Ghrelin Gene Products and the Regulation of Food Intake and Gut Motility

2009 ◽  
Vol 61 (4) ◽  
pp. 430-481 ◽  
Author(s):  
Chih-Yen Chen ◽  
Akihiro Asakawa ◽  
Mineko Fujimiya ◽  
Shou-Dong Lee ◽  
Akio Inui
Keyword(s):  
Food Intake ◽  
Gene Products ◽  
Gut Motility ◽  
Ghrelin Gene

At the Cutting Edge: Ghrelin Gene Products in Food Intake and Gut Motility

2008 ◽  
Vol 89 (1) ◽  
pp. 9-17 ◽  
Author(s):  
Chih-Yen Chen ◽  
Mineko Fujimiya ◽  
Akihiro Asakawa ◽  
Full-Young Chang ◽  
Juei-Tang Cheng ◽  
...  
Keyword(s):  
Food Intake ◽  
Cutting Edge ◽  
Gene Products ◽  
Gut Motility ◽  
Ghrelin Gene

scholarly journals Ghrelin gene products rescue cultured adult rat hippocampal neural stem cells from high glucose insult

2016 ◽  
Vol 57 (3) ◽  
pp. 171-184 ◽  
Author(s):  
Sehee Kim ◽  
Chanyang Kim ◽  
Seungjoon Park
Keyword(s):  
Stem Cells ◽  
Neural Stem Cells ◽  
High Glucose ◽  
Hippocampal Neurogenesis ◽  
Adult Hippocampal Neurogenesis ◽  
Gene Products ◽  
Growth Hormone Secretagogue ◽  
Phosphohistone H3 ◽  
Ghrelin Gene ◽  
Hippocampal Neural Stem Cells

Adult hippocampal neurogenesis is decreased in type 2 diabetes, and this impairment appears to be important in cognitive dysfunction. Previous studies suggest that ghrelin gene products (acylated ghrelin (AG), unacylated ghrelin (UAG) and obestatin (OB)) promote neurogenesis. Therefore, we hypothesize that ghrelin gene products may reduce the harmful effects of high glucose (HG) on hippocampal neural stem cells (NSCs). The aim of this study was to investigate the role of these peptides on the survival of cultured hippocampal NSCs exposed to HG insult. Treatment of hippocampal NSCs with AG, UAG or OB inhibited HG-induced cell death and apoptosis. Exposure of cells to the growth hormone secretagogue receptor 1a antagonist abolished the protective effects of AG against HG toxicity, whereas those of UAG or OB were preserved. All three peptides attenuated HG-induced decrease in BrdU-labeled and phosphohistone-H3-labeled cells. We also investigated the effects of ghrelin gene products on the regulation of apoptosis at the mitochondrial level. AG, UAG or OB rescued hippocampal NSCs from HG insult by inhibiting intracellular and mitochondrial reactive oxygen species generation and stabilizing mitochondrial transmembrane potential. In addition, cells treated with ghrelin gene products showed an increased Bcl-2 and decreased Bax levels, thereby increasing the Bcl-2/Bax ratio, inhibiting cytochrome c release and preventing caspase-3 activation. Finally, AG-, UAG- or OB-mediated protection was dependent on the activities of adenosine monophosphate-activated protein kinase/uncoupling protein 2 pathway. Our data indicate that ghrelin gene products may act as survival factors that preserve mitochondrial function and inhibit oxidative stress-induced apoptosis.

Neuroendocrine and metabolic activities of ghrelin gene products

Peptides ◽  
2011 ◽  
Vol 32 (11) ◽  
pp. 2323-2332 ◽  
Author(s):  
Alessandra Baragli ◽  
Fabio Lanfranco ◽  
Stefano Allasia ◽  
Riccarda Granata ◽  
Ezio Ghigo
Keyword(s):  
Gene Products ◽  
Ghrelin Gene ◽  
Metabolic Activities

Somatostatin administration modifies food intake, body weight, and gut motility in rat

Peptides ◽  
1998 ◽  
Vol 19 (6) ◽  
pp. 991-997 ◽  
Author(s):  
Giuseppe Scalera ◽  
Giorgio Tarozzi
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Gut Motility

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.

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