پپتید-1 ترشح گلوکاگون مانند در بولیمیا
|کد مقاله||سال انتشار||مقاله انگلیسی||ترجمه فارسی||تعداد کلمات|
|32528||2009||4 صفحه PDF||سفارش دهید||محاسبه نشده|
Publisher : Elsevier - Science Direct (الزویر - ساینس دایرکت)
Journal : Psychiatry Research, Volume 169, Issue 1, 30 August 2009, Pages 82–85
Blood concentrations of the satiety-inducing glucagon-like peptide-1 (GLP-1) were compared in 20 bulimic patients and 20 healthy controls to examine whether secretory impairment of the peptide could be involved in bulimia nervosa (BN). Basal GLP-1 concentrations were measured by means of an enzyme-linked immunosorbent assay (ELISA) in blood samples taken four times over a 12-h period (08.00h, 12.00h, 16.00h, 20.00h) and seven times over a 3-h period following administration of a test meal. Eating-related and non-eating related patients' psychopathological aspects were measured by the use of a battery of ad hoc rating scales (Eating Disorder Inventory-2 = EDI-2, Bulimic Investigation test-Edinburgh = B.I.T.E., Montgomery–Åsberg Depression Rating Scale = MADRS, Spielberger State-Trait Anxiety Inventory = STAI, Yale–Brown–Cornell Eating Disorder Scale = YBC-EDS). Basal GLP-1 values were higher in patients than in controls only in the blood samples taken at 16.00h, whereas no difference between patients and controls was observed in GLP-1 concentrations in response to the test meal stimulation. GLP-1 levels correlated positively with bingeing–vomiting frequency, with B.I.T.E. scores and the “bulimia” subitem scores of the EDI-2 scale, and negatively with the “ascetism” subitem score of the same scale.
Peripherally secreted hormones and peptides influence brain hunger–satiety regulating centers by crossing the blood-brain barrier via the area postrema and the subfornical organ, or by activating centripetal neuronal pathways. In experimental animals and human studies, the C-terminal 31-aminoacid glucagon-like peptide-1 (GLP-1), a glucose and fat dependent (insulinotropic) incretin, has been found to inhibit the feeling of hunger and to induce satiety, significantly reducing energy intake and prospective energy consumption. The peptide diminishes gastric emptying rate, gastrin secretion and gut motility. All these effects have been tentatively suggested, among other hypotheses, to underlie the increased feeling of satiety after feeding (Flint et al., 1998, Flint et al., 2001, Verdick et al., 2001, Vettor et al., 2002, De Graaf et al., 2004, Stanley et al., 2004, Meier and Nauck, 2005 and Lopez et al., 2007). GLP-1 derives from preproglucagon, and is secreted by intestinal L-cells primarily in the ileum and by the pancreas. The peptide is also expressed in the central nervous system, specifically in the nucleus of the tractus solitarius whose neurons project into the hypothalamic nuclei, in particular into the arcuate and paraventricular nuclei (Stanley et al., 2004). GLP-1 acts on specific GLP-1 receptors (Lejeune et al., 2006). The release of the peptide increases between 5 and 30 min after food ingestion, proportionally with meal calorie intake (Vilsboll et al., 2003 and Frost et al., 2003). Altered feelings of hunger and satiety have been reported to occur in patients with anorexia nervosa (AN) (Rolls et al., 1992). In these patients, basal GLP-1 secretion was found either significantly higher (Tomasik et al., 2005 and Germain et al., 2007) or lower (D'Alessio et al., 1989) than normal, and highly correlated with glucose concentrations, whereas responses to a standard test meal and to an oral glucose tolerance test were lower than normal. These discordant results may be due to the patients' selection and to the different degrees of severity and duration of the disease, which could decrease (duration) or increase (severity) the secretion of the satiety-inducing peptide. To date, pertinent data about patients with bulimia nervosa (BN) are lacking. Since feelings of satiety have been repeatedly reported to be impaired in BN (Walsh et al., 1989, Rolls et al., 1992 and Kissileff et al., 1996), we hypothesized that the secretion of GLP-1 could be impaired in BN patients. That is why in a group of bulimic patients, in an active phase of the disease, we have examined the secretion of GLP-1, in basal conditions four times over a 12-h period and then after a mixed test meal in a separate experiment. The aim of the study was to see whether or not the satiety-inducing GLP-1 secretion is impaired in bulimic patients in basal conditions and after food stimulation, such alterations possibly being responsible for the abnormal type of relationship with food, and whether the impairments may correlate with the patients' psychopathological aspects.