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      Regulation of Food Intake by Inflammatory Cytokines in the Brain

      review-article
      Author(s): a , a, b
      Publication date (Electronic):
      Journal: Neuroendocrinology
      Publisher: S. Karger AG
      Keywords: Hypothalamus, Inflammatory cytokines, Feeding, Cachexia

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          Abstract

          A number of inflammatory cytokines are synthesized and released after activation of the immune system. In addition to other biological effects, these cytokines can potently inhibit food intake. Cytokine-mediated inhibition of food intake is of particular importance because excessive production of peripheral inflammatory cytokines is often associated with the cachexia-anorexia syndrome seen in some chronic diseases. The weight loss in cachexia is associated with an increase in morbidity and mortality. Understanding how cytokines regulate food intake may be crucial in enhancing quality of life and facilitating recovery in patients exhibiting cachexia. This review describes the main inflammatory cytokines that influence food intake and explores how peripheral cytokines communicate with hypothalamic nuclei to influence feeding.

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          Interleukin-6-deficient mice develop mature-onset obesity.

          Ville Wallenius, Kristina Wallenius, Bo Ahrén … (2002)
          The immune-modulating cytokine interleukin-6 (IL-6) is expressed both in adipose tissue and centrally in hypothalamic nuclei that regulate body composition. We investigated the impact of loss of IL-6 on body composition in mice lacking the gene encoding IL-6 (Il6-/- mice) and found that they developed mature-onset obesity that was partly reversed by IL-6 replacement. The obese Il6-/- mice had disturbed carbohydrate and lipid metabolism, increased leptin levels and decreased responsiveness to leptin treatment. To investigate the possible mechanism and site of action of the anti-obesity effect of IL-6, we injected rats centrally and peripherally with IL-6 at low doses. Intracerebroventricular, but not intraperitoneal IL-6 treatment increased energy expenditure. In conclusion, centrally acting IL-6 exerts anti-obesity effects in rodents.
          Article 0 comments Cited 288 times – based on 0 reviews     Review now
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            Neurogenesis in the hypothalamus of adult mice: potential role in energy balance.

            Maia V Kokoeva, Huali Yin, Jeffrey Flier (2005)
            Ciliary neurotrophic factor (CNTF) induces weight loss in obese rodents and humans, and for reasons that are not understood, its effects persist after the cessation of treatment. Here we demonstrate that centrally administered CNTF induces cell proliferation in feeding centers of the murine hypothalamus. Many of the newborn cells express neuronal markers and show functional phenotypes relevant for energy-balance control, including a capacity for leptin-induced phosphorylation of signal transducer and activator of transcription 3 (STAT3). Coadministration of the mitotic blocker cytosine-beta-d-arabinofuranoside (Ara-C) eliminates the proliferation of neural cells and abrogates the long-term, but not the short-term, effect of CNTF on body weight. These findings link the sustained effect of CNTF on energy balance to hypothalamic neurogenesis and suggest that regulated hypothalamic neurogenesis in adult mice may play a previously unappreciated role in physiology and disease.
            Article 0 comments Cited 169 times – based on 0 reviews     Review now
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              Deficiency of interleukin-18 in mice leads to hyperphagia, obesity and insulin resistance.

              Mihai Netea, Ki Kim, M. Baak … (2006)
              Here we report the presence of hyperphagia, obesity and insulin resistance in knockout mice deficient in IL-18 or IL-18 receptor, and in mice transgenic for expression of IL-18 binding protein. Obesity of Il18-/- mice resulted from accumulation of fat tissue based on increased food intake. Il18-/- mice also had hyperinsulinemia, consistent with insulin resistance and hyperglycemia. Insulin resistance was secondary to obesity induced by increased food intake and occurred at the liver level as well as at the muscle and fat-tissue level. The molecular mechanisms responsible for the hepatic insulin resistance in the Il18-/- mice involved an enhanced expression of genes associated with gluconeogenesis in the liver of Il18-/- mice, resulting from defective phosphorylation of STAT3. Recombinant IL-18 (rIL-18) administered intracerebrally inhibited food intake. In addition, rIL-18 reversed hyperglycemia in Il18-/- mice through activation of STAT3 phosphorylation. These findings indicate a new role of IL-18 in the homeostasis of energy intake and insulin sensitivity.
              Article 0 comments Cited 124 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (publisher-id): NEN
                Journal ID (nlm-ta): Neuroendocrinology
                Journal ID (doi): 10.1159/issn.0028-3835
                Title: Neuroendocrinology
                Publisher: S. Karger AG
                ISBN: 978-3-8055-8457-9
                ISBN: 978-3-8055-8458-6
                ISSN (Print): 0028-3835
                ISSN (Electronic): 1423-0194
                Publication date Subscription-year: 2007
                Publication date (Print): November 2007
                Publication date (Electronic): 07 September 2007
                Volume: 86
                Issue: 3
                Pages: 183-190
                Affiliations
                aLaboratory of Integrative Immunology and Behaviour, Division of Nutritional Sciences and bDepartment of Animal Sciences, University of Illinois Urbana-Champaign, Urbana, Ill., USA
                Article
                Publisher ID: 108280 Other ID: Neuroendocrinology 2007;86:183–190
                DOI: 10.1159/000108280
                PubMed ID: 17823502
                SO-VID: e16424fe-1274-4eb4-970e-9d5544f8f256
                Copyright © © 2007 S. Karger AG, Basel
                License:

                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.

                History
                Page count
                Figures: 1, Tables: 1, References: 103, Pages: 8
                Categories
                Subject: Paper

                ScienceOpen disciplines: Endocrinology & Diabetes,Neurology,Nutrition & Dietetics,Sexual medicine,Internal medicine,Pharmacology & Pharmaceutical medicine
                Keywords: Feeding,Inflammatory cytokines,Hypothalamus,Cachexia
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes, Neurology, Nutrition & Dietetics, Sexual medicine, Internal medicine, Pharmacology & Pharmaceutical medicine
                Keywords: Feeding, Inflammatory cytokines, Hypothalamus, Cachexia

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