Growth hormone secretagogue receptor signalling affects high‐fat intake independently of plasma levels of ghrelin and LEAP 2, in a 4‐day binge eating model

2019 ◽  
Vol 31 (10) ◽  
Author(s):  
María Paula Cornejo ◽  
Daniel Castrogiovanni ◽  
Helgi B. Schiöth ◽  
Mirta Reynaldo ◽  
Jacky Marie ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Binge Eating ◽  
Plasma Levels ◽  
Fat Intake ◽  
High Fat ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Receptor Signalling

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

Sleep enhances nocturnal plasma ghrelin levels in healthy subjects

2004 ◽  
Vol 286 (6) ◽  
pp. E963-E967 ◽  
Author(s):  
Andrea Dzaja ◽  
Mira A. Dalal ◽  
Hubertus Himmerich ◽  
Manfred Uhr ◽  
Thomas Pollmächer ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Sleep Deprivation ◽  
Plasma Levels ◽  
Slow Wave Sleep ◽  
Sleep Stages ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Nocturnal Increase ◽  
Ghrelin Secretion

Ghrelin, an endogenous ligand of the growth hormone secretagogue receptor, has been shown to promote slow-wave sleep (SWS, non-REM sleep stages 3 and 4). Plasma levels of ghrelin are dependent on food intake and increase in sleeping subjects during the early part of the night. It is unknown whether sleep itself affects ghrelin levels or whether circadian networks are involved. Therefore, we studied the effect of sleep deprivation on nocturnal ghrelin secretion. In healthy male volunteers, plasma levels of ghrelin, cortisol, and human growth hormone (hGH) were measured during two experimental sessions of 24 h each: once when the subjects were allowed to sleep between 2300 and 0700 and once when they were kept awake throughout the night. During sleep, ghrelin levels increased during the early part of the night and decreased in the morning. This nocturnal increase was blunted during sleep deprivation, and ghrelin levels increased only slightly until the early morning. Ghrelin secretion during the first hours of sleep correlated positively with peak hGH concentrations. We conclude that the nocturnal increase in ghrelin levels is more likely to be caused by sleep-associated processes than by circadian influences. During the first hours of sleep, ghrelin might promote sleep-associated hGH secretion and contribute to the promotion of SWS.

scholarly journals Estradiol Replacement Improves High-Fat Diet-Induced Obesity by Suppressing the Action of Ghrelin in Ovariectomized Rats

Nutrients ◽  
2020 ◽  
Vol 12 (4) ◽  
pp. 907
Author(s):  
Naoko Yokota-Nakagi ◽  
Haruka Takahashi ◽  
Mizuho Kawakami ◽  
Akira Takamata ◽  
Yuki Uchida ◽  
...  
Keyword(s):  
Growth Hormone ◽  
High Fat Diet ◽  
Ovariectomized Rats ◽  
Mrna Levels ◽  
High Fat ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue ◽  
Protein Levels ◽  
Ovx Rats ◽  
Hypothalamic Arcuate Nucleus

This study aims to investigate the effects of estradiol replacement on the orexigenic action of ghrelin in ovariectomized (OVX) obese rats fed with a high-fat diet (HFD). Four weeks after OVX at 9 weeks of age, Wistar rats were subcutaneously implanted with either 17β-estradiol (E2) or placebo (Pla) pellets and started on HFD feeding. After 4 weeks, growth hormone-releasing peptide (GHRP)-6, a growth hormone secretagogue receptor (GHSR) agonist injected intraperitoneally, induced changes in HFD intake, and c-Fos-positive neurons in the hypothalamic arcuate nucleus (ARC) were measured in both groups. The ghrelin protein and mRNA levels, as well as GHSR protein in stomach, were analyzed by Western blotting and real-time PCR. HFD increased energy intake and body weight in the Pla group, while it temporarily reduced these in the E2 group. GHRP-6 enhanced HFD intake and activated neurons in the ARC only in the Pla group. Furthermore, gastric ghrelin and GHSR protein levels were lower in the E2 group than in the Pla group, but plasma acyl ghrelin levels were similar in both groups. Our results suggest that E2 replacement improves obesity by inhibiting the orexigenic action of ghrelin via downregulation of ghrelin and its receptor in stomach in HFD-fed OVX rats.

scholarly journals The Ghrelin/Growth Hormone Secretagogue Receptor System Is Involved in the Rapid and Sustained Antidepressant-Like Effect of Paeoniflorin

2021 ◽  
Vol 15 ◽  
Author(s):  
Yuan Zhang ◽  
Min-Zhen Zhu ◽  
Xi-He Qin ◽  
Yuan-Ning Zeng ◽  
Xin-Hong Zhu
Keyword(s):  
Growth Hormone ◽  
Plasma Levels ◽  
Antidepressant Drugs ◽  
Chronic Mild Stress ◽  
Mild Stress ◽  
Growth Hormone Secretagogue Receptor ◽  
Receptor System ◽  
Growth Hormone Secretagogue ◽  
Sustained Effects ◽  
Total Ghrelin

Major depressive disorder (MDD) is a debilitating mental illness affecting people worldwide. Although significant progress has been made in the development of therapeutic agents to treat this condition, fewer than half of all patients respond to currently available antidepressants, highlighting the urgent need for the development of new classes of antidepressant drugs. Here, we found that paeoniflorin (PF) produced rapid and sustained antidepressant-like effects in multiple mouse models of depression, including the forced swimming test and exposure to chronic mild stress (CMS). Moreover, PF decreased the bodyweight of mice without affecting food intake and glucose homeostasis, and also reduced the plasma levels of total ghrelin and the expression of ghrelin O-acyltransferase in the stomach; however, the plasma levels of ghrelin and the ghrelin/total ghrelin ratio were unaffected. Furthermore, PF significantly increased the expression of growth hormone secretagogue receptor 1 alpha (GHSR1α, encoded by the Ghsr gene) in the intestine, whereas the levels of GHSR1α in the brain were only marginally downregulated following subchronic PF treatment. Finally, the genetic deletion of Ghsr attenuated the antidepressant-like effects of PF in mice exposed to CMS. These results suggested that increased GHSR1α expression in the intestine mediates the antidepressant-like effects of PF. Understanding peripheral ghrelin/GHSR signaling may provide new insights for the screening of antidepressant drugs that produce fast-acting and sustained effects.

Novel Isoxazole Carboxamides as Growth Hormone Secretagogue Receptor (GHS-R) Antagonists.

ChemInform ◽  
2005 ◽  
Vol 36 (4) ◽  
Author(s):  
Bo Liu ◽  
Gang Liu ◽  
Zhili Xin ◽  
Michael D. Serby ◽  
Hongyu Zhao ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Growth Hormone Secretagogue Receptor ◽  
Growth Hormone Secretagogue

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.

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