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Deletion of ghrelin impairs neither growth nor appetite

Academic Article
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Overview

authors

  • Sun, Y. X.
  • Ahmed, S.
  • Smith, Roy

publication date

  • November 2003

journal

  • Molecular and Cellular Biology  Journal

abstract

  • Pharmacological studies show that ghrelin stimulates growth hormone release, appetite, and fat deposition, but ghrelin's physiological role in energy homeostasis has not been established. Ghrelin was also proposed to regulate leptin and insulin release and to be important for the normal function of stomach, heart, kidney, lung, testis, and placenta. To help determine a definable physiological role for ghrelin, we generated ghrelin-null mice. In contrast to predictions made from the pharmacology of ghrelin, ghrelin-null mice are not anorexic dwarfs; their size, growth rate, food intake, body composition, reproduction, gross behavior, and tissue pathology are indistinguishable from wild-type littermates. Fasting produces identical decreases in serum leptin and insulin in null and wild-type mice. Ghrelin-null mice display normal responses to starvation and diet-induced obesity. As in wild-type mice, the administration of exogenous ghrelin stimulates appetite in null mice. Our data show that ghrelin is not critically required for viability, fertility, growth, appetite, bone density, and fat deposition and not likely to be a direct regulator of leptin and insulin. Therefore, antagonists of ghrelin are unlikely to have broad utility as antiobesity agents.

subject areas

  • Animals
  • Appetite
  • Base Sequence
  • DNA
  • Fasting
  • Female
  • Ghrelin
  • Growth
  • Insulin
  • Lac Operon
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • Obesity
  • Peptide Hormones
  • Pregnancy
  • RNA, Messenger
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Identity

PubMed Central ID

  • PMC262394

International Standard Serial Number (ISSN)

  • 0270-7306

Digital Object Identifier (DOI)

  • 10.1128/mcb.23.22.7973-7981.2003

PubMed ID

  • 14585959
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Additional Document Info

start page

  • 7973

end page

  • 7981

volume

  • 23

issue

  • 22

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