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      Effects of Galanin-Like Peptide on Food Intake and the Hypothalamo-Pituitary-Thyroid Axis

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          Abstract

          Galanin-like peptide (GALP) is a novel hypothalamic peptide synthesised in neurons in the arcuate nucleus which project to the paraventricular nucleus (PVN). GALP has recently been identified as an orexigenic peptide. In this study we aimed to further characterise the hypothalamic action of this peptide in energy homeostasis. Firstly, we investigated the orexigenic effect of GALP in the PVN and compared its effects with galanin and galanin 2–29. Secondly, we examined the effect of PVN administration of GALP and galanin on circulating thyroid-stimulating hormone (TSH). PVN administration of GALP significantly increased the food intake of satiated rats 1 h after administration at doses of 0.3, 1 and 3 nmol. In comparison with paraventricular administration of galanin, GALP was a more potent orexigen, whereas galanin 2–29, the relatively selective GAL R2 agonist, had no effect on food intake. Both GALP and galanin administration (1 nmol) into the PVN significantly decreased the level of circulating TSH. To investigate the mechanism of these effects, we examined the effect of GALP and galanin application on neuropeptide release from hypothalamic explants in vitro. GALP peptide (100 n M) stimulated the release of the orexigenic peptide neuropeptide Y from hypothalamic explants and decreased the release of the anorectic peptide cocaine-and-amphetamine-regulated transcript, whereas galanin (100 n M) peptide had no significant effect on the release of either peptide. Both GALP (100 n M) and galanin (100 n M) inhibited the release thyrotrophin-releasing hormone. These data suggest that in the PVN, GALP may play a role in energy homeostasis by stimulating food intake and suppressing TSH release.

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          Most cited references 7

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          Mice lacking melanin-concentrating hormone are hypophagic and lean.

          Feeding is influenced by hypothalamic neuropeptides that promote (orexigenic peptides) or inhibit feeding. Of these, neuropeptide Y (NPY) in the arcuate nucleus and melanin-concentrating hormone (MCH) and orexins/hypocretins in the lateral hypothalamus have received attention because their expression is increased during fasting and because they promote feeding when administered centrally. Surprisingly, absence of the orexigenic neuropeptide NPY fails to alter feeding or body weight in normal mice. As deficiency of a single component of the pathway that limits food intake (such as leptin or receptors for melanocortin-4) causes obesity, it has been suggested that orexigenic signals are more redundant than those limiting food intake. To define further the physiological role of MCH and to test the redundancy of orexigenic signals, we generated mice carrying a targeted deletion of the MCH gene. MCH-deficient mice have reduced body weight and leanness due to hypophagia (reduced feeding) and an inappropriately increased metabolic rate, despite their reduced amounts of both leptin and arcuate nucleus pro-opiomelanocortin messenger RNA. Our results show that MCH is a critical regulator of feeding and energy balance which acts downstream of leptin and the melanocortin system, and that deletion of a gene encoding a single orexigenic peptide can result in leanness.
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            CART peptides in the central control of feeding and interactions with neuropeptide Y.

            While CART peptides have been implicated as novel, putative peptide neurotransmitters/cotransmitters, behavioral effects of these peptides have not yet been demonstrated. In this study, we show the first behavioral effect of CART peptides. I.c.v. administration of CART peptide fragments inhibits feeding in rats. Moreover, injection of an antibody to CART peptide 82-103 stimulates feeding, suggesting that endogenous CART peptides exert an inhibitory tone on feeding. Injection of CART peptide 82-103 five min before NPY reduces the increase in feeding caused by injection of NPY alone. Also, in light microscopic immunohistochemical studies, NPY-positive varicosities were observed around CART peptide-positive cell bodies in the paraventricular nucleus of the hypothalamus. These data suggest functional interactions between CART peptides and NPY. These results indicate that CART peptides play a role in the control of food intake by the brain.
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              Isolation and cDNA cloning of a novel galanin-like peptide (GALP) from porcine hypothalamus.

               H Onda,  S Kumano,  T Kurokawa (1999)
              Galanin is a widely distributed neuropeptide with a variety of physiological functions. Three galanin receptor subtypes, GALR1, GALR2, and GALR3, have been reported. We isolated a novel galanin-like peptide (GALP) from porcine hypothalamus by observing its activity for increasing [(35)S]GTPgammaS binding to a membrane preparation of GALR2-transfected cells. The peptide had 60 amino acid residues and a non-amidated C terminus. The amino acid sequence of GALP-(9-21) was completely identical to that of galanin-(1-13). A cloned porcine GALP cDNA indicated that GALP was processed from a 120-amino acid GALP precursor protein. The structures of rat and human GALP-(1-60) were deduced from cloned cDNA, which indicated that the amino acid sequences 1-24 and 41-53 were highly conserved between humans, rats, and pigs. Receptor binding studies revealed that porcine GALP-(1-60) had a high affinity for the GALR2 receptor (IC(50) = 0.24 nM) and a lower affinity for the GALR1 receptor (IC(50) = 4.3 nM). In contrast, galanin showed high affinity for the GALR1 (IC(50) = 0.097 nM) and GALR2 receptors (IC(50) = 0.48 nM). GALP is therefore an endogenous ligand that preferentially binds the GALR2 receptor, whereas galanin is relatively non-selective.
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                Author and article information

                Journal
                NEN
                Neuroendocrinology
                10.1159/issn.0028-3835
                Neuroendocrinology
                S. Karger AG
                0028-3835
                1423-0194
                2003
                February 2003
                10 March 2003
                : 77
                : 2
                : 125-131
                Affiliations
                Division of Metabolic Medicine, Faculty of Medicine, Imperial College of Science Technology and Medicine, Hammersmith Campus, London, UK
                Article
                68648 Neuroendocrinology 2003;77:125–131
                10.1159/000068648
                12624534
                © 2003 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: 3, References: 33, Pages: 7
                Categories
                Behavioural Neuroendocrinology

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