scholarly journals Central infusion of glucagon-like peptide-1-(7–36) amide (GLP-1) receptor antagonist attenuates lithium chloride-induced c-Fos induction in rat brainstem

1998 ◽  
Vol 801 (1-2) ◽  
pp. 164-170 ◽  
Author(s):  
Todd E Thiele ◽  
Randy J Seeley ◽  
David D'Alessio ◽  
John Eng ◽  
Ilene L Bernstein ◽  
...  
Keyword(s):  
Receptor Antagonist ◽  
Lithium Chloride ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Rat Brainstem

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 Role of CNS Glucagon-Like Peptide-1 (7-36) Amide Receptors in Mediating the Visceral Illness Effects of Lithium Chloride

2000 ◽  
Vol 20 (4) ◽  
pp. 1616-1621 ◽  
Author(s):  
Randy J. Seeley ◽  
Kathleen Blake ◽  
Paul A. Rushing ◽  
Stephen Benoit ◽  
John Eng ◽  
...  
Keyword(s):  
Lithium Chloride ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Properties of native and in vitro glycosylated forms of the glucagon-like peptide-1 receptor antagonist exendin (9–39)

Metabolism ◽  
1999 ◽  
Vol 48 (6) ◽  
pp. 716-724 ◽  
Author(s):  
Janet A. Meurer ◽  
Jerry R. Colca ◽  
Philip S. Burton ◽  
Åke P. Elhammer
Keyword(s):  
Receptor Antagonist ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Glucagon-Like Peptide-1 Counteracts Oxidative Stress-Dependent Apoptosis of Human Cardiac Progenitor Cells by Inhibiting the Activation of the c-Jun N-terminal Protein Kinase Signaling Pathway

Endocrinology ◽  
2012 ◽  
Vol 153 (12) ◽  
pp. 5770-5781 ◽  
Author(s):  
L. Laviola ◽  
A. Leonardini ◽  
M. Melchiorre ◽  
M. R. Orlando ◽  
A. Peschechera ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Protein Kinase ◽  
Receptor Antagonist ◽  
Progenitor Cells ◽  
Cell Apoptosis ◽  
Human Heart ◽  
Cardiac Progenitor Cells ◽  
Terminal Protein ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Abstract Increased apoptosis of cardiac progenitor cells (CPCs) has been proposed as a mechanism of myocardial damage and dysfunction. Glucagon-like peptide-1 (GLP-1) has been shown to improve heart recovery and function after ischemia and to promote cell survival. The protective effects of GLP-1 on oxidative stress-induced apoptosis were investigated in human CPCs isolated from human heart biopsies. Mesenchymal-type cells were isolated from human heart biopsies, exhibited the marker profile of CPCs, differentiated toward the myocardiocyte, adipocyte, chondrocyte, and osteocyte lineages under appropriate culture conditions, and expressed functional GLP-1 receptors. CPCs were incubated with GLP-1 with or without hydrogen peroxide (H2O2). Phospho- and total proteins were detected by immunoblotting and immunofluorescence analysis. Gene expression was evaluated by quantitative RT-PCR. The role of the canonical GLP-1 receptor was assessed by using the receptor antagonist exendin(9–39) and receptor-specific silencer small interfering RNAs. Cell apoptosis was quantified by an ELISA assay and by flow cytometry-detected Annexin V. Exposure of CPCs to H2O2 induced a 2-fold increase in cell apoptosis, mediated by activation of the c-Jun N-terminal protein kinase (JNK) pathway. Preincubation of CPCs with GLP-1 avoided H2O2-triggered JNK phosphorylation and nuclear localization, and protected CPCs from apoptosis. The GLP-1 effects were markedly reduced by coincubation with the receptor antagonist exendin(9–39), small interfering RNA-mediated silencing of the GLP-1 receptor, and pretreatment with the protein kinase A inhibitor H89. In conclusion, activation of GLP-1 receptors prevents oxidative stress-mediated apoptosis in human CPCs by interfering with JNK activation and may represent an important mechanism for the cardioprotective effects of GLP-1.

scholarly journals The glucagon‐like peptide‐1 receptor antagonist exendin‐9 elevates blood pressure and worsens renal function in SHR (1136.18)

2014 ◽  
Vol 28 (S1) ◽  
Author(s):  
Gabriela Aragao ◽  
Maria Shimizu ◽  
Ana Davel ◽  
Antonio Seguro ◽  
Alicia McDonough ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Function ◽  
Receptor Antagonist ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Mechanisms underlying the prokinetic effects of endogenous glucagon-like peptide-1 in the rat proximal colon

2021 ◽  
Author(s):  
Hiroyuki Nakamori ◽  
Koji Iida ◽  
Hikaru Hashitani
Keyword(s):  
Fatty Acids ◽  
Receptor Antagonist ◽  
Short Chain Fatty Acids ◽  
Proximal Colon ◽  
Afferent Neurons ◽  
L Cells ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Peristaltic Contractions ◽  
Stimulation Of

Glucagon-like peptide-1 (GLP-1), a well-known insulin secretagogue, is released from enteroendocrine L cells both luminally and basolaterally to exert different effects. Basolaterally released GLP-1 increases epithelial ion transport by activating CGRP-containing enteric afferent neurons. Although bath-applied GLP-1 reduced the contractility of colonic segments, GLP-1-induced stimulation of afferent neurons could also accelerate peristaltic contractions. Here, the roles of endogenous GLP-1 in regulating colonic peristalsis were investigated using isolated colonic segments. Isolated segments of rat proximal colon were placed in an organ bath, serosally perfused with oxygenated physiological salt solution and luminally perfused with degassed 0.9% saline. Colonic wall motion was recorded using a video camera and converted into spatio-temporal maps. Intraluminal administration of GLP-1 (100 nM) stimulating the secretion of GLP-1 from L cells increased the frequency of oro-aboral propagating peristaltic contractions. The acceleratory effect of GLP-1 was blocked by luminally-applied exendin-3 (9-39) (100 nM), a GLP-1 receptor antagonist. GLP-1-induced acceleration of peristaltic contractions was also prevented by bath-applied BIBN4069 (1 μM), a CGRP receptor antagonist. In colonic segments that had been exposed to bath-applied capsaicin (100 nM) that desensitizes extrinsic afferents, GLP-1 was still capable of exerting its prokinetic effect. Stimulation of endogenous GLP-1 secretion with a luminally-applied cocktail of short-chain fatty acids (1 mM) increased the frequency of peristaltic waves in an exendin-3 (9-39)-sensitive manner. Thus, GLP-1 activates CGRP-expressing intrinsic afferents to accelerate peristalsis in the proximal colon. Short-chain fatty acids appear to stimulate endogenous GLP-1 secretion from L cells resulting in the acceleration of colonic peristalsis.

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