Hypothalamic neuropeptides are thought to contribute to the pathophysiology of eating disorders. In an animal model with chronic abnormalities of energy expenditure, appetitive behavior, and body weight, without acute food restriction, we found alterations in peripheral levels of adrenocorticotropic hormone and corticosterone, but no alterations in the expression of neuropeptides genes that are known to regulate ingestive behavior and food intake acutely. Our data suggest that activation of hypothalamic-pituitary-adrenal function in activity anorexia may not be due to increased transcription of corticotropin-releasing hormone gene, but might be related to posttranscriptional events or to other neuropeptides, such as arginine vasopressin. Furthermore, we suggest that abnormalities in neuropeptides observed in eating disorders may be caused by acute food restriction, rather than by chronic hyperactivity, anorexia, and low weight.