Receptors for the incretin glucagon-like peptide-1 are expressed on neurons in the central nervous system

Neuroreport ◽  
2009 ◽  
Vol 20 (13) ◽  
pp. 1161-1166 ◽  
Author(s):  
Alison Hamilton ◽  
Christian Hölscher
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
The Central Nervous System ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Central Nervous System Regulation of Intestinal Lipoprotein Metabolism by Glucagon-Like Peptide-1 via a Brain–Gut Axis

2015 ◽  
Vol 35 (5) ◽  
pp. 1092-1100 ◽  
Author(s):  
Sarah Farr ◽  
Christopher Baker ◽  
Mark Naples ◽  
Jennifer Taher ◽  
Jahangir Iqbal ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Lipoprotein Metabolism ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Preproglucagon neurons in the hindbrain have IL-6 receptor-α and show Ca2+ influx in response to IL-6

2016 ◽  
Vol 311 (1) ◽  
pp. R115-R123 ◽  
Author(s):  
Fredrik Anesten ◽  
Marie K. Holt ◽  
Erik Schéle ◽  
Vilborg Pálsdóttir ◽  
Frank Reimann ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Food Intake ◽  
Extracellular Space ◽  
Solitary Tract ◽  
Neuronal Marker ◽  
Reporter Mice ◽  
The Central Nervous System ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
The Brain

Neuronal circuits in the hypothalamus and hindbrain are of importance for control of food intake, energy expenditure, and fat mass. We have recently shown that treatment with exendin-4 (Ex-4), an analog of the proglucagon-derived molecule glucagon-like peptide 1 (GLP-1), markedly increases mRNA expression of the cytokine interleukin-6 (IL-6) in the hypothalamus and hindbrain and that this increase partly mediates the suppression of food intake and body weight by Ex-4. Endogenous GLP-1 in the central nervous system (CNS) is produced by preproglucagon (PPG) neurons of the nucleus of the solitary tract (NTS) in the hindbrain. These neurons project to various parts of the brain, including the hypothalamus. Outside the brain, IL-6 stimulates GLP-1 secretion from the gut and pancreas. In this study, we aim to investigate whether IL-6 can affect GLP-1-producing PPG neurons in the nucleus of the solitary tract (NTS) in mouse hindbrain via the ligand binding part of the IL-6 receptor, IL-6 receptor-α (IL-6Rα). Using immunohistochemistry, we found that IL-6Rα was localized on PPG neurons of the NTS. Recordings of these neurons in GCaMP3/GLP-1 reporter mice showed that IL-6 enhances cytosolic Ca2+ concentration in neurons capable of expressing PPG. We also show that the Ca2+ increase originates from the extracellular space. Furthermore, we found that IL-6Rα was localized on cells in the caudal hindbrain expressing immunoreactive NeuN (a neuronal marker) or CNP:ase (an oligodendrocyte marker). In summary, IL-6Rα is present on PPG neurons in the NTS, and IL-6 can stimulate these cells by increasing influx of Ca2+ to the cytosol from the extracellular space.

scholarly journals Role of Central Nervous System Glucagon-Like Peptide-1 Receptors in Enteric Glucose Sensing

Diabetes ◽  
2008 ◽  
Vol 57 (10) ◽  
pp. 2603-2612 ◽  
Author(s):  
C. Knauf ◽  
P. D. Cani ◽  
D.-H. Kim ◽  
M. A. Iglesias ◽  
C. Chabo ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Glucose Sensing ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Direct Control of Brown Adipose Tissue Thermogenesis by Central Nervous System Glucagon-Like Peptide-1 Receptor Signaling

Diabetes ◽  
2012 ◽  
Vol 61 (11) ◽  
pp. 2753-2762 ◽  
Author(s):  
S. H. Lockie ◽  
K. M. Heppner ◽  
N. Chaudhary ◽  
J. R. Chabenne ◽  
D. A. Morgan ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Adipose Tissue ◽  
Brown Adipose Tissue ◽  
Receptor Signaling ◽  
Direct Control ◽  
Brown Adipose ◽  
Brown Adipose Tissue Thermogenesis ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Peripheral and Central GLP-1 Receptor Populations Mediate the Anorectic Effects of Peripherally Administered GLP-1 Receptor Agonists, Liraglutide and Exendin-4

Endocrinology ◽  
2011 ◽  
Vol 152 (8) ◽  
pp. 3103-3112 ◽  
Author(s):  
Scott E. Kanoski ◽  
Samantha M. Fortin ◽  
Myrtha Arnold ◽  
Harvey J. Grill ◽  
Matthew R. Hayes
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Body Weight ◽  
Food Intake ◽  
Vagal Afferents ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Long Acting ◽  
Higher Doses ◽  
Cns Delivery

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.

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