scholarly journals Ghrelin and Des-Acyl Ghrelin Promote Differentiation and Fusion of C2C12 Skeletal Muscle Cells

2007 ◽  
Vol 18 (3) ◽  
pp. 986-994 ◽  
Author(s):  
Nicoletta Filigheddu ◽  
Viola F. Gnocchi ◽  
Marco Coscia ◽  
Miriam Cappelli ◽  
Paolo E. Porporato ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Ectopic Expression ◽  
Cell Types ◽  
C2c12 Cells ◽  
Growth Hormone Secretagogue Receptor ◽  
Endocrine Activity ◽  
Growth Hormone Secretagogue ◽  
Inhibition Of Proliferation ◽  
Acyl Ghrelin

Ghrelin is an acylated peptidyl gastric hormone acting on the pituitary and hypothalamus to stimulate appetite, adiposity, and growth hormone release, through activation of growth hormone secretagogue receptor (GHSR)-1a receptor. Moreover, ghrelin features several activities such as inhibition of apoptosis, regulation of differentiation, and stimulation or inhibition of proliferation of several cell types. Ghrelin acylation is absolutely required for both GHSR-1a binding and its central endocrine activities. However, the unacylated ghrelin form, des-acyl ghrelin, which does not bind GHSR-1a and is devoid of any endocrine activity, is far more abundant than ghrelin in plasma, and it shares with ghrelin some of its cellular activities. Inhere we show that both ghrelin and des-acyl ghrelin stimulate proliferating C2C12 skeletal myoblasts to differentiate and to fuse into multinucleated myotubes in vitro through activation of p38. Consistently, both ghrelin and des-acyl ghrelin inhibit C2C12 proliferation in growth medium. Moreover, the ectopic expression of ghrelin in C2C12 enhances differentiation and fusion of these myoblasts in differentiation medium. Finally, we show that C2C12 cells do not express GHSR-1a, but they do contain a common high-affinity binding site recognized by both acylated and des-acylated ghrelin, suggesting that the described activities on C2C12 are likely mediated by this novel, yet unidentified receptor for both ghrelin forms.

Ghrelin and des-acyl ghrelin both inhibit isoproterenol-induced lipolysis in rat adipocytes via a non-type 1a growth hormone secretagogue receptor

2004 ◽  
Vol 498 (1-3) ◽  
pp. 27-35 ◽  
Author(s):  
Giampiero Muccioli ◽  
Nicoletta Pons ◽  
Corrado Ghè ◽  
Filomena Catapano ◽  
Riccarda Granata ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Rat Adipocytes ◽  
Acyl Ghrelin

scholarly journals Acute intravenous acyl ghrelin infusion induces thirst but does not affect sodium excretion: two randomized, double-blind, placebo-controlled crossover studies in hypopituitary patients

2019 ◽  
Vol 181 (1) ◽  
pp. 23-30
Author(s):  
Esben T Vestergaard ◽  
Niels Møller ◽  
René Frydensbjerg Andersen ◽  
Søren Rittig ◽  
Jens Otto Lunde Jørgensen
Keyword(s):  
Growth Hormone ◽  
Urinary Excretion ◽  
Sodium Excretion ◽  
Plasma Osmolality ◽  
Sodium Absorption ◽  
Growth Hormone Secretagogue Receptor ◽  
Double Blind ◽  
Growth Hormone Secretagogue ◽  
Crossover Studies ◽  
Acyl Ghrelin

Objective Acyl ghrelin, which is the endogenous ligand for the growth hormone secretagogue receptor, potently stimulates pituitary growth hormone release, and to some degree adrenocorticotropic hormone and prolactin. Ghrelin is also orexigenic and has recently been shown to stimulate renal sodium absorption in rodent models. Increased thirst sensation has been observed as a side effect of acyl ghrelin administration in some human studies. The objective of this clinical trial was to investigate the direct effects of acyl ghrelin on thirst sensation and sodium excretion in hypopituitary patients. Design Hypopituitary patients on stable replacement with hydrocortisone and growth hormone were investigated in two double-blind and placebo-controlled crossover studies. The patients received a 5-h intravenous infusion of acyl ghrelin (5 pmol/kg/min in the first study and 1 pmol/kg/min in the second study). Thirst sensation was measured on a Visual Analog Scale (VAS). In the second study plasma osmolality, vasopressin, copeptin, water intake, diuresis and urinary excretion of sodium and creatinine were measured. Results In the initial study, acyl ghrelin (5 pmol/kg/min) increased thirst sensation (time × treatment analysis of variance for the effect of acyl ghrelin infusion P = 0.003). In the second study acyl ghrelin (1 pmol/kg/min) also increased thirst (P = 0.04) but did not affect urinary excretion of either sodium or water. Conclusions We demonstrate that acyl ghrelin infusion increases thirst sensation, without affecting sodium excretion or diuresis in human subjects.

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 Des-Acyl Ghrelin Induces Food Intake by a Mechanism Independent of the Growth Hormone Secretagogue Receptor

Endocrinology ◽  
2006 ◽  
Vol 147 (5) ◽  
pp. 2306-2314 ◽  
Author(s):  
Koji Toshinai ◽  
Hideki Yamaguchi ◽  
Yuxiang Sun ◽  
Roy G. Smith ◽  
Akihiro Yamanaka ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Food Intake ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Acyl Ghrelin

scholarly journals Metabolic and Cardiovascular Effects of Ghrelin

2010 ◽  
Vol 2010 ◽  
pp. 1-7 ◽  
Author(s):  
Manfredi Tesauro ◽  
Francesca Schinzari ◽  
Miriam Caramanti ◽  
Renato Lauro ◽  
Carmine Cardillo
Keyword(s):  
Nitric Oxide ◽  
Growth Hormone ◽  
Cardiovascular Effects ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Amino Acid Peptide

Ghrelin, an endogenous ligand for the growth hormone secretagogue receptor, is synthesized as a preprohormone and then proteolytically processed to yield a 28-amino acid peptide. This peptide was originally reported to induce growth hormone release; large evidence, however, has indicated many other physiological activities of ghrelin, including regulation of food intake and energy balance, as well as of lipid and glucose metabolism. Ghrelin receptors have been detected in the hypothalamus and the pituitary, but also in the cardiovascular system, where ghrelin exerts beneficial hemodynamic activities. Ghrelin administration acutely improves endothelial dysfunction by increasing nitric oxide bioavailability and normalizes the altered balance between endothelin-1 and nitric oxide within the vasculature of patients with metabolic syndrome. Other cardiovascular effects of ghrelin include improvement of left ventricular contractility and cardiac output, as well as reduction of arterial pressure and systemic vascular resistance. In addition, antinflammatory and antiapoptotic actions of ghrelin have been reported both in vivo and in vitro. This review summarizes the most recent findings on the metabolic and cardiovascular effects of ghrelin through GH-dependent and -independent mechanisms and the possible role of ghrelin as a therapeutic molecule for treating cardiovascular diseases.

scholarly journals Growth hormone secretagogue receptor in dopamine neurons controls appetitive and consummatory behaviors towards high-fat diet in ad-libitum fed mice

2020 ◽  
Vol 119 ◽  
pp. 104718
Author(s):  
María Paula Cornejo ◽  
Franco Barrile ◽  
Daniela Cassano ◽  
Julieta Paola Aguggia ◽  
Guadalupe García Romero ◽  
...  
Keyword(s):  
Growth Hormone ◽  
High Fat Diet ◽  
Dopamine Neurons ◽  
High Fat ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Ad Libitum
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