Scripps VIVO scripps research logo

  • Index
  • Log in
  • Home
  • People
  • Organizations
  • Research
  • Events
Search form
As of April 1st VIVO Scientific Profiles will no longer updated for faculty, and the link to VIVO will be removed from the library website. Faculty profile pages will continue to be updated via Interfolio. VIVO will continue being used behind the scenes to update graduate student profiles. Please contact helplib@scripps.edu if you have questions.
How to download citations from VIVO | Alternative profile options

Des-acyl ghrelin induces food intake by a mechanism independent of the growth hormone secretagogue receptor

Academic Article
uri icon
  • Overview
  • Identity
  • Additional Document Info
  • View All
scroll to property group menus

Overview

authors

  • Toshinai, K.
  • Yamaguchi, H.
  • Sun, Y. X.
  • Smith, Roy
  • Yamanaka, A.
  • Sakurai, T.
  • Date, Y.
  • Mondal, M. S.
  • Shimbara, T.
  • Kawagoe, T.
  • Murakami, N.
  • Miyazato, M.
  • Kangawa, K.
  • Nakazato, M.

publication date

  • May 2006

journal

  • Endocrinology  Journal

abstract

  • Ghrelin, an acylated peptide produced predominantly in the stomach, stimulates feeding and GH secretion via interactions with the GH secretagogue type 1a receptor (GHS-R1a), the functionally active form of the GHS-R. Ghrelin molecules exist in the stomach and hypothalamus as two major endogenous forms, a form acylated at serine 3 (ghrelin) and a des-acylated form (des-acyl ghrelin). Acylation is indispensable for the binding of ghrelin to the GHS-R1a. Ghrelin enhances feeding via the neuronal pathways of neuropeptide Y and orexin, which act as orexigenic peptides in the hypothalamus. We here studied the effect of des-acyl ghrelin on feeding behavior. Intracerebroventricular (icv) administration of rat des-acyl ghrelin to rats or mice fed ad libitum stimulated feeding during the light phase; neither ip nor icv administration of des-acyl ghrelin to fasting mice suppressed feeding. The icv administration of des-acyl ghrelin induced the expression of Fos, a marker of neuronal activation, in orexin-expressing neurons of the lateral hypothalamic area, but not neuropeptide Y-expressing neurons of the arcuate nucleus. Peripheral administration of des-acyl ghrelin to rats or mice did not affect feeding. Although icv administration of ghrelin did not induce food intake in GHS-R-deficient mice, it did in orexin-deficient mice. In contrast, icv administration of des-acyl ghrelin stimulated feeding in GHS-R-deficient mice, but not orexin-deficient mice. Des-acyl ghrelin increased the intracellular calcium concentrations in isolated orexin neurons. Central des-acyl ghrelin may activate orexin-expressing neurons, perhaps functioning in feeding regulation through interactions with a target protein distinct from the GHS-R.

subject areas

  • Animals
  • Calcium
  • Chromatography, High Pressure Liquid
  • Cytosol
  • Feeding Behavior
  • Ghrelin
  • Growth Hormone
  • Hypothalamus
  • Intracellular Signaling Peptides and Proteins
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Movement
  • Neurons
  • Neuropeptide Y
  • Neuropeptides
  • Orexin Receptors
  • Orexins
  • Peptide Hormones
  • Peptides
  • Proto-Oncogene Proteins c-fos
  • Rats
  • Receptors, G-Protein-Coupled
  • Receptors, Ghrelin
  • Receptors, Neuropeptide
  • Stomach
  • Time Factors
scroll to property group menus

Identity

International Standard Serial Number (ISSN)

  • 0013-7227

Digital Object Identifier (DOI)

  • 10.1210/en.2005-1357

PubMed ID

  • 16484324
scroll to property group menus

Additional Document Info

start page

  • 2306

end page

  • 2314

volume

  • 147

issue

  • 5

©2022 The Scripps Research Institute | Terms of Use | Powered by VIVO

  • About
  • Contact Us
  • Support