• Made available online as an Accepted Preprint 10 March 2010
  • Accepted Preprint first posted online on 10 March 2010

Acute food deprivation reduces expression of diazepam-binding inhibitor, the precursor of the anorexigenic octadecaneuropeptide ODN, in mouse glial cells

  1. M C Tonon1,2
  1. 1Inserm U982, Laboratory of Neuronal and Neuroendocrine Communication and Differentiation
    2University of Rouen, European Institute for Peptide Research (IFRMP 23), Regional Platform for Cell Imaging of Normandy (PRIMACEN), University of Rouen, 76821 Mont-Saint-Aignan, France
    3Department of Anesthesiology and Critical Care, Rouen University Hospital, 7600 Rouen, France
    4Research Center in Molecular Endocrinology, Oncology and Genetics, Laval University Hospital Center, Quebec City, Quebec, Canada G1V4G2
  1. (Correspondence should be addressed to M C Tonon at Inserm U982, Laboratory of Neuronal and Neuroendocrine Communication and Differentiation, European Institute for Peptide Research (IFRMP 23), University of Rouen; Email: marie-christine.tonon{at}univ-rouen.fr)

Abstract

In the central nervous system of mammals, the gene encoding diazepam-binding inhibitor (DBI) is exclusively expressed in glial cells. Previous studies have shown that central administration of a DBI processing product, the octadecaneuropeptide ODN, causes a marked inhibition of food consumption in rodents. Paradoxically, however, the effect of food restriction on DBI gene expression has never been investigated. Here, we show that in mice, acute fasting dramatically reduces DBI mRNA levels in the hypothalamus and the ependyma bordering the third and lateral ventricles. I.p. injection of insulin, but not of leptin, selectively stimulated DBI expression in the lateral ventricle area. These data support the notion that glial cells, through the production of endozepines, may relay peripheral signals to neurons involved in the central regulation of energy homeostasis.

  • Revision received 27 January 2010
  • Accepted 9 March 2010
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