Serum S100B Protein Is Increased in Fasting Rats

Netto, Cristina Brinckmann Oliveira; Conte, Sabrina; Leite, Marina Concli; Pires, Caroline; Martins, Tiago Leal; Vidal, Penélope Rogers; Benfato, Mara da Silveira; Giugliani, Roberto; Gonçalves, Carlos‐Alberto

doi:10.1016/j.arcmed.2005.11.005

Cited by 58 publications

(49 citation statements)

References 24 publications

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“…Future studies in larger samples may focus on drug-naive schizophrenic subjects and the comparison of different standardized treatment regimens to further elucidate the suggested link between S100B and abnormal energy metabolism. The six genome-wide association studies (GWAS) completed in bipolar disorder (BD) [1][2][3][4][5][6] have revealed some promising association signals that have been replicated in independent study samples, 7 but the mechanism by which these genes increase disease susceptibility has remained unresolved. Here, our goal was (i) to replicate the best results from the study by Sklar et al, 2008 4 and also the highest ranking imputed SNPs from the WTCCC study 1 and (ii) to define the effect of the Figure 1 Elevated S100B serum concentrations (a) and an increased C-peptide/glucose ratio (b), indicating insulin resistance, were schizophrenia related.…”

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confidence: 99%

“…3,4 S100B secretion from adipocytes is reduced by insulin and is activated by physiological factors such as stress and fasting. 5,6 Therefore, weight gain or adipocyte dysfunction, including insulin insensitivity, could offer important alternative explanations for elevated S100B levels, given the increased prevalence of metabolic syndrome in schizophrenic patients and their firstdegree relatives. 7 The assumption of such extracerebral origins of altered S100B levels in schizophrenia is challenged by findings of elevated S100B in cerebrospinal fluid and postmortem brain tissue.…”

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confidence: 99%

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Elevated S100B levels in schizophrenia are associated with insulin resistance

et al. 2009

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confidence: 99%

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Elevated S100B levels in schizophrenia are associated with insulin resistance

et al. 2009

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“…An immunoelectron microscopic study suggested that S100B may be involved in the regulation of lipolysis 59 . The release of S100B from adipocytes is reduced by insulin, and activated by physiological factors such as stress (catecholamines and adrenocorticotropic hormone (ACTH)) or fasting [60][61][62] . Given the increased prevalence of obesity and metabolic syndrome in patients and their first degree relatives, an increase in adipose tissue mass or changes in insulin metabolism, such as insulin resistance are likely to play a major role in increased S100B levels in schizophrenia.…”

Section: Potential Links Between S100b and The Pathogenesis Of Schizomentioning

confidence: 99%

“…However, future studies of psychoses in animal models are necessary in order to clarify whether this mechanism is contributing to a hyperactive dopaminergic system in limbic brain regions, which has been observed in schizophrenia. 53 ] S100B is a potential marker of blood-brain barrier dysfunction [animal experiments and magnetic resonance imaging after osmotic blood-brain barrier disruption 50 ] Impaired glucose utilization hypothesis S100B may increase intracellular energy supply by activating glycolysis (fructose-1,6-bisphosphate aldolase) and glycogenolysis (phosphoglucomutase) [binding assays 71,72 ] Association of increased blood levels of S100B with insulin resistance [serum analyses in schizophrenia patients 64 ], release of S100B from adipose tissue is regulated by fasting, insulin and adrenalin [animal and cell culture experiments 60,62,80,81 ] Cerebral deficiency in glucose supply → increased S100B release from astro-and oligodendroglial cells/glucose oversupply → reduced S100B production and secretion in astrocytes [cell culture experiments 8,67,68 ] The glutamate hypothesis is the second most frequent neurotransmitter hypothesis of schizophrenia. It postulates that the N-methyl-D-aspartate (NMDA) glutamate receptor function is compromised.…”

Section: Potential Links Between S100b and The Pathogenesis Of Schizomentioning

confidence: 99%

Os possíveis papéis da S100B na esquizofrenia

Steiner

Bernstein

Bogerts

et al. 2012

Arch. Clin. Psychiatry (São Paulo)

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Background: Scientific evidence for increased S100B concentrations in the peripheral blood of acutely ill schizophrenia patients is consistent. In the past, this finding was mainly considered to reflect astroglial or blood-brain barrier dysfunction. Methods: Using Entrez, PubMed was searched for articles published on or before June 15, 2011, including electronic early release publications, in order to determine other potential links between S100B and current hypotheses for schizophrenia. Results: S100B is potentially associated with the dopamine and glutamate hypotheses. Supporting the glial hypothesis, an increased expression of S100B has been detected in cortical astrocytes of paranoid schizophrenia cases, while decreased oligodendrocytic expression has been observed in residual schizophrenia. Recently, the neuroinflammation hypothesis of schizophrenia has gained attention. S100B may act as a cytokine after secretion from glial cells, CD8+ lymphocytes and NK cells, activating monocytes and microglial cells. Moreover, S100B exhibits adipokine-like properties and may be dysregulated in schizophrenia due to disturbances in insulin signaling, leading to the increased release of S100B and free fatty acids from adipose tissue. Discussion: Dysregulation of pathways related to S100B appears to play a role in schizophrenia. However, S100B is expressed in different cell types and is involved in many regulatory processes. Currently, "the most important" mechanism related to schizophrenia cannot be determined.

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“…Serum concentrations of S100B, a marker of astroglial cell death, are inversely proportional to age, with the youngest children having the highest concentrations (Gazzolo et al, 2003b;Portela et al, 2002). It has been hypothesized that age-related changes in the bloodbrain barrier, and/or age-dependent release of S100B from adipocytes and chondrocytes, may be the cause of the agedependence seen with this marker (Donato, 2007;Goncalves et al, 2010;Holtkamp et al, 2008;Netto et al, 2006).…”

Section: Developmental Considerationsmentioning

confidence: 99%

Common Data Elements for Pediatric Traumatic Brain Injury: Recommendations from the Biospecimens and Biomarkers Workgroup

Berger

Beers²,

Papa

et al. 2012

Journal of Neurotrauma

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Biospecimens represent a critically important resource in pediatric brain injury research. Data from these specimens can be used to identify and classify injury, understand the molecular mechanisms underlying different types of brain injury, and ultimately identify therapeutic targets to tailor treatments for individual patient needs. To realize the full potential of biospecimens in pediatric traumatic brain injury (TBI), standardization and adoption of best practice guidelines are needed to ensure the quality and consistency of specimens. Multiple groups, including the National Cancer Institute (NCI), the International Society for Biological and Environmental Repositories (ISBER), and the Organisation for Economic Co-operation and Development (OECD), have previously published best practice guidelines for biospecimen resources. Recommendations have also been provided by the Biospecimens and Biomarkers Workgroup of the interagency TBI Common Data Elements (CDE) initiative. The recommendations from all of these sources, however, focus exclusively on adult biospecimen collection. There are no published pediatric-specific biospecimen collection guidelines. An additional workgroup was formed to specifically address this gap. The aim of the Pediatric TBI CDE Biospecimens and Biomarkers Workgroup was to provide recommendations for best practice guidelines to standardize the quality and accessibility of biospecimens for pediatric brain injury research in general, and for pediatric TBI research in particular. Consensus recommendations were developed by review of previously published adult-specific recommendations, including the recommendations of the original TBI Common Data Elements Biospecimens and Biomarkers Workgroup, and by participation in the interagency workshop ''Common Data Elements for TBI Research: Pediatric Considerations,'' held in Houston, Texas in March of 2010. These recommendations represent expert opinion on this subject. The authors of this article were members of the Biospecimens Workgroup. We hope that with adoption of these best practices, future investigators will be able to obtain biospecimens in a consistent way that meets the needs of pediatric patients, and helps to accelerate acquisition of pediatric-specific biomarker data.

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Serum S100B Protein Is Increased in Fasting Rats

Cited by 58 publications

References 24 publications

Elevated S100B levels in schizophrenia are associated with insulin resistance

Elevated S100B levels in schizophrenia are associated with insulin resistance

Os possíveis papéis da S100B na esquizofrenia

Common Data Elements for Pediatric Traumatic Brain Injury: Recommendations from the Biospecimens and Biomarkers Workgroup

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