scholarly journals Sympathetic Modulation By Glucagon Like Peptide 1 And Melanocortin 4 Receptors In The Carotid Body Of Wistar Rats

2021 ◽  
Vol 35 (S1) ◽  
Author(s):  
Pratik Thakkar ◽  
Audrys Pauza ◽  
David Murphy ◽  
Julian Paton
Keyword(s):  
Carotid Body ◽  
Wistar Rats ◽  
Sympathetic Modulation ◽  
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.

Diet-induced obesity enhances postprandial glucagon-like peptide-1 secretion in Wistar rats, but not in diabetic Goto-Kakizaki rats

2020 ◽  
pp. 1-13
Author(s):  
Jukkrapong Pinyo ◽  
Hiroshi Hara ◽  
Tohru Hira
Keyword(s):  
Wistar Rats ◽  
Control Diet ◽  
Postprandial Glucose ◽  
Diabetic Rats ◽  
Gk Rats ◽  
Obesity And Diabetes ◽  
Male Wistar Rats ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Insulin Responses

Abstract Glucagon-like peptide-1 (GLP-1) is postprandially secreted from enteroendocrine L-cells and enhances insulin secretion. Currently, it is still controversial whether postprandial GLP-1 responses are altered in obesity and diabetes. To address the issue and to find out possible factors related, we compared postprandial GLP-1 responses in normal rats and in diabetic rats chronically fed an obesogenic diet. Male Wistar rats and diabetic Goto-Kakizaki (GK) rats were fed either a control diet or a high-fat/high-sucrose (HFS, 30 % fat and 40 % sucrose) diet for 26 weeks. Meal tolerance tests were performed for monitoring postprandial responses after a liquid diet administration (62·76 kJ/kg body weight) every 4 or 8 weeks. Postprandial glucose, GLP-1 and insulin responses in Wistar rats fed the HFS diet (WH) were higher than Wistar rats fed the control diet (WC). Although GK rats fed the HFS diet (GH) had higher glycaemic responses than GK rats fed the control diet (GC), these groups had similar postprandial GLP-1 and insulin responses throughout the study. Jejunal and ileal GLP-1 contents were increased by the HFS diet only in Wistar rats. Furthermore, mRNA expression levels of fatty acid receptors (Ffar1) in the jejunum were mildly (P = 0·053) increased by the HFS diet in Wistar rats, but not in GK rats. These results demonstrate that postprandial GLP-1 responses are enhanced under an obesogenic status in normal rats, but not in diabetic rats. Failure of adaptive enhancement of GLP-1 response in GK rats could be partly responsible for the development of glucose intolerance.

scholarly journals Glucagon Shows Higher Sensitivity than Insulin to Grapeseed Proanthocyanidin Extract (GSPE) Treatment in Cafeteria-Fed Rats

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1084
Author(s):  
Carme Grau-Bové ◽  
Iris Ginés ◽  
Raúl Beltrán-Debón ◽  
Ximena Terra ◽  
MTeresa Blay ◽  
...  
Keyword(s):  
Wistar Rats ◽  
Endocrine Pancreas ◽  
Receptor Expression ◽  
Cafeteria Diet ◽  
Β Cells ◽  
Glucose Stimulation ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Pre Treatment ◽  
Higher Sensitivity

The endocrine pancreas plays a key role in metabolism. Procyanidins (GSPE) targets β-cells and glucagon-like peptide-1 (GLP-1)-producing cells; however, there is no information on the effects of GSPE on glucagon. We performed GSPE preventive treatments administered to Wistar rats before or at the same time as they were fed a cafeteria diet during 12 or 17 weeks. We then measured the pancreatic function and GLP-1 production. We found that glucagonemia remains modified by GSPE pre-treatment several weeks after the treatment has finished. The animals showed a higher GLP-1 response to glucose stimulation, together with a trend towards a higher GLP-1 receptor expression in the pancreas. When the GSPE treatment was administered every second week, the endocrine pancreas behaved differently. We show here that glucagon is a more sensitive parameter than insulin to GSPE treatments, with a secretion that is highly linked to GLP-1 ileal functionality and dependent on the type of treatment.

Effects of glucagon-like peptide-1-(7–36)-amide on pancreatic islet and intestinal blood perfusion in Wistar rats and diabetic GK rats

2007 ◽  
Vol 112 (6) ◽  
pp. 345-351 ◽  
Author(s):  
Annika M. Svensson ◽  
Claes-Göran Östenson ◽  
Suad Efendic ◽  
Leif Jansson
Keyword(s):  
Blood Flow ◽  
Pancreatic Islet ◽  
Wistar Rats ◽  
Blood Perfusion ◽  
Glucose Administration ◽  
Gk Rats ◽  
Islet Blood Flow ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Pre Treatment

The aim of the present study was to evaluate the effects of GLP-1 [glucagon-like peptide-1-(7–36)-amide] on total pancreatic, islet and intestinal blood perfusion in spontaneously hyperglycaemic GK rats and normal Wistar rats using a microsphere technique. GK rats had hyperglycaemia and increased pancreatic and islet blood flow. Blood glucose concentrations were not affected when measured shortly (8 min) after GLP-1 administration in either GK or Wistar rats. GLP-1 had no effects on baseline pancreatic or islet blood flow in Wistar rats, but did prevent the blood flow increase normally seen following glucose administration to these animals. In GK rats, administration of GLP-1 decreased both pancreatic and islet blood flow. Glucose administration to the GK rats decreased pancreatic and islet blood flow. This decrease was not affected by pre-treatment with GLP-1. We conclude that administration of GLP-1 leads to a decrease in the augmented blood flow seen in islets of diabetic GK rats. The GLP-1-induced action on islet blood perfusion may modulate output of islet hormones and contribute to the antidiabetogenic effects of the drug in Type 2 diabetes (non-insulin-dependent diabetes).

scholarly journals Liraglutide Preserves Intracellular Calcium Handling in Isolated Murine Myocytes Exposed to Oxidative Stress

2017 ◽  
pp. 889-895 ◽  
Author(s):  
S. PALEE ◽  
S. C. CHATTIPAKORN ◽  
N. CHATTIPAKORN
Keyword(s):  
Oxidative Stress ◽  
Decay Rate ◽  
Intracellular Calcium ◽  
Wistar Rats ◽  
Calcium Handling ◽  
Isolated Cardiomyocytes ◽  
Before And After ◽  
Male Wistar Rats ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

In ischemic/reperfusion (I/R) injured hearts, severe oxidative stress occurs and is associated with intracellular calcium (Ca2+) overload. Glucagon-Like Peptide-1 (GLP-1) analogues have been shown to exert cardioprotection in I/R heart. However, there is little information regarding the effects of GLP-1 analogue on the intracellular Ca2+ regulation in the presence of oxidative stress. Therefore, we investigated the effects of GLP-1 analogue, (liraglutide, 10 µM) applied before or after hydrogen peroxide (H2O2, 50 µM) treatment on intracellular Ca2+ regulation in isolated cardiomyocytes. We hypothesized that liraglutide can attenuate intracellular Ca2+ overload in cardiomyocytes under H2O2-induced cardiomyocyte injury. Cardiomyocytes were isolated from the hearts of male Wistar rats. Isolated cardiomyocytes were loaded with Fura-2/AM and fluorescence intensity was recorded. Intracellular Ca2+ transient decay rate, intracellular Ca2+ transient amplitude and intracellular diastolic Ca2+ levels were recorded before and after treatment with liraglutide. In H2O2 induced severe oxidative stressed cardiomyocytes (which mimic cardiac I/R) injury, liraglutide given prior to or after H2O2 administration effectively increased both intracellular Ca2+ transient amplitude and intracellular Ca2+ transient decay rate, without altering the intracellular diastolic Ca2+ level. Liraglutide attenuated intracellular Ca2+ overload in H2O2-induced cardiomyocyte injury and may be responsible for cardioprotection during cardiac I/R injury by preserving physiological levels of calcium handling during the systolic and diastolic phases of myocyte activation.

scholarly journals Endogenous Activation of Glucagon-Like Peptide-1 Receptor Contributes to Blood Pressure Control

Hypertension ◽  
2020 ◽  
Vol 76 (3) ◽  
pp. 839-848
Author(s):  
Flavia L. Martins ◽  
Matthew A. Bailey ◽  
Adriana C.C. Girardi
Keyword(s):  
Blood Pressure ◽  
Proximal Tubule ◽  
Wistar Rats ◽  
Renin Angiotensin System ◽  
Pressure Control ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Relevant Effect ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

The pharmacological administration of GLP-1R (glucagon-like peptide-1 receptor) agonists reduces blood pressure (BP) in type 2 diabetes mellitus and nondiabetic patients. This study tested the hypothesis that endogenous GLP-1R signaling influences the regulation of BP. To this end, SHRs (spontaneously hypertensive rats) and Wistar rats were treated with the GLP-1R antagonist Ex9 (exendin-9) or vehicle for 4 weeks. Rats receiving the GLP-1R agonist Ex4 (exenatide) were used as an additional control. We found that blockade of baseline GLP-1R signaling by Ex9 increased systolic BP in both SHR and Wistar rats, compared with vehicle-treated animals, while Ex4 only reduced systolic BP in SHR. Higher systolic BP induced by Ex9 was accompanied by reduced lithium clearance and lower levels of NHE3 (Na + /H + exchanger isoform 3) phosphorylation at the serine 552, indicative of increased proximal tubule sodium reabsorption. Additionally, urinary AGT (angiotensinogen) and renal cortical concentration of Ang II (angiotensin II) were enhanced by Ex9. Conversely, Ex4 decreased both urinary AGT and cortical Ang II but exclusively in SHRs. Moreover, both SHR and Wistar rats treated with Ex9 displayed hyperinsulinemia as compared with vehicle-treated rats, whereas Ex4 reduced fasting insulin concentration in SHR. Collectively, these results suggest that endogenous GLP-1R signaling exerts a physiologically relevant effect on BP control, which may be attributable, in part, to its tonic actions on the proximal tubule NHE3-mediated sodium reabsorption, intrarenal renin-angiotensin system, and insulin sensitivity. The possible role of impaired GLP-1R signaling in the pathogenesis of hypertension warrants further investigation.

Effects of glucagon-like peptide-1 (GLP-1) on gastric accommodation, emptying and satiety in humans

2001 ◽  
Vol 120 (5) ◽  
pp. A74-A74
Author(s):  
S AROS ◽  
D KIM ◽  
D BURTON ◽  
G THOMFORDE ◽  
A VELLA ◽  
...  
Keyword(s):  
Gastric Accommodation ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1
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