scholarly journals Reproductive performance of male mice after hypothalamic ghrelin administration

Reproduction ◽  
2018 ◽  
Vol 156 (2) ◽  
pp. 121-132 ◽  
Author(s):  
María Belén Poretti ◽  
Camila Frautschi ◽  
Eugenia Luque ◽  
Santiago Bianconi ◽  
Ana Carolina Martini ◽  
...  
Keyword(s):  
Food Intake ◽  
Plasma Levels ◽  
Sperm Concentration ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Artificial Cerebrospinal Fluid ◽  
Orexigenic Peptide ◽  
Metabolic Conditions ◽  
Histological Morphology

It has been demonstrated that food intake and reproductive physiology are both simultaneously modulated to optimize reproductive success under fluctuating metabolic conditions. Ghrelin (GHRL) is an orexigenic peptide identified as the endogenous ligand of the growth hormone secretagogue receptor that is being investigated for its potential role on reproduction. Considering that data available so far are still limited and characterization of GHRL action mechanism on the reproductive system has not been fully elucidated, we studied the participation of hypothalamus in GHRL effects on sperm functional activity, plasma levels of gonadotropins and histological morphology in mice testes after hypothalamic infusion of 0.3 or 3.0 nmol/day GHRL or artificial cerebrospinal fluid (ACSF) at different treatment periods. We found that GHRL 3.0 nmol/day administration for 42 days significantly reduced sperm concentration (GHRL 3.0 nmol/day = 14.05 ± 2.44 × 106/mL vs ACSF = 20.33 ± 1.35 × 106/mL,P < 0.05) and motility (GHRL 3.0 nmol/day = 59.40 ± 4.20% vs ACSF = 75.80 ± 1.40%,P < 0.05). In addition, histological studies showed a significant decrease percentage of spermatogonia (GHRL 3.0 nmol/day = 6.76 ± 0.68% vs ACSF = 9.56 ± 0.41%,P < 0.05) and sperm (GHRL 3.0 nmol/day = 24.24 ± 1.92% vs ACSF = 31.20 ± 3.06%,P < 0.05). These results were associated with a significant reduction in luteinizing hormone and testosterone plasma levels (P < 0.05). As GHRL is an orexigenic peptide, body weight and food intake were measured. Results showed that GHRL increases both parameters; however, the effect did not last beyond the first week of treatment. Results presented in this work confirm that central GHRL administration impairs spermatogenesis and suggest that this effect is mediated by inhibition of hypothalamic–pituitary–gonadal axis.

scholarly journals Evidence Supporting a Role for Constitutive Ghrelin Receptor Signaling in Fasting-Induced Hyperphagia in Male Mice

Endocrinology ◽  
2017 ◽  
Vol 159 (2) ◽  
pp. 1021-1034 ◽  
Author(s):  
Gimena Fernandez ◽  
Agustina Cabral ◽  
María F Andreoli ◽  
Alexandra Labarthe ◽  
Céline M'Kadmi ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Food Intake ◽  
Peptide Hormone ◽  
Negative Energy ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Ghrelin Receptor ◽  
Orexigenic Peptide ◽  
Hypothalamic Arcuate Nucleus

Abstract Ghrelin is a potent orexigenic peptide hormone that acts through the growth hormone secretagogue receptor (GHSR), a G protein–coupled receptor highly expressed in the hypothalamus. In vitro studies have shown that GHSR displays a high constitutive activity, whose physiological relevance is uncertain. As GHSR gene expression in the hypothalamus is known to increase in fasting conditions, we tested the hypothesis that constitutive GHSR activity at the hypothalamic level drives the fasting-induced hyperphagia. We found that refed wild-type (WT) mice displayed a robust hyperphagia that continued for 5 days after refeeding and changed their food intake daily pattern. Fasted WT mice showed an increase in plasma ghrelin levels, as well as in GHSR expression levels and ghrelin binding sites in the hypothalamic arcuate nucleus. When fasting-refeeding responses were evaluated in ghrelin- or GHSR-deficient mice, only the latter displayed an ∼15% smaller hyperphagia, compared with WT mice. Finally, fasting-induced hyperphagia of WT mice was significantly smaller in mice centrally treated with the GHSR inverse agonist K-(D-1-Nal)-FwLL-NH2, compared with mice treated with vehicle, whereas it was unaffected in mice centrally treated with the GHSR antagonists D-Lys3-growth hormone–releasing peptide 6 or JMV2959. Taken together, genetic models and pharmacological results support the notion that constitutive GHSR activity modulates the magnitude of the compensatory hyperphagia triggered by fasting. Thus, the hypothalamic GHSR signaling system could affect the set point of daily food intake, independently of plasma ghrelin levels, in situations of negative energy balance.

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.

Design and characterization of a fluorescent ghrelin analog for imaging the growth hormone secretagogue receptor 1a

2011 ◽  
Vol 172 (1-3) ◽  
pp. 69-76 ◽  
Author(s):  
Rebecca McGirr ◽  
Mark S. McFarland ◽  
Jillian McTavish ◽  
Leonard G. Luyt ◽  
Savita Dhanvantari
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue

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

Characterization of a Monoclonal Antibody Specific for the Growth Hormone Secretagogue Receptor

2017 ◽  
Vol 36 (2) ◽  
pp. 37-43 ◽  
Author(s):  
Katia Crotta ◽  
Claudia Casnici ◽  
Noemi Tonna ◽  
Donatella Lattuada ◽  
Fabio Bianco ◽  
...  
Keyword(s):  
Monoclonal Antibody ◽  
Growth Hormone ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue

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&lt;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.

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.

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