بولیمیا(پرخوری عصبی)؛ نقص اولیه در محور هیپوتالاموس -هیپوفیز-آدرنال؟
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|32504||2006||4 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Appetite, Volume 46, Issue 2, March 2006, Pages 164–167
Bulimia nervosa has been associated with impaired satiety, decreased resting metabolic rate and abnormal neuroendocrine regulation. The aim of this study was to investigate the diurnal cortisol secretion and the pituitary-adrenal response to corticotropin-releasing hormone (CRH) in subjects suffering from bulimia nervosa. Eight female subjects with remitted bulimia nervosa, ages 24–56, and 8 sex- and weight-matched controls volunteered to participate. After an overnight fast they were admitted to the Clinical Research Center for 24 hour recording of plasma cortisol secretion. Blood were drawn every 2nd hour from 8 AM. After another overnight fast, the subjects performed a 120-min CRH test (100 μg i.v.), drawn for measurements of adrenocorticotropin releasing hormone (ACTH) and cortisol. Compared to the control group (CG), the diurnal cortisol secretions in the bulimic group (BG) decreased at time points 6 AM to 2 PM. In the CRH test, the ACTH response was significantly stronger in the BG than in the CG. Similar observations were found for cortisol, although not at significant levels. Remitted bulimic patients exhibit a neuroendocrine pattern of decreased HPA axis activity with a hyperreactivity to CRH. This may indicate a complex and so far poorly understood neuroendocrine dysregulation of HPA axis associated with the disease.
The eating disorder bulimia nervosa is characterized by recurrent episodes of uncontrolled over-eating, often involving extremely large amounts of high-calorie foods, compensatory behavior to avoid weight gain, and related behavioral and physiological symptoms (Christopher & Harrison, 2003). Although this disorder is of great interest to the public, to clinicians and to researchers, the mechanisms underlying the various symptoms typical of this disease are complex and badly understood. There is a genetic predisposition, and certain specific environmental risk factors have been implicated. Numerous studies have been performed in order to describe the neuroendocrine characteristics of the bulimics, and the eating behavior has been reported as an impaired post-digestive satiety, associated with a diminished responsiveness in satiety-related pathways (Kissileff et al., 1996). Several neurotransmitters have been associated with food intake and satiety (Kaye et al., 1990 and Weltzin et al., 1991), and most attention has been focused on the limbic–hypothalamic–pituitary (HPA) axis that plays a crucial role in afferent and efferent signaling of satiety and hunger (Schwartz, Baskin, Kaiyala, & Woods, 1999). Studies have shown either normal (Fichter et al., 1990 and Vescovi et al., 1996) or increased (Ferrari et al., 1997, Koo-Loeb et al., 2000 and Monteleone et al., 2001) circadian secretion of cortisol in bulimics. Therefore, unlike patients with anorexia nervosa who with few exceptions have a hyper reactivity in the HPA axis (Licinio, 1996), the activity in the HPA axis in bulimia nervosa is more heterogeneous. The objective of this study was therefore to investigate the circadian rhythm of cortisol and the HPA axis in female subjects suffering from bulimia nervosa. We studied remitted bulimia patients in order to prevent secondary neuroendocrine disturbances to conditions such as overeating and psychological stress observed in an active phase of the disease.