Reduced fasting plasma levels of diazepam-binding inhibitor in adolescents with anorexia nervosa
Version of Record online: 29 APR 2013
Copyright © 2013 Wiley Periodicals, Inc.
International Journal of Eating Disorders
Volume 46, Issue 6, pages 626–629, September 2013
How to Cite
Conti, E., Tremolizzo, L., Bomba, M., Uccellini, O., Rossi, M. S., Raggi, M. E., Neri, F., Ferrarese, C. and Nacinovich, R. (2013), Reduced fasting plasma levels of diazepam-binding inhibitor in adolescents with anorexia nervosa. Int. J. Eat. Disord., 46: 626–629. doi: 10.1002/eat.22129
- Issue online: 23 AUG 2013
- Version of Record online: 29 APR 2013
- Manuscript Accepted: 27 JAN 2013
- Manuscript Revised: 7 JAN 2013
- University of Milano-Bicocca, Italy
- diazepam-binding inhibitor;
- anorexia nervosa;
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.
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.
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.
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)