TY - JOUR
T1 - Inhibitory effect of ghrelin on food intake is mediated by the corticotropin-releasing factor system in neonatal chicks
AU - Saito, Ei Suke
AU - Kaiya, Hiroyuki
AU - Tachibana, Tetsuya
AU - Tomonaga, Shozo
AU - Denbow, D. Michel
AU - Kangawa, Kenji
AU - Furuse, Mitsuhiro
N1 - Funding Information:
This study was supported by a Grant-in-Aid for Scientific Research from Japan Society for the Promotion of Science, and in part by a Grant-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan. We are grateful to Yasuo Kitajima, Masaru Matsumoto, Yoshiharu Minamitake at the Daiichi Suntory Pharma, Institute for Medicinal Research and Development, Gunma, Japan for synthesizing chicken ghrelin.
PY - 2005/2/15
Y1 - 2005/2/15
N2 - It is known that, in rats, central and peripheral ghrelin increases food intake mainly through activation of neuropeptide Y (NPY) neurons. In contrast, intracerebroventricular (ICV) injection of ghrelin inhibits food intake in neonatal chicks. We examined the mechanism governing this inhibitory effect in chicks. The ICV injection of ghrelin or corticotropin-releasing factor (CRF), which also inhibits feeding and causes hyperactivity in chicks. Thus, we examined the interaction of ghrelin with CRF and the hypothalamo-pituitary- adrenal (HPA) axis. The ICV injection of ghrelin increased plasma corticosterone levels in a dose-dependent or a time-dependent manner. Co-injection of a CRF receptor antagonist, astressin, attenuated ghrelin-induced plasma corticosterone increase and anorexia. In addition, we also investigated the effect of ghrelin on NPY-induced food intake and on expression of hypothalamic NPY mRNA. Co-injection of ghrelin with NPY inhibited NPY-induced increase in food intake, and the ICV injection of ghrelin did not change NPY mRNA expression. These results indicate that central ghrelin does not interact with NPY as seen in rodents, but instead inhibits food intake by interacting with the endogenous CRF and its receptor.
AB - It is known that, in rats, central and peripheral ghrelin increases food intake mainly through activation of neuropeptide Y (NPY) neurons. In contrast, intracerebroventricular (ICV) injection of ghrelin inhibits food intake in neonatal chicks. We examined the mechanism governing this inhibitory effect in chicks. The ICV injection of ghrelin or corticotropin-releasing factor (CRF), which also inhibits feeding and causes hyperactivity in chicks. Thus, we examined the interaction of ghrelin with CRF and the hypothalamo-pituitary- adrenal (HPA) axis. The ICV injection of ghrelin increased plasma corticosterone levels in a dose-dependent or a time-dependent manner. Co-injection of a CRF receptor antagonist, astressin, attenuated ghrelin-induced plasma corticosterone increase and anorexia. In addition, we also investigated the effect of ghrelin on NPY-induced food intake and on expression of hypothalamic NPY mRNA. Co-injection of ghrelin with NPY inhibited NPY-induced increase in food intake, and the ICV injection of ghrelin did not change NPY mRNA expression. These results indicate that central ghrelin does not interact with NPY as seen in rodents, but instead inhibits food intake by interacting with the endogenous CRF and its receptor.
UR - http://www.scopus.com/inward/record.url?scp=9944264980&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=9944264980&partnerID=8YFLogxK
U2 - 10.1016/j.regpep.2004.09.003
DO - 10.1016/j.regpep.2004.09.003
M3 - Article
C2 - 15582733
AN - SCOPUS:9944264980
SN - 0167-0115
VL - 125
SP - 201
EP - 208
JO - Regulatory Peptides
JF - Regulatory Peptides
IS - 1-3
ER -