Glucagon-like Peptide-1 and the Central/Peripheral Nervous System: Crosstalk in Diabetes

2017 ◽  
Vol 28 (2) ◽  
pp. 88-103 ◽  
Author(s):  
Giovanna Muscogiuri ◽  
Ralph A. DeFronzo ◽  
Amalia Gastaldelli ◽  
Jens J. Holst
Keyword(s):  
Nervous System ◽  
Peripheral 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 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 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.

scholarly journals Intermittent Hypoxia Up-Regulates Gene Expressions of Peptide YY (PYY), Glucagon-like Peptide-1 (GLP-1), and Neurotensin (NTS) in Enteroendocrine Cells

2019 ◽  
Vol 20 (8) ◽  
pp. 1849 ◽  
Author(s):  
Ryogo Shobatake ◽  
Asako Itaya-Hironaka ◽  
Akiyo Yamauchi ◽  
Mai Makino ◽  
Sumiyo Sakuramoto-Tsuchida ◽  
...  
Keyword(s):  
Nervous System ◽  
Intermittent Hypoxia ◽  
Peptide Yy ◽  
Trichostatin A ◽  
Sleep Apnea Syndrome ◽  
Enteroendocrine Cells ◽  
Mrna Levels ◽  
Gene Expressions ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The patients with sleep apnea syndrome are exposed to intermittent hypoxia (IH) during sleep. We previously demonstrated the IH-induced up-regulation of the mRNA levels of anorexigenic peptides proopiomelanocortin (POMC), and cocaine- and amphetamine-regulated transcript (CART) in human neuronal cells. Appetite is regulated not only by the central nervous system but also by the peptides from gastrointestinal tract. Here, we investigated the effects of IH on the gene expression(s) of appetite-inhibiting gut hormones. Human enteroendocrine Caco-2 and mouse STC-1 cells were exposed to IH [64 cycles of 5 min hypoxia (1% O2) and 10 min normoxia (21% O2)] or normoxia for 24 h. Real-time RT-PCR revealed that IH significantly increased the mRNA levels of peptide YY (PYY), glucagon-like peptide-1 (GLP-1), and neurotensin (NTS) in Caco-2 and STC-1 cells. ELISA showed that the concentrations of PYY, GLP-1, and NTS in the culture medium were significantly increased by IH. The mRNA levels of PYY, GLP-1, and NTS were significantly up-regulated even in normoxia by Trichostatin A (TSA) and were significantly decreased even in IH by 5-azacytidine (5AZC), suggesting that IH increases PYY, GLP-1, and NTS mRNAs via alterations in the chromatin structure in enteroendocrine cells. IH might have an anorexigenic influence on the enteric nervous system.

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