Ghrelin

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Abstract

Background

The gastrointestinal peptide hormone ghrelin was discovered in 1999 as the endogenous ligand of the growth hormone secretagogue receptor. Increasing evidence supports more complicated and nuanced roles for the hormone, which go beyond the regulation of systemic energy metabolism.

Scope of review

In this review, we discuss the diverse biological functions of ghrelin, the regulation of its secretion, and address questions that still remain 15 years after its discovery.

Major conclusions

In recent years, ghrelin has been found to have a plethora of central and peripheral actions in distinct areas including learning and memory, gut motility and gastric acid secretion, sleep/wake rhythm, reward seeking behavior, taste sensation and glucose metabolism.

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Most cited references 389

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Comprehensive analysis of mRNA methylation reveals enrichment in 3' UTRs and near stop codons.

Kate D Meyer, Yogesh Saletore, Paul Zumbo … (2012)

Methylation of the N(6) position of adenosine (m(6)A) is a posttranscriptional modification of RNA with poorly understood prevalence and physiological relevance. The recent discovery that FTO, an obesity risk gene, encodes an m(6)A demethylase implicates m(6)A as an important regulator of physiological processes. Here, we present a method for transcriptome-wide m(6)A localization, which combines m(6)A-specific methylated RNA immunoprecipitation with next-generation sequencing (MeRIP-Seq). We use this method to identify mRNAs of 7,676 mammalian genes that contain m(6)A, indicating that m(6)A is a common base modification of mRNA. The m(6)A modification exhibits tissue-specific regulation and is markedly increased throughout brain development. We find that m(6)A sites are enriched near stop codons and in 3' UTRs, and we uncover an association between m(6)A residues and microRNA-binding sites within 3' UTRs. These findings provide a resource for identifying transcripts that are substrates for adenosine methylation and reveal insights into the epigenetic regulation of the mammalian transcriptome. Copyright © 2012 Elsevier Inc. All rights reserved.

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A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity.

Timothy Frayling, Nicholas J Timpson, Michael N. Weedon … (2007)

Obesity is a serious international health problem that increases the risk of several common diseases. The genetic factors predisposing to obesity are poorly understood. A genome-wide search for type 2 diabetes-susceptibility genes identified a common variant in the FTO (fat mass and obesity associated) gene that predisposes to diabetes through an effect on body mass index (BMI). An additive association of the variant with BMI was replicated in 13 cohorts with 38,759 participants. The 16% of adults who are homozygous for the risk allele weighed about 3 kilograms more and had 1.67-fold increased odds of obesity when compared with those not inheriting a risk allele. This association was observed from age 7 years upward and reflects a specific increase in fat mass.

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Ghrelin is a growth-hormone-releasing acylated peptide from stomach.

M. Kojima, H Hosoda, Y Date … (1999)

Small synthetic molecules called growth-hormone secretagogues (GHSs) stimulate the release of growth hormone (GH) from the pituitary. They act through GHS-R, a G-protein-coupled receptor for which the ligand is unknown. Recent cloning of GHS-R strongly suggests that an endogenous ligand for the receptor does exist and that there is a mechanism for regulating GH release that is distinct from its regulation by hypothalamic growth-hormone-releasing hormone (GHRH). We now report the purification and identification in rat stomach of an endogenous ligand specific for GHS-R. The purified ligand is a peptide of 28 amino acids, in which the serine 3 residue is n-octanoylated. The acylated peptide specifically releases GH both in vivo and in vitro, and O-n-octanoylation at serine 3 is essential for the activity. We designate the GH-releasing peptide 'ghrelin' (ghre is the Proto-Indo-European root of the word 'grow'). Human ghrelin is homologous to rat ghrelin apart from two amino acids. The occurrence of ghrelin in both rat and human indicates that GH release from the pituitary may be regulated not only by hypothalamic GHRH, but also by ghrelin.

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Author and article information

Contributors

M.H. Tschöp

Journal

Journal ID (nlm-ta): Mol Metab

Journal ID (iso-abbrev): Mol Metab

Title: Molecular Metabolism

Publisher: Elsevier

ISSN (Electronic): 2212-8778

Publication date PMC-release: 21 March 2015

Publication date Collection: June 2015

Publication date (Electronic): 21 March 2015

Volume: 4

Issue: 6

Pages: 437-460

Affiliations

[1 ]Institute for Diabetes and Obesity, Helmholtz Zentrum München, München, Germany

[2 ]Department of Physiology, Centro de Investigación en Medicina Molecular y Enfermedades Crónicas, University of Santiago de Compostela (CIMUS)-Instituto de Investigación Sanitaria (IDIS)-CIBER Fisiopatología de la Obesidad y Nutrición (CIBERobn), Santiago de Compostela, Spain

[3 ]Division of Endocrinology, Department of Medicine, Beth Israel Deaconess Medical Center, Boston, MA, USA

[4 ]Department of Physiology, Faculty of Medicine, Monash University, Melbourne, Victoria, Australia

[5 ]Applied Cachexia Research, Department of Cardiology, Charité Universitätsmedizin Berlin, Germany

[6 ]Department of Pediatrics and Pediatric Endocrinology, Hospital Infantil Universitario Niño Jesús, Instituto de Investigación La Princesa, Madrid, Spain

[7 ]Department of Pediatrics, Universidad Autónoma de Madrid and CIBER Fisiopatología de la obesidad y nutrición, Instituto de Salud Carlos III, Madrid, Spain

[8 ]Centre for Obesity Research, University College London, London, United Kingdom

[9 ]Metabolic Disease Institute, Division of Endocrinology, Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA

[10 ]Tulane University Health Sciences Center, Endocrinology and Metabolism Section, Peptide Research Section, New Orleans, LA, USA

[11 ]Division of Endocrinology, Diabetes and Metabolism, Dept. of Medical Sciences, University of Torino, Torino, Italy

[12 ]Department of Medicine, Santiago de Compostela University, Complejo Hospitalario Universitario de Santiago (CHUS), CIBER de Fisiopatologia Obesidad y Nutricion (CB06/03), Instituto Salud Carlos III, Santiago de Compostela, Spain

[13 ]Duke Molecular Physiology Institute, Duke University, Durham, NC, USA

[14 ]Translational Research Center for Gastrointestinal Disorders, University of Leuven, Leuven, Belgium

[15 ]New York Obesity Nutrition Research Center, Department of Medicine, St Luke's-Roosevelt Hospital Center, Columbia University College of Physicians and Surgeons, New York, NY, USA

[16 ]Department of Pharmacology & Molecular Sciences, The Johns Hopkins University School of Medicine, Baltimore, MD, USA

[17 ]Monash Obesity & Diabetes Institute, Monash University, Clayton, Victoria, Australia

[18 ]Division of Metabolism, Endocrinology and Nutrition, Department of Medicine, University of Washington School of Medicine, Seattle, WA, USA

[19 ]McConnell Brain Imaging Centre, Montreal Neurological Institute, McGill University, Montreal, Quebec, Canada

[20 ]Dept of Neurobiology, Yale University School of Medicine, New Haven, CT, USA

[21 ]Department of Physiology/Endocrinology, Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden

[22 ]Department of Physiology, School of Medicine, Instituto de Investigacion Sanitaria (IDIS), University of Santiago de Compostela, Spain

[23 ]Department of Psychology, Institute of Diabetes, Obesity and Metabolism, University of Pennsylvania, Philadelphia, PA, USA

[24 ]Department of Diabetes, Obesity and Metabolism, Oregon National Primate Research Center, Oregon Health & Science University, Beaverton, OR, USA

[25 ]Comprehensive Diabetes Center, University of Alabama School of Medicine, Birmingham, AL, USA

[26 ]Division of Diabetes, Obesity, and Metabolism, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, OR 97006, USA

[27 ]NuMe Health, 1441 Canal Street, New Orleans, LA 70112, USA

[28 ]Departments of Psychiatry and Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA

[29 ]Department of Neuroscience and Pharmacology, University of Copenhagen, Copenhagen N, Denmark

[30 ]Department of Psychosomatic Internal Medicine, Kagoshima University Graduate School of Medical and Dental Sciences, Kagoshima, Japan

[31 ]Institute of Neuroscience and Physiology, The Sahlgrenska Academy at the University of Gothenburg, Gothenburg, Sweden

[32 ]Medizinische Klinik I, Universitätsklinikum Schleswig-Holstein Campus Lübeck, Lübeck, Germany

[33 ]Centre for Endocrinology, William Harvey Research Institute, Barts and the London, Queen Mary University of London, London, UK

[34 ]New York Obesity Research Center, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY, USA

[35 ]Diabetes Complications Research Centre, Conway Institute, University College Dublin, Ireland

[36 ]Division of Neurology, Respirology, Endocrinology and Metabolism, Department of Internal Medicine, Faculty of Medicine, University of Miyazaki, Kiyotake, Miyazaki, Japan

[37 ]Division of Endocrinology and Metabolism, University of Virginia, Charlottesville, VA, USA

[38 ]Department of Internal Medicine, Department of Medicine, University of Cincinnati College of Medicine, Cincinnati, OH, USA

[39 ]Department of Neuroscience and Pharmacology, Laboratory for Molecular Pharmacology, The Panum Institute, University of Copenhagen, Copenhagen, Denmark

[40 ]Department of Surgery, University of Michigan School of Medicine, Ann Arbor, MI, USA

[41 ]Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA

[42 ]Department of Genetics and Development, Columbia University, New York, NY, USA

[43 ]Department of Medicine, Erasmus University MC, Rotterdam, The Netherlands

[44 ]Rhythm Pharmaceuticals, Boston, MA, USA

[45 ]Departments of Internal Medicine and Psychiatry, The University of Texas Southwestern Medical Center, Dallas, TX, USA

[46 ]Molecular Genetics, Institute of Life Science, Kurume University, Kurume, Japan

[47 ]National Cerebral and Cardiovascular Center Research Institute, Osaka, Japan

[48 ]The Scripps Research Institute, Florida Department of Metabolism & Aging, Jupiter, FL, USA

[49 ]Program in Integrative Cell Signaling and Neurobiology of Metabolism, Section of Comparative Medicine, Yale University School of Medicine, New Haven, CT, USA

[50 ]Division of Metabolic Diseases, Department of Medicine, Technical University Munich, Munich, Germany

Author notes

[∗ ]Corresponding author. Institute for Diabetes and Obesity, Helmholtz Zentrum München, München, Germany. matthias.tschoep@ 123456helmholtz-muenchen.de

[51]

R.G. Smith, T. Horvath, and M.H. Tschöp contributed equally to this work.

Article

Publisher ID: S2212-8778(15)00060-5

DOI: 10.1016/j.molmet.2015.03.005

PMC ID: 4443295

PubMed ID: 26042199

SO-VID: f6b6d823-e6d2-4f09-b11a-3d2b9e04e247

License:

This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).

History

Date received : 28 January 2015

Date revision received : 11 March 2015

Date accepted : 11 March 2015

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Ghrelin

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Abstract

Background

Scope of review

Major conclusions

Related collections

UCL: UN SDG 03 Good Health and Well-Being

Most cited references 389

Comprehensive analysis of mRNA methylation reveals enrichment in 3' UTRs and near stop codons.

A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity.

Ghrelin is a growth-hormone-releasing acylated peptide from stomach.

Author and article information

Contributors

Journal

Affiliations

Author notes

Article

History

Categories

Comments

Comment on this article

Similar content 242

Cited by 333

Most referenced authors 4,848