Diazepam binding inhibitor (DBI) in the plasma of pediatric and adult epileptic patients

Ferrarese, Carlo; Cogliati, Tiziana; Tortorella, Rachele; Zucca, Claudio; Bogliun, G.; Beghi, Ettore; Passoni, Davide; Zoia, Chiara Paola; Begni, Barbara; Airoldi, Larissa; Alho, Hannu; Frattola, L.

doi:10.1016/s0920-1211(97)00074-0

Cited by 19 publications

(19 citation statements)

References 14 publications

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“…The complex mechanisms of PBRs involvement in neurodegenerative diseases needs to be researched in the near future. Ferrarese et al (in 1998) analyzed the plasma DBI concentrations in pediatric and adult epileptic patients and found significantly higher levels that was particularly strikingly in drug-resistant patients, as compared to the agerelated controls. The authors considered that plasma DBI levels could be used as a peripheral biological marker of epilepsy and anticonvulsant drug responsiveness [31].…”

Section: Discussionmentioning

confidence: 99%

The Role of Peripheral Benzodiazepine Receptors (PBRs) in CNS Pathophysiology

Lang

2002

CMC

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The peripheral benzodiazepine receptors (PBRs) have been identified to bind selectively benzodiazepine ligands and an isoquinoline carboxamide derivative PK 11195 with high affinity. PBRs are present in the central nervous system (CNS), peripheral tissues, and most organs in the human body. PBRs are different from the central benzodiazepine receptors (CBRs) related to the nerve cell membrane GABA(A) receptor and are thought to play several physiological and pathophysiological functions in the CNS and immune system due to their meanly localization in glial cells, the mitochondrial outer membrane of peripheral cells and blood leucocytes and to their important roles in steroidogenesis, cell proliferation and differentiation. Recent research has shown that the density of PBRs is significantly increased in CNS several disorders, such as epilepsy, multiple sclerosis, cerebral ischemia, astrocytoma, brain injury and neurodegenerative diseases. Recent progress in the pharmacology of PBRs is reviewed here with respect to the functions in the brain and peripheral tissues including apoptosis, immune system modulation, seizure promotion, reactions of anticonvulsants on peripheral blood cells, and adverse drug reactions (ADR) of anticonvulsants.

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Section: Discussionmentioning

confidence: 99%

The Role of Peripheral Benzodiazepine Receptors (PBRs) in CNS Pathophysiology

Lang

2002

CMC

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“…DBI represents an endogenous specific PBR ligand and was assessed in this work as well, hypothesizing that adjustment of this peptide plasma levels might occur taking into account the reported differences in the cognate receptor on PBMC membranes [4]. DBI plasma levels have been assessed before in epileptic patients finding elevated values in adult generalized epilepsy and in drug-resistant both paediatric and adult patients [21]. A DBI alteration in this patient population was analogously hypothesized based on our group's previous report of a differential expression of PBR in PBMC obtained from drug-treated epileptic patients and of a significantly lower receptor density in drug-resistant patients when compared to newly diagnosed patients and to normal age-related controls [24,25].…”

Section: Discussionmentioning

confidence: 99%

“…Multivariate analysis was performed. Moreover, an attempt at calculating sample size for this pilot study was made a priori, based on our previously published plasma DBI data assessed in a healthy paediatric population [21], concurrently hypothesizing a plasma DBI change of 50% in BPD patients (similar magnitude with respect to the previously shown 65% reduction of PBR B max in PBMC [4], corresponding to the number of DBI cognate receptors). With α = 0.05, power (two-tailed) was high (>90%) hypothesizing of recruiting 12 subjects for group.…”

Section: Methodsmentioning

confidence: 99%

Diazepam Binding Inhibitor and Dehydroepiandrosterone Sulphate Plasma Levels in Borderline Personality Disorder Adolescents

Conti

Nacinovich²,

Bomba³

et al. 2013

Neuropsychobiology

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Background: Borderline personality disorder (BPD) patients display a complex and heterogeneous clinical phenotype that plausibly implies variable underlying pathogenic mechanisms. A dysregulation of peripheral benzodiazepine receptors has previously been shown in BPD peripheral tissues, implying possible alterations of its ligand, the diazepam binding inhibitor (DBI) or of the downstream products of its activation, i.e. neuroactive steroids. Methods: The aim of this work consisted in assessing, by ELISA, fasting plasma levels of DBI and dehydroepiandrosterone sulphate (DHEA-S), including cortisol and the cortisol-to-DHEA-S molar ratio (CDR), in 17 BPD adolescents versus 13 healthy controls, testing the possibility that clinical scales related to depressive or anxious traits (CDI, STAI-Y) or to disease severity (BPDCL) might be associated with a selective dysregulation of these parameters. Results: DBI plasma levels were unchanged, while DHEA-S ones were significantly increased (approx. 70%) and the CDR decreased in BPD patients. No meaningful correlations with clinical variables emerged. Conclusion: Our results indicate that a dysfunction of the neurosteroid system might be operative in BPD in spite of unchanged DBI plasma levels and that DHEA-S might represent a generalized trait marker for the altered stress response that is associated with this disorder.

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“…On the strengths of this function, plasma ACBP concentration was considered as a biological marker of epilepsy [27] and neuropsychiatric disorders [28]. Recently, Conditional logistic regression analysis (sex and age were matching variables).…”

Section: Discussionmentioning

confidence: 99%

Association of acyl‐CoA‐binding protein (ACBP) single nucleotide polymorphisms and type 2 diabetes in two German study populations

Nitz

Gieger

Grallert

et al. 2007

Molecular Nutrition Food Res

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The human acyl-CoA-binding protein (ACBP) is a potential candidate gene of type 2 diabetes (T2D), since it plays a central role in determining the intracellular concentration of activated fatty acids which contribute to insulin resistance. The aim of our study was to evaluate whether single nucleotide polymorphisms (SNPs) of the ACBP gene are associated with risk of T2D. Genotyping of eight SNPs (rs2084202, rs3731607, rs8192501, rs8192504, rs2244135, rs2276596, rs8192506, rs2289948) was performed in 192 incident T2D subjects and 384 matched controls of the European Prospective Investigation into Cancer and Nutrition-Potsdam cohort. A putative promoter SNP (rs2084202) of splice variant ACBP 1c showed decreased risk of T2D (odds ratio (OR) 0.63, 95% CI 0.41-0.96). The haplotype, that contained the mutant base of rs2084202 showed similar evidence for the association with disease risk as single SNP rs2084202. In a second population-based study, Cooperative Health Research in the Augsburg Region of 226 individuals with T2D and 863 control subjects a borderline significant association between rs2084202 and T2D (OR 0.72, 95% CI 0.51-1.01) was observed. In summary, we obtained evidence from two Caucasian study populations that the minor allele of ACBP rs2084202 might be associated with reduced risk of T2D.

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Diazepam binding inhibitor (DBI) in the plasma of pediatric and adult epileptic patients

Cited by 19 publications

References 14 publications

The Role of Peripheral Benzodiazepine Receptors (PBRs) in CNS Pathophysiology

The Role of Peripheral Benzodiazepine Receptors (PBRs) in CNS Pathophysiology

Diazepam Binding Inhibitor and Dehydroepiandrosterone Sulphate Plasma Levels in Borderline Personality Disorder Adolescents

Association of acyl‐CoA‐binding protein (ACBP) single nucleotide polymorphisms and type 2 diabetes in two German study populations

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