S100B in underweight and weight-recovered patients with anorexia nervosa

Ehrlich, Stefan; Salbach‐Andrae, Harriet; Weiss, Deike; Burghardt, Roland; Goldhahn, Klaus; Craciun, Eugenia Maria; Franke, L.; Uebelhack, Ralf; Klapp, Burghard F.; Lehmkuhl, Ulrike

doi:10.1016/j.psyneuen.2008.03.004

Cited by 18 publications

(15 citation statements)

References 34 publications

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“…This finding may explain previous reports indicating a direct relationship between S100B blood levels with body weight in anorexia nervosa: Effect sizes that were obtained from data given for anorexic subjects by Ehrlich et al [59] before and after weight gain (i.e., mean ± SD of BMI: initially 14.5 ± 1.3, after >10% weight gain 17.1 ± 0.9; mean ± SD of S100B levels: initially 0.095 ± 0.041 μ g/l, finally: 0.128 ± 0.063 μ g/l) and by Holtkamp et al [60] after 21 weeks of weight gain (mean ± SD of BMI: initially 14.8 ± 1.3, finally 17.0 ± 1.2; mean ± SD of S100B levels: initially 0.077 ± 0.023 μ g/l, finally 0.107 ± 0.035 μ g/l) were 0.81 and 1.3, respectively. In conclusion, S100B blood levels are directly related to BMI across an extensive range of nutritional states spanning from starvation to extreme obesity.…”

Section: S100b Serum Is Correlated With Body Mass Index and A-fabpsupporting

confidence: 78%

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

Steiner

Myint

Schiltz

et al. 2010

Cardiovascular Psychiatry and Neurology

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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.

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Section: S100b Serum Is Correlated With Body Mass Index and A-fabpsupporting

confidence: 78%

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

Steiner

Myint

Schiltz

et al. 2010

Cardiovascular Psychiatry and Neurology

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show abstract

“…The suspicion that body weight could affect serum S100B levels was examined in a study in bipolar patients [39]. Two independent studies in anorexic patients indicate a relationship between serum S100B and body weight [40, 41]. However, an appropriate study about this issue was performed only more recently [42].…”

Section: Is S100b Released By Adipocytes?mentioning

confidence: 99%

Adipocytes as an Important Source of Serum S100B and Possible Roles of This Protein in Adipose Tissue

Gonçalves

Leite

Guerra

2010

Cardiovascular Psychiatry and Neurology

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Adipocytes contain high levels of S100B and in vitro assays indicate a modulated secretion of this protein by hormones that regulate lipolysis, such as glucagon, adrenaline, and insulin. A connection between lipolysis and S100B release has been proposed but definitive evidence is lacking. Although the biological significance of extracellular S100B from adipose tissue is still unclear, it is likely that this tissue might be an important source of serum S100B in situations related, or not, to brain damage. Current knowledge does not preclude the use of this protein in serum as a marker of brain injury or astroglial activation, but caution is recommended when discussing the significance of changes in serum levels where S100B may function as an adipokine, a neurotrophic cytokine, or an alarmin.

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“…Etiopatogenetic mechanism of cerebral alterations are not still completely explained. First hypothesis that volume reductions are related to neuron death has not been confirmed either by neuro-biochemical [17], histological studies [18] or by improvement of brain alterations with weight restoration [10]. The current hypothesis, summarized in Swayze’s study [8], include: i) decreased serum proteins resulting in decreased colloidal osmotic pressure and a shift of fluid from the intravascular space into the subarachnoid spaces [19]; ii) partial regeneration of damaged neurons and their axons with possible regeneration of myelin [20]; iii) loss of lean body tissue mass [21]; iv) increased urine and serum cortisol levels [22]; v) decreased protein synthesis resulting in loss of dendritic spines, a reduction in the number of synaptic junctions, and delayed synaptogenesis [7].…”

Section: Introductionmentioning

confidence: 99%

Impact of speed and magnitude of weight loss on the development of brain trophic changes in adolescents with anorexia nervosa: a case control study

et al. 2013

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BackgroundAnorexia nervosa commonly arises during adolescence and is associated with more than one medical morbidity. Abnormalities in brain structure (defined as “pseudoatrophy”) are common in adolescents with anorexia nervosa; however, their correlations with endocrinological profiles and clinical parameters are still unclear. In particular, no study has described the impact of BMI (body mass index) variations (speed and magnitude of weight loss) on cerebral trophism changes.MethodsEleven adolescents with anorexia nervosa and 8 healthy controls underwent cerebral MRI (magnetic resonance imaging) examination to obtain global and partial volumes (gray matter, white matter and cerebrospinal fluid) and clinical evaluation. The Mann-Whitney U test was used to compare partial volumes and clinical variables between cases and controls. The Spearman non-parametric test was performed in order to explore correlations between the variables studied.ResultsThe patients diagnosed with AN showed significantly increased cerebrospinal fluid (CSF) volumes and decreased total gray (GM) and white matter (WM) volumes. The degree of weight loss (deltaBMI) correlated inversely with the GM volume; the increase of CSF compartment correlated directly with the rapidity of weight loss (DeltaBMI/disease duration).ConclusionsThis study suggests a correlation between cerebral alterations in AN and the speed and magnitude of weight loss, and outlines its importance for the therapeutic treatment.

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S100B in underweight and weight-recovered patients with anorexia nervosa

Cited by 18 publications

References 34 publications

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

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

Adipocytes as an Important Source of Serum S100B and Possible Roles of This Protein in Adipose Tissue

Impact of speed and magnitude of weight loss on the development of brain trophic changes in adolescents with anorexia nervosa: a case control study

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