Journal
PHARMACOLOGY BIOCHEMISTRY AND BEHAVIOR
Volume 97, Issue 1, Pages 25-33Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pbb.2010.04.016
Keywords
Anorexia; Eating disorders; Dietary fat; Sugar; Taste reward; Restricted access; Homovanillic acid; Catechol o-methyltransferase; Methylphenidate
Funding
- NIH [DK078484, DK080899, DC000240]
- Jane B Barsumian Trust Fund
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Central dopaminergic mechanisms are involved in the motivational aspects of eating and food choices 1 his review focuses on human and animal data investigating the importance of dopamine on binge eating behaviors Early work examining dopamine metabolites in the cerebrospinal fluid and plasma of bulimic individuals suggested decreased dopamine turnover during the active phase of the illness While neuroimaging studies of dopamine mechanisms in bulimia nervosa (BN) and binge eating disorder (BID) are limited genetic studies in humans have implicated an increased frequency of dopamine transporter and associated D2 receptor polymorphisms with binge pathology Recent studies in rodent models of dietary induced binge eating (DIBE) have investigated plausible dopamine mechanisms involved in sustaining binge eating behaviors In DIBE models highly palatable foods (fats sugars and their combination) as well as restricted access conditions appear to promote ingestive responses and result in sustained dopamine stimulation within the nucleus accumbens Taken together with studies on the comorbidity of illicit drug use and eating disorders the data reviewed here support a role for dopamine in perpetuating the compulsive feeding patterns of BN and BED As such we propose that sustained stimulation of the dopamine systems by bingeing promoted by preexisting conditions (e g genetic traits dietary restraint stress etc) results in progressive impairments of dopamine signaling To disrupt this vicious cycle novel research-based treatment options aiming at the neural substrates of compulsive eating patterns are necessary (C) 2010 Elsevier Inc All rights reserved
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