scholarly journals Ghrelin Enhances Appetite and Increases Food Intake in Humans

2001 ◽  
Vol 86 (12) ◽  
pp. 5992-5992 ◽  
Author(s):  
A. M. Wren ◽  
L. J. Seal ◽  
M. A. Cohen ◽  
A. E. Brynes ◽  
G. S. Frost ◽  
...  
Keyword(s):  
Food Intake ◽  
Free Choice ◽  
Saline Infusion ◽  
Endogenous Ligand ◽  
Growth Hormone Secretagogue Receptor ◽  
Double Blind ◽  
Growth Hormone Secretagogue ◽  
Clear Cut ◽  
Healthy Humans ◽  
Paracetamol Absorption

Ghrelin is a recently identified endogenous ligand for the growth hormone secretagogue receptor. It is synthesized predominantly in the stomach and found in the circulation of healthy humans. Ghrelin has been shown to promote increased food intake, weight gain and adiposity in rodents. The effect of ghrelin on appetite and food intake in man has not been determined. We investigated the effects of intravenous ghrelin (5.0 pmol/kg/min) or saline infusion on appetite and food intake in a randomised double-blind cross-over study in nine healthy volunteers. There was a clear-cut increase in energy consumed by every individual from a free-choice buffet (mean increase 28 ± 3.9%, p<0.001) during ghrelin compared with saline infusion. Visual analogue scores for appetite were greater during ghrelin compared to saline infusion. Ghrelin had no effect on gastric emptying as assessed by the paracetamol absorption test. Ghrelin is the first circulating hormone demonstrated to stimulate food intake in man. Endogenous ghrelin is a potentially important new regulator of the complex systems controlling food intake and body weight.

Effect of chronic hyperghrelinemia on ingestive action of ghrelin

2006 ◽  
Vol 290 (3) ◽  
pp. R803-R808 ◽  
Author(s):  
Wei Wei ◽  
Xiang Qi ◽  
Jason Reed ◽  
Jeff Ceci ◽  
Hui-Qun Wang ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Food Intake ◽  
Transgenic Mice ◽  
Growth Response ◽  
Fat Pad ◽  
Endogenous Ligand ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Gh Secretion ◽  
Ghrelin Gene

The stomach hormone ghrelin is the endogenous ligand for the growth hormone secretagogue receptor (GHS-R). Systemic administration of ghrelin will cause elevations in growth hormone (GH) secretion, food intake, adiposity, and body growth. Ghrelin also affects insulin secretion, gastric acid secretion, and gastric motility. Several reports indicate that repeated or continuous activation of GHS-R by exogenous GHSs or ghrelin results in a diminished GH secretory response. The purpose of this study was to examine the extent to which the acute stimulation of food intake by exogenous ghrelin is altered by chronic hyperghrelinemia in transgenic mice that overexpress the human ghrelin gene. The present findings show that the orexigenic action of exogenous ghrelin is not diminished by a chronic hyperghrelinemia and indicate that the food ingestive pathway of the GHS-R is not susceptible to desensitization. In contrast, the epididymal fat pad growth response, like the GH response, to exogenous ghrelin is blunted in ghrelin transgenic mice with chronic hyperghrelinemia.

scholarly journals Intraportal Infusion of Ghrelin Could Inhibit Glucose-Stimulated GLP-1 Secretion by Enteric Neural Net in Wistar Rat

2014 ◽  
Vol 2014 ◽  
pp. 1-7 ◽  
Author(s):  
Xiyao Zhang ◽  
Wensong Li ◽  
Ping Li ◽  
Manli Chang ◽  
Xu Huang ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Food Intake ◽  
Portal Vein ◽  
Wistar Rat ◽  
Inhibitory Effect ◽  
Neural Net ◽  
Incretin Effect ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Intraportal Infusion

As a regulator of food intake and energy metabolism, the role of ghrelin in glucose metabolism is still not fully understood. In this study, we determined the in vivo effect of ghrelin on incretin effect. We demonstrated that ghrelin inhibited the glucose-stimulated release of glucagon-like peptide-1 (GLP-1) when infused into the portal vein of Wistar rat. Hepatic vagotomy diminished the inhibitory effect of ghrelin on glucose-stimulated GLP-1 secretion. In addition, phentolamine, a nonselective α receptor antagonist, could recover the decrease of GLP-1 release induced by ghrelin infusion. Pralmorelin (an artificial growth hormone release peptide) infusion into the portal vein could also inhibit the glucose-stimulated release of GLP-1. And growth hormone secretagogue receptor antagonist, [D-lys3]-GHRP-6, infusion showed comparable increases of glucose stimulated GLP-1 release compared to ghrelin infusion into the portal vein. The data showed that intraportal infusion of ghrelin exerted an inhibitory effect on GLP-1 secretion through growth hormone secretagogue receptor 1α (GHS1α receptor), which indicated that the downregulation of ghrelin secretion after food intake was necessary for incretin effect. Furthermore, our results suggested that the enteric neural net involved hepatic vagal nerve and sympathetic nerve mediated inhibition effect of ghrelin on incretin effect.

scholarly journals Assessing the role of the growth hormone secretagogue receptor in motivational learning and food intake.

2009 ◽  
Vol 123 (5) ◽  
pp. 1058-1065 ◽  
Author(s):  
Alexander W. Johnson ◽  
Rebecca Canter ◽  
Michela Gallagher ◽  
Peter C. Holland
Keyword(s):  
Growth Hormone ◽  
Food Intake ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue

Bombesin Reduces Food Intake after a Preload in Man by a Cholecystokinin-Independent Mechanism

1993 ◽  
Vol 85 (3) ◽  
pp. 277-280 ◽  
Author(s):  
R. J. Lieverse ◽  
J. B. M. J. Jansen ◽  
A. A. M. Masclee ◽  
C. B. H. W. Lamers
Keyword(s):  
Food Intake ◽  
Receptor Antagonist ◽  
Healthy Subjects ◽  
Saline Infusion ◽  
Blind Study ◽  
Double Blind Study ◽  
Double Blind ◽  
Cholecystokinin Receptor ◽  
Independent Mechanism

1. A double-blind study was undertaken to determine whether the infusion of bombesin inhibits the intake of a carbohydrate-rich meal, consumed 15 min after a 300 ml banana shake, in nine lean healthy subjects and whether the possible inhibition of food intake by bombesin is mediated by cholecystokinin. 2. The amount of food eaten during infusion of bombesin (267 ±60 g) and bombesin combined with the cholecystokinin-receptor antagonist loxiglumide (269±39g) was slightly (P = 0.09) less than during saline infusion (384 ± 40 g). In addition, preprandial feelings of hunger were significantly less during infusion of both bombesin and bombesin combined with loxiglumide. 3. In conclusion, infusion of bombesin tends to inhibit the intake of a carbohydrate-rich meal after a preload by a cholecystokinin-independent mechanism.

Radiofluorination of Non-activated Aromatic Prosthetic Groups for Synthesis and Evaluation of Fluorine-18 Labelled Ghrelin(1-8) Analogues

2021 ◽  
Author(s):  
Marina D Childs ◽  
Lihai Yu ◽  
Michael Kovacs ◽  
Leonard G Luyt
Keyword(s):  
Growth Hormone ◽  
Molecular Imaging ◽  
Differentially Expressed ◽  
Endogenous Ligand ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Disease States ◽  
Prosthetic Groups

The growth hormone secretagogue receptor 1a (GHSR) is differentially expressed in various disease states compared to healthy tissues and thus is a target for molecular imaging. The endogenous ligand for...

scholarly journals Molecular characterization of the bovine <i>GHRL</i> gene (Short Communication)

2009 ◽  
Vol 52 (1) ◽  
pp. 79-84 ◽  
Author(s):  
F. G. Colinet ◽  
D. Portetelle ◽  
R. Renaville
Keyword(s):  
Growth Hormone ◽  
Amino Acid ◽  
Short Communication ◽  
Hormone Secretion ◽  
Growth Hormone Secretion ◽  
Endogenous Ligand ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Amino Acid Peptide

Abstract. Bovine ghrelin, a 27 amino acid peptide, has been identified in oxyntic glands of the abomasum. It is an endogenous ligand for growth hormone secretagogue receptor and stimulates food intake and growth hormone secretion. The bovine GHRL gene was completely sequenced and consists of five exons and four introns. Like mouse and human GHRL genes, we found that the bovine GHRL gene also contains a first non-coding exon of 21 bp. The bovine GHRL gene codes for 116 amino acid peptide named preproghrelin which contains the ghrelin peptide and another peptide similar to obestatin. Sequence analysis revealed eight polymorphisms, which are located in the non-coding sequence of the gene.

scholarly journals Ghrelin in the lateral parabrachial nucleus influences the excitability of glucosensing neurons, increases food intake and body weight

2020 ◽  
Vol 9 (12) ◽  
pp. 1168-1177
Author(s):  
Caishun Zhang ◽  
Junhua Yuan ◽  
Qian Lin ◽  
Manwen Li ◽  
Liuxin Wang ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Firing Rate ◽  
Body Weight Gain ◽  
Parabrachial Nucleus ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Lateral Parabrachial Nucleus

Ghrelin plays a pivotal role in the regulation of food intake, body weight and energy metabolism. However, these effects of ghrelin in the lateral parabrachial nucleus (LPBN) are unexplored. C57BL/6J mice and GHSR−/− mice were implanted with cannula above the right LPBN and ghrelin was microinjected via the cannula to investigate effect of ghrelin in the LPBN. In vivo electrophysiological technique was used to record LPBN glucose-sensitive neurons to explore potential udnderlying mechanisms. Microinjection of ghrelin in LPBN significantly increased food intake in the first 3 h, while such effect was blocked by [D-Lys3]-GHRP-6 and abolished in GHSR−/− mice. LPBN ghrelin microinjection also significantly increased the firing rate of glucose-excited (GE) neurons and decreased the firing rate of glucose-inhibited (GI) neurons. Additionally, LPBN ghrelin microinjection also significantly increased c-fos expression. Chronic ghrelin administration in the LPBN resulted in significantly increased body weight gain. Meanwhile, no significant changes were observed in both mRNA and protein expression levels of UCP-1 in BAT. These results demonstrated that microinjection of ghrelin in LPBN could increase food intake through the interaction with growth hormone secretagogue receptor (GHSR) in C57BL/6J mice, and its chronic administration could also increase body weight gain. These effects might be associated with altered firing rate in the GE and GI neurons.

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