Energy Policy

Topics: Hypothalamus, Growth hormone, Leptin Pages: 22 (7518 words) Published: April 16, 2013
0013-7227/01/$03.00/0 Printed in U.S.A.

Endocrinology 142(10):4163– 4169 Copyright © 2001 by The Endocrine Society

Minireview: Ghrelin and the Regulation of Energy Balance—A Hypothalamic Perspective TAMAS L. HORVATH, SABRINA DIANO, PETER SOTONYI, MARK HEIMAN, ¨ MATTHIAS TSCHOP AND

Reproductive Neuroscience Unit (T.L.H., S.D.), Department of Obstetrics and Gynecology and Department of Neurobiology (T.L.H.), Yale Medical School, New Haven, Connecticut 06520; Department of Anatomy and Histology (P.S.), Faculty of Veterinary Science, Szent Istvan University, Budapest, Hungary 1400; and Lilly Research Laboratories (M.H., M.T.), Eli Lilly & Co., Indianapolis, Indiana 46285 The recently discovered hormone, ghrelin, has been recognized as an important regulator of GH secretion and energy homeostasis. Orexigenic and adipogenic ghrelin is produced by the stomach, intestine, placenta, pituitary, and possibly in the hypothalamus. The concentration of circulating ghrelin, principally derived from the stomach, is influenced by acute and chronic changes in nutritional state. To date, most studies focused on the role of ghrelin in GH secretion or its function in complementing leptin action to prevent energy deficits. The potential significance of ghrelin in the etiology of obesity and cachexia as well as in the regulation of growth processes is the subject of ongoing discussions. A large quantity of information based on clinical trials and experimental studies with ghrelin and previously available synthetic ghrelin receptor agonists (GH secretagogues) must now be integrated with a rapidly increasing amount of data on the central regulation of metabolism and appetite. In this overview, we summarize recent findings and strategies on the integration of ghrelin into neuroendocrine networks that regulate energy homeostasis. (Endocrinology 142: 4163– 4169, 2001)


BESITY AND RELATED disorders are among the leading causes of illness and mortality in the developed world (1). To better understand the pathophysiological mechanisms that underlie metabolic disorders, increasing attention has been paid to central regulatory elements in energy homeostasis, including food intake and energy expenditure (2–5). The past two decades have provided overwhelming evidence of the critical role that hypothalamic peptidergic systems play in the central regulation of appetite and metabolism (6, 7). The discovery of ghrelin (8 –11) and its influence on appetite, fuel utilization, body weight, and body composition that is complementary to ghrelin’s GHreleasing effect (12) adds yet another component to the complexity in the central regulation of energy balance. Discovery of Ghrelin

Reverse pharmacology may be an appropriate term to describe the road to ghrelin’s discovery. First, synthetic agonists with ghrelin-like activity [GH-releasing peptides (GHRPs) and GH secretagogues (GHSs)] were discovered by Bowers and co-workers in the late seventies (9, 13–15), followed by the cloning of ghrelin-GHS-receptor (GHS-R) in 1996 by Smith and co-workers (16 –18). Subsequently, the elegant studies by Kojima and co-workers led to the identification of an acylated 28 residue peptide as an endogenous bioactive ligand for the GHS-R (8 –11). It was called ghrelin, a term that contains “ghre-” as the etymological root for “growth” in many languages. “GH” and “relin,” a suffix for releasing substances in generic names according to the USP Abbreviations: AGRP, Agouti-related protein; GHRP, GH-releasing peptide; GHS, GH-secretagogue; GHS-R, GHS receptor.

Dictionary of USAN and International Drug Names, also represents an abbreviation for “growth-hormone-release,” a characteristic effect of ghrelin (8, 11). The Ser3-acylation that seems to be responsible for bioactivity of ghrelin is a modification that has been observed for the first time in mammalian physiology. There are no data to support the tempting speculation that the purpose of this modification is to increase...
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