scholarly journals Agouti-Related Protein Segments Outside of the Receptor Binding Core Are Required for Enhanced Short- and Long-term Feeding Stimulation

2011 ◽  
Vol 7 (2) ◽  
pp. 395-402 ◽  
Author(s):  
Michael E. Madonna ◽  
Jennifer Schurdak ◽  
Ying-kui Yang ◽  
Stephen Benoit ◽  
Glenn L. Millhauser
animal ◽  
2016 ◽  
Vol 10 (7) ◽  
pp. 1182-1191 ◽  
Author(s):  
I.M. Aparicio ◽  
P. Martin Muñoz ◽  
G.M. Salido ◽  
F.J. Peña ◽  
J.A. Tapia

Biochemistry ◽  
2001 ◽  
Vol 40 (51) ◽  
pp. 15520-15527 ◽  
Author(s):  
Joseph C. McNulty ◽  
Darren A. Thompson ◽  
Kimberly A. Bolin ◽  
Jill Wilken ◽  
Gregory S. Barsh ◽  
...  

Pharmacology ◽  
2017 ◽  
Vol 100 (3-4) ◽  
pp. 153-160 ◽  
Author(s):  
Unbin Chae ◽  
Ju-Sik Min ◽  
Hyun Hee Leem ◽  
Hyun-Shik Lee ◽  
Hong Jun Lee ◽  
...  

Chrysophanic acid, or chrysophanol, is an anthraquinone found in Rheum palmatum, which was used in the preparation of oriental medicine in ancient China. The hippocampus plays a major role in controlling the activities of the short- and long-term memory. It is one of the major regions affected by excessive cell death in Alzheimer's disease. Therefore, neuronal cell-death modulation in the hippocampus is important for maintaining neuronal function. We investigated chrysophanol's effects on glutamate-induced hippocampal neuronal cell death. Chrysophanol reduced glutamate-induced cell death via suppression of proapoptotic factors and reactive oxygen species generation. Furthermore, it downregulated glutamate-induced mitochondrial fission by inhibiting dynamin-related protein 1 (Drp1) dephosphorylation. Thus, chrysophanol suppressed hippocampal neuronal cell death via inhibition of Drp1-dependent mitochondrial fission, and can be used as a therapeutic agent for treating neuronal cell death-mediated neurodegenerative diseases.


Endocrinology ◽  
2004 ◽  
Vol 145 (10) ◽  
pp. 4645-4652 ◽  
Author(s):  
Mads Tang-Christensen ◽  
Niels Vrang ◽  
Sylvia Ortmann ◽  
Martin Bidlingmaier ◽  
Tamas L. Horvath ◽  
...  

Abstract Ghrelin was recently identified as an endogenous ligand of the GH secretagogue receptor. The novel peptide hormone is produced by gastric A-like cells, and circulating levels rise before feeding, suggestive of ghrelin as an endogenous hunger factor. ghrelin stimulates food intake and promotes adiposity after peripheral or central administration, likely by activating hypothalamic neurons expressing the orexigenic neuropeptides neuropeptide Y (NPY) and agouti-related protein (AGRP). To examine whether ghrelin-induced feeding resembles NPY and AGRP [AGRP fragment (83–132)] induced orexia, we compared the short- and long-term orexigenic capacity of the three peptides. A single intracerebroventricular injection of ghrelin (0.2, 1.0, and 5.0 μg) increased food intake in a dose-dependent manner. A prolonged and uncompensated increase in feeding was seen after the highest dose of ghrelin. The prolonged effects on feeding (+72 h) closely resembled those of AGRP (83–132) but not NPY. Surprisingly, ghrelin injections reduced overall locomotor activity by 20% during the first 24-h observation period. AGRP (83–132) had similar effects on locomotor behavior, whereas NPY had no effect. In summary, ghrelin causes long-term increases of food intake and, like AGRP, plays a previously unknown role as a suppressor of spontaneous physical activity. Expanding the current model of food intake control to include mechanisms regulating physical activity may promote our understanding of two major etiological factors causing obesity.


Neuroreport ◽  
2001 ◽  
Vol 12 (6) ◽  
pp. 1281-1284 ◽  
Author(s):  
Xin-Yun Lu ◽  
Janet R. Nicholson ◽  
Huda Akil ◽  
Stanley J. Watson

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