Reduced fasting plasma levels of diazepam-binding inhibitor in adolescents with anorexia nervosa

ABSTRACT Objective Altered expression and/or function, both peripherally and centrally, of various neuropeptides is involved in the neurophysiology of anorexia nervosa (AN). Diazepam‐binding inhibitor (DBI) is an interesting peptide for understanding this crosstalk. The aim of this work was to asses...

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Veröffentlicht in:The International journal of eating disorders 2013-09, Vol.46 (6), p.626-629
Hauptverfasser: Conti, Elisa, Tremolizzo, Lucio, Bomba, Monica, Uccellini, Orlando, Rossi, Maria Sara, Raggi, Maria Elisabetta, Neri, Francesca, Ferrarese, Carlo, Nacinovich, Renata
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Sprache:eng
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Zusammenfassung:ABSTRACT Objective Altered expression and/or function, both peripherally and centrally, of various neuropeptides is involved in the neurophysiology of anorexia nervosa (AN). Diazepam‐binding inhibitor (DBI) is an interesting peptide for understanding this crosstalk. The aim of this work was to assess fasting plasma levels of DBI and leptin in patients with AN. Method Twenty‐four AN adolescents were recruited together with 10 age‐comparable healthy controls. Neuropeptide determinations were performed on plasma samples by enzyme‐linked immunosorbent assays. Patients with AN were further characterized for the presence of a depressive state or anxiety by using, respectively, the Children's Depression Inventory or the State‐Trait Anxiety Inventory form Y. Results Levels of both plasma DBI and leptin were reduced in patients with AN (∼40 and ∼70%, respectively). DBI levels displayed a tendency to increase in the presence of a depressive state, although not with anxiety, whereas leptin levels correlated exclusively with body mass index. Discussion These data further extend our knowledge of neuropeptide dysfunction in AN, and plasma DBI may represent a marker for this disease, in particular considering its correlation with comorbid mood disorders. © 2013 Wiley Periodicals, Inc. (Int J Eat Disord 2013; 46:626–629)
ISSN:0276-3478
1098-108X
DOI:10.1002/eat.22129