT receptor blocker or vehicle, followed by synthetic GLP-1 [(7–36) amide]. Subsequent food intake was monitored as before. The anorexigenic effect of OT was eliminated in rats pretreated with the GLP-1 receptor antagonist. Conversely, GLP-1-induced anorexia was not affected by blockade of OT receptors. In a separate immunocytochemical study, OT-positive terminals were found closely apposed to GLP-1-positive perikarya, and central infusion of OT activated c-Fos expression in GLP-1 neurons. These findings implicate endogenous GLP-1 receptor signaling as an important downstream mediator of anorexia in rats after activation of central OT neural pathways.

A functional role for central glucagon-like peptide-1 receptors in lithium chloride-induced anorexia

1999 ◽  
Vol 277 (5) ◽  
pp. R1537-R1540 ◽  
Author(s):  
Linda Rinaman
Keyword(s):  
Food Intake ◽  
Receptor Antagonist ◽  
Lithium Chloride ◽  
Neural Pathways ◽  
Sprague Dawley ◽  
Receptor Signalling ◽  
Sprague Dawley Rats ◽  
Licl Treatment ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The present study sought to determine whether central glucagon-like peptide-1 (GLP-1)-receptor signalling contributes to the anorexigenic effects of systemically administered lithium chloride (LiCl). Male Sprague-Dawley rats with chronic intracerebroventricular (ICV) cannulas were acclimated to a feeding schedule that included daily 30-min access to palatable mash. In the first experiment, ICV infusion of a GLP-1-receptor antagonist [exendin-4-(3—39)] significantly attenuated (10 μg dose) or completely blocked (20 μg dose) the inhibition of food intake produced by subsequent ICV infusion of GLP-1-(7—36) amide (5 μg). In the second experiment, rats were infused with 0, 10, or 20 μg of the GLP-1-receptor antagonist ICV, followed by injection of 0.15 M LiCl (50 mg/kg ip) or the same volume of 0.15 M NaCl. The ability of LiCl treatment to suppress food intake was significantly attenuated in rats that were pretreated with the GLP-1-receptor antagonist. These results support the view that central mechanisms underlying LiCl-induced anorexia include a prominent role for endogenous GLP-1 neural pathways.

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.

scholarly journals Potential modulation of plasma ghrelin and glucagon-like peptide-1 by anorexigenic cannabinoid compounds, SR141716A (rimonabant) and oleoylethanolamide

2004 ◽  
Vol 92 (5) ◽  
pp. 757-761 ◽  
Author(s):  
Patrice D. Cani ◽  
Maite Lasa Montoya ◽  
Audrey M. Neyrinck ◽  
Nathalie M. Delzenne ◽  
Didier M. Lambert
Keyword(s):  
Gastrointestinal Tract ◽  
Food Intake ◽  
Receptor Antagonist ◽  
Food Consumption ◽  
Cannabinoid Receptor ◽  
Short Term ◽  
Cannabinoid Compounds ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Fasted Rats

The CB1 cannabinoid receptor antagonist, N-piperidino-5-(4-chlorophenyl)-1-(2,4-dichlorophenyl)-4-methylpyrazole-3-carboxamide (rimonabant; SR141716A), and oleoylethanolamide (OEA) are known to reduce food consumption, by, at least partially, a peripheral regulation of feeding. The effects of systemic SR141716A or OEA (5 mg/kg) administrations on food consumption in 24 h food-deprived and fed rats were investigated. In fasted rats, SR141716A and OEA produced an inhibition in food intake measurable the first 20 min following injection. The increase in ghrelin levels observed in the vehicle-injected rats was abolished in animals receiving OEA and significantly reduced with SR141716A. Neither OEA nor SR141716A modified glucagon-like peptide-1 (7–36) amide portal levels 20 min after the administration. In fed rats, plasma ghrelin levels of SR141716A- and OEA-treated rats were 35% lower as compared with those of the vehicle-injected rats. These results show an influence of cannabinoid agents on circulating ghrelin levels and suggest that their short-term action on appetite seems to be in accordance with the control of secretion of gastrointestinal orexigenic peptides, mainly expressed in the upper part of the gastrointestinal tract.

scholarly journals Hindbrain Oxytocin Receptors Contribute to the Effects of Circulating Oxytocin on Food Intake in Male Rats

Endocrinology ◽  
2014 ◽  
Vol 155 (8) ◽  
pp. 2845-2857 ◽  
Author(s):  
Jacqueline M. Ho ◽  
Vishwanath T. Anekonda ◽  
Benjamin W. Thompson ◽  
Mingyan Zhu ◽  
Robert W. Curry ◽  
...  
Keyword(s):  
Food Intake ◽  
Male Rats ◽  
Predominant Role ◽  
Catecholaminergic Neurons ◽  
Downstream Target ◽  
Oxytocin Receptors ◽  
Electrophysiological Studies ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Catecholamine Neurons

Oxytocin (OT)-elicited hypophagia has been linked to neural activity in the nucleus of the solitary tract (NTS). Because plasma OT levels increase after a meal, we hypothesized that circulating OT acts at both peripheral and hindbrain OT receptors (OTRs) to limit food intake. To initially determine whether circulating OT inhibits food intake by acting at hindbrain OTRs, we pretreated rats with an OTR antagonist administered into the fourth ventricle (4V) followed by either central or systemic OT administration. Administration of the OTR antagonist into the 4V blocked anorexia induced by either 4V or ip injection of OT. However, blockade of peripheral OTRs also weakened the anorectic response to ip OT. Our data suggest a predominant role for hindbrain OTRs in the hypophagic response to peripheral OT administration. To elucidate central mechanisms of OT hypophagia, we tested whether OT activates NTS catecholaminergic neurons. OT (ip) increased the number of NTS cells expressing c-Fos, of which 10%–15% were catecholaminergic. Furthermore, electrophysiological studies in mice revealed that OT stimulated 47% (8 of 17) of NTS catecholamine neurons through a presynaptic mechanism. However, OT-elicited hypophagia did not appear to require activation of α1-adrenoceptors, and blockade of glucagon-like peptide-1 receptors similarly did not attenuate anorexia induced by OT. These findings demonstrate that OT elicits satiety through both central and peripheral OTRs and that although catecholamine neurons are a downstream target of OT signaling in the NTS, the hypophagic effect is mediated independently of α1-adrenoceptor signaling.

scholarly journals Endogenous Glucagon-like Peptide-1 Receptor Signaling in the Nucleus Tractus Solitarius is Required for Food Intake Control

2016 ◽  
Vol 42 (7) ◽  
pp. 1471-1479 ◽  
Author(s):  
Amber L Alhadeff ◽  
Blake D Mergler ◽  
Derek J Zimmer ◽  
Christopher A Turner ◽  
David J Reiner ◽  
...  
Keyword(s):  
Food Intake ◽  
Nucleus Tractus Solitarius ◽  
Receptor Signaling ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Intake Control

scholarly journals Paraventricular Thalamic Control of Food Intake and Reward: Role of Glucagon-Like Peptide-1 Receptor Signaling

2017 ◽  
Vol 42 (12) ◽  
pp. 2387-2397 ◽  
Author(s):  
Zhi Yi Ong ◽  
Jing-Jing Liu ◽  
Zhiping P Pang ◽  
Harvey J Grill
Keyword(s):  
Food Intake ◽  
Receptor Signaling ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Dose combinations of exendin-4 and salmon calcitonin produce additive and synergistic reductions in food intake in nonhuman primates

2010 ◽  
Vol 299 (3) ◽  
pp. R945-R952 ◽  
Author(s):  
Nicholas T. Bello ◽  
Matthew H. Kemm ◽  
Erica M. Ofeldt ◽  
Timothy H. Moran
Keyword(s):  
Food Intake ◽  
Salmon Calcitonin ◽  
Meal Size ◽  
Reduce Food Intake ◽  
Additive Effects ◽  
Daily Food ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
The Individual ◽  
Access To Food

Glucagon-like peptide-1 (GLP-1) and amylin mediate the feedback control of eating by seemingly separate, but overlapping mechanisms. This study examined the effects of combined doses of the GLP-1 agonist, exendin-4 (Ex-4), and the amylin analog, salmon calcitonin (sCT), on food intake and meal patterns in adult male rhesus monkeys. Monkeys received intramuscular injections of Ex-4 (0, 0.1, 0.32, or 0.56 μg/kg), sCT (0, 0.1, or 0.32 μg/kg), or combinations thereof before a 6-h daily access to food. Dose combinations produced reductions in food intake that were significantly greater than those produced by the individual doses. Surface plots of the hourly intake indicated a synergistic interaction at lower doses of Ex-4 and sCT during the first 4 h of feeding and additive effects at hours 5 and 6. Meal pattern analysis revealed the combinational doses reduced average meal size and meal frequency by additive interactions, whereas infra-additive effects were apparent at lower doses for first meal size. Combinational doses were further characterized by administration of repeated daily injections of 0.56 μg/kg Ex-4 + 0.32 μg/kg sCT for 5 days. This resulted in sustained reductions in daily food intake (>70% from saline baseline) for 5 days with residual reductions (∼48% from saline baseline) persisting on day 1 following the injections. In contrast, when pair-fed an identical amount of daily food, there was a compensatory food intake increase on day 1 following the pair-feeding (∼132% of saline baseline). Such data suggest Ex-4 and sCT interact in an overall additive fashion to reduce food intake and further the understanding of how GLP-1 and amylin agonist combinations influence feeding behavior.

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