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      Differences in the Appetite-Stimulating Effect of Orexin, Neuropeptide Y and Ghrelin among Young, Adult and Old Rats

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          Abstract

          Aging is associated with a progressive decrease in appetite and food intake. The appetite-stimulating peptides orexin A, neuropeptide Y (NPY) and ghrelin are known to play a critical role in food intake. In this study, the stimulatory effect of intracerebroventricular administration of these peptides on food intake was compared among young (4 months old), adult (11 months old) and old (24–27 months old) male Wistar rats. A stainless steel cannula was implanted stereotactically into the left lateral ventricle. After a 7-day recovery period, different doses of orexin A (0.25–3 nmol), NPY and ghrelin (0.03–1 nmol) were injected into the left lateral ventricle without anesthesia. Food consumption was measured at 1, 2 and 4 h after injection. We also examined the plasma levels of acylated and desacyl ghrelin in young and old rats by ELISA. Intracerebroventricular administration of orexin A and NPY stimulated food intake in young and adult rats, but no effects were observed at any dose in old rats. Ghrelin increased food intake in a dose-dependent manner in all groups, and the effect of ghrelin was reduced with advancing age. Neither the acylated nor the desacyl plasma ghrelin level differed significantly between young and old rats. In conclusion, the orexigenic effect of the peptides orexin A, NPY and ghrelin decreased in old rats, and this reduction may have been responsible for the age-related decrease in food intake.

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          Most cited references 15

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          Orexins and Orexin Receptors: A Family of Hypothalamic Neuropeptides and G Protein-Coupled Receptors that Regulate Feeding Behavior

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            Neuropeptide Y--a novel brain peptide with structural similarities to peptide YY and pancreatic polypeptide.

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              Ghrelin, an endogenous growth hormone secretagogue, is a novel orexigenic peptide that antagonizes leptin action through the activation of hypothalamic neuropeptide Y/Y1 receptor pathway.

              Ghrelin, an endogenous ligand for growth hormone secretagogue (GHS) receptor originally isolated from the stomach, occurs in the hypothalamic arcuate nucleus and may play a role in energy homeostasis. Synthetic GHSs have activated the hypothalamic arcuate neurons containing neuropeptide Y (NPY), suggesting the involvement of NPY in some of ghrelin actions. This study was designed to elucidate the role of ghrelin in the regulation of food intake. A single intracerebroventricular (ICV) injection of ghrelin (5-5,000 ng/rat) caused a significant and dose-related increase in cumulative food intake in rats. Ghrelin (500 ng/rat) was also effective in growth hormone-deficient spontaneous dwarf rats. Hypothalamic NPY mRNA expression was increased in rats that received a single ICV injection of ghrelin (500 ng/rat) (approximately 160% of that in vehicle-treated groups, P < 0.05). The ghrelin's orexigenic effect was abolished dose-dependently by ICV co-injection of NPY Y1 receptor antagonist (10-30 microg/rat). The leptin-induced inhibition of food intake was reversed by ICV co-injection of ghrelin in a dose-dependent manner (5-500 ng/rat). Leptin reduced hypothalamic NPY mRNA expression by 35% (P < 0.05), which was abolished by ICV co-injection of ghrelin (500 ng/rat). This study provides evidence that ghrelin is an orexigenic peptide that antagonizes leptin action through the activation of hypothalamic NPY/Y1 receptor pathway.
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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2005
                May 2006
                31 May 2006
                : 82
                : 5-6
                : 256-263
                Affiliations
                Department of Clinical Physiology, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan
                Article
                92754 Neuroendocrinology 2005;82:256–263
                10.1159/000092754
                16721031
                © 2005 S. Karger AG, Basel

                Copyright: All rights reserved. No part of this publication may be translated into other languages, reproduced or utilized in any form or by any means, electronic or mechanical, including photocopying, recording, microcopying, or by any information storage and retrieval system, without permission in writing from the publisher. Drug Dosage: The authors and the publisher have exerted every effort to ensure that drug selection and dosage set forth in this text are in accord with current recommendations and practice at the time of publication. However, in view of ongoing research, changes in government regulations, and the constant flow of information relating to drug therapy and drug reactions, the reader is urged to check the package insert for each drug for any changes in indications and dosage and for added warnings and precautions. This is particularly important when the recommended agent is a new and/or infrequently employed drug. Disclaimer: The statements, opinions and data contained in this publication are solely those of the individual authors and contributors and not of the publishers and the editor(s). The appearance of advertisements or/and product references in the publication is not a warranty, endorsement, or approval of the products or services advertised or of their effectiveness, quality or safety. The publisher and the editor(s) disclaim responsibility for any injury to persons or property resulting from any ideas, methods, instructions or products referred to in the content or advertisements.

                Page count
                Figures: 4, References: 31, Pages: 8
                Categories
                Original Paper

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