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Tang-Christensen, M.* ; Vrang, N.* ; Ortmann, S.* ; Bidlingmaier, M.* ; Horvath, T.L.* ; Tschöp, M.H.

Central administration of ghrelin and agouti-related protein (83-132) increases food intake and decreases spontaneous locomotor activity in rats.

Endocrinology 145, 4645-4652 (2004)
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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 microg) 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.
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Publication type Article: Journal article
Document type Scientific Article
Language english
Publication Year 2004
HGF-reported in Year 2004
ISSN (print) / ISBN 0013-7227
e-ISSN 1945-7170
Journal Endocrinology
Quellenangaben Volume: 145, Issue: 10, Pages: 4645-4652 Article Number: , Supplement: ,
Publisher Endocrine Society
Publishing Place Chevy Chase, Md.
Reviewing status Peer reviewed
PubMed ID 15231700
Erfassungsdatum 2020-02-20