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Expression and activity of P‐glycoprotein (MDR1/ABCB1) in peripheral blood mononuclear cells from patients with anorexia nervosa compared with healthy controls
Author(s) -
Storch Caroline Henrike,
Nikendei Christoph,
Schild Sandra,
Haefeli Walter Emil,
Weiss Johanna,
Herzog Wolfgang
Publication year - 2008
Publication title -
international journal of eating disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.785
H-Index - 138
eISSN - 1098-108X
pISSN - 0276-3478
DOI - 10.1002/eat.20519
Subject(s) - p glycoprotein , peripheral blood mononuclear cell , anorexia nervosa , medicine , endocrinology , flow cytometry , transporter , reuptake , pharmacology , immunology , biology , serotonin , receptor , eating disorders , psychiatry , gene , biochemistry , antibiotics , multiple drug resistance , in vitro
Objective: Pharmacotherapeutic strategies for treatment of anorexia nervosa (AN) are characterized by limited success. Some drugs used (antipsychotics, selective serotonin reuptake inhibitors) are transported by P‐glycoprotein (P‐gp), a transporter with major impact on pharmacokinetics of substrate drugs. Biochemical alterations seen in AN patients could lead to increased expression and/or activity of P‐gp and therefore to diminished access of drugs to the brain. The aim of our study was to investigate expression and activity levels of P‐gp in peripheral blood mononuclear cells (PBMCs) in AN patients. Method: PBMCs of 16 AN patients and 16 controls were isolated. Activity of P‐gp was determined by flow cytometry and expression was quantified by reverse‐transcriptase‐real‐time‐polymerase‐chain‐reaction. Results: Neither a significant difference in P‐gp expression (AN: 0.00154 ± 0.00088 [ MDR1 /β2 mg], control: 0.00244 ± 0.0013 [ MDR1 /β2 mg ], p = .138) nor a difference in P‐gp activity (rhodamine123 ratio AN: 1.79 ± 0.73, control: 2.03 ± 0.42, p = .20) between AN patients and healthy controls could be detected. In contrast to previous studies, expression and activity of P‐gp correlated significantly ( p = .0031). Conclusion: Failure in pharmacotherapy with P‐gp substrates in AN patients are probably neither caused by different P‐gp expression nor activity levels. © 2008 by Wiley Periodicals, Inc. Int J Eat Disord 2008