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      Ghrelin and the central regulation of feeding and energy balance

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          Abstract

          Ghrelin was discovered in 1999 as growth hormone secretagouge released from the gut. Soon after it was recognized that ghrelin is a fundamental driver of appetite in rodents and humans and that its mode of action requires alteration of hypothalamic circuit function. Here we review aspects of ghrelin's action that revolve around the central nervous system with the goal to highlight these pathways in integrative physiology of metabolism regulation including ghrelin's cross-talk with the action of the adipose hormone, leptin.

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          Obesity and the regulation of energy balance.

          B Spiegelman, J Flier (2001)
          Article 0 comments Cited 253 times – based on 0 reviews     Review now
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            Rapid rewiring of arcuate nucleus feeding circuits by leptin.

            Shirly Pinto, Aaron Roseberry, Hongyan Liu … (2004)
            The fat-derived hormone leptin regulates energy balance in part by modulating the activity of neuropeptide Y and proopiomelanocortin neurons in the hypothalamic arcuate nucleus. To study the intrinsic activity of these neurons and their responses to leptin, we generated mice that express distinct green fluorescent proteins in these two neuronal types. Leptin-deficient (ob/ob) mice differed from wild-type mice in the numbers of excitatory and inhibitory synapses and postsynaptic currents onto neuropeptide Y and proopiomelanocortin neurons. When leptin was delivered systemically to ob/ob mice, the synaptic density rapidly normalized, an effect detectable within 6 hours, several hours before leptin's effect on food intake. These data suggest that leptin-mediated plasticity in the ob/ob hypothalamus may underlie some of the hormone's behavioral effects.
            Article 0 comments Cited 236 times – based on 0 reviews     Review now
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              UCP2 mediates ghrelin's action on NPY/AgRP neurons by lowering free radicals.

              Zane Andrews, Zhong-Wu Liu, Nicholas Walllingford … (2008)
              The gut-derived hormone ghrelin exerts its effect on the brain by regulating neuronal activity. Ghrelin-induced feeding behaviour is controlled by arcuate nucleus neurons that co-express neuropeptide Y and agouti-related protein (NPY/AgRP neurons). However, the intracellular mechanisms triggered by ghrelin to alter NPY/AgRP neuronal activity are poorly understood. Here we show that ghrelin initiates robust changes in hypothalamic mitochondrial respiration in mice that are dependent on uncoupling protein 2 (UCP2). Activation of this mitochondrial mechanism is critical for ghrelin-induced mitochondrial proliferation and electric activation of NPY/AgRP neurons, for ghrelin-triggered synaptic plasticity of pro-opiomelanocortin-expressing neurons, and for ghrelin-induced food intake. The UCP2-dependent action of ghrelin on NPY/AgRP neurons is driven by a hypothalamic fatty acid oxidation pathway involving AMPK, CPT1 and free radicals that are scavenged by UCP2. These results reveal a signalling modality connecting mitochondria-mediated effects of G-protein-coupled receptors on neuronal function and associated behaviour.
              Article 0 comments Cited 198 times – based on 0 reviews     Review now
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                Author and article information

                Journal
                Journal ID (nlm-ta): Indian J Endocrinol Metab
                Journal ID (iso-abbrev): Indian J Endocrinol Metab
                Journal ID (publisher-id): IJEM
                Title: Indian Journal of Endocrinology and Metabolism
                Publisher: Medknow Publications & Media Pvt Ltd (India )
                ISSN (Print): 2230-8210
                ISSN (Electronic): 2230-9500
                Publication date (Print): December 2012
                Volume: 16
                Issue: Suppl 3
                Pages: S617-S626
                Affiliations
                [1] Department of Neuroscience, Carlton University, Ottawa, ON, Canada
                [1 ] Program in Integrative Cell Signaling and Neurobiology of Metabolism, Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT, USA
                Author notes
                Corresponding Author: Prof. Tamas L. Horvath, BML 330, 310 Cedar St., New Haven CT 06520, USA. E-mail: tamas.horvath@ 123456yale.edu
                Article
                Publisher ID: IJEM-16-617
                DOI: 10.4103/2230-8210.105580
                PMC ID: 3602992
                PubMed ID: 23565498
                SO-VID: 8b60f3af-6f6d-4fcb-af09-574733426770
                Copyright © Copyright: © Indian Journal of Endocrinology and Metabolism
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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                Categories
                Subject: Review Article

                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: food intake,ghrelin,hypothalamus,neuropeptide y,proopiomelanocortin
                Data availability:
                ScienceOpen disciplines: Endocrinology & Diabetes
                Keywords: food intake, ghrelin, hypothalamus, neuropeptide y, proopiomelanocortin

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