Table of Contents
Cardiovascular Psychiatry and Neurology
Volume 2010 (2010), Article ID 480707, 11 pages
Review Article

S100B Serum Levels in Schizophrenia Are Presumably Related to Visceral Obesity and Insulin Resistance

1Department of Psychiatry, University of Magdeburg, Leipziger Str. 44, 39120 Magdeburg, Germany
2Department of Psychiatry, University of Munich, Nußbaumstr. 7, 80336 Munich, Germany
3Institute of Clinical Chemistry & Pathobiochemistry, University of Magdeburg, Leipziger Str. 44, 39120 Magdeburg, Germany
4Max-Planck-Institute for Human Cognitive and Brain Sciences, P.O. Box 500355, 04103 Leipzig, Germany
5Day Clinic of Cognitive Neurology, University of Leipzig, 04103 Leipzig, Germany

Received 8 January 2010; Accepted 31 March 2010

Academic Editor: Claus W. Heizmann

Copyright © 2010 Johann Steiner et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Elevated blood levels of S100B in schizophrenia have so far been mainly attributed to glial pathology, as S100B is produced by astro- and oligodendroglial cells and is thought to act as a neurotrophic factor with effects on synaptogenesis, dopaminergic and glutamatergic neutrotransmission. However, adipocytes are another important source of S100B since the concentration of S100B in adipose tissue is as high as in nervous tissue. Insulin is downregulating S100B in adipocytes, astrocyte cultures and rat brain. As reviewed in this paper, our recent studies suggest that overweight, visceral obesity, and peripheral/cerebral insulin resistance may be pivotal for at least part of the elevated S100B serum levels in schizophrenia. In the context of this recently identified framework of metabolic disturbances accompanying S100B elevation in schizophrenia, it rather has to be attributed to systemic alterations in glucose metabolism than to be considered a surrogate marker for astrocyte-specific pathologies.