peptide-yy and Bulimia

Normal weight bulimia nervosa, a disorder of unknown etiology, is characterized by bingeing and purging behavior, disturbances of mood, and neuroendocrine abnormalities. Bulimic women have alterations of neurotransmitter systems known to contribute to the modulation of feeding, mood, and neuroendocrine function. Bulimic patients have increased cerebrospinal fluid concentrations of peptide YY (PYY), a peptide which is a potent stimulant of feeding in experimental animals. It has been suggested that increased brain PYY activity could contribute to the powerful and uncontrollable drive of bulimic patients to binge. It also has been reported that bulimics have impaired satiety and secretion of cholecystokinin, a peptide known to induce satiety and reduce food intake in animals and humans. Most data show that bulimic women have alterations of serotonin and norepinephrine activity. In animals, serotonin appears to have effects on eating behavior (inhibition) that are opposite to the actions of endogenous norepinephrine (activation) at alpha 2 receptors in the hypothalamus. Bingeing behavior is consistent with an overactivity of the hypothalamic alpha-noradrenergic system, an underactivity of hypothalamic serotonergic systems, or a combination of both defects. In summary, it is possible that bulimic patients have a trait-related disturbance of one or more neurotransmitter systems that could cause their appetitive dysregulation. Alternatively, these neurotransmitter disturbances may be secondary to extremes of dietary intake. Nonetheless, such neurotransmitter disturbances may contribute to a high recidivism rate. That is, bulimic patients could enter a vicious cycle in which pathologic feeding sustains and provokes continued pathologic feeding behavior. Moreover, the self-reinforcing effects of bulimia, such as decreased anxiety or food craving, may be mediated through behavior-induced changes in neurotransmission.

Topics: Animals; Brain; Bulimia; Cholecystokinin; Eating; Feeding Behavior; Female; Humans; Hypothalamus; Neurotransmitter Agents; Norepinephrine; Peptide YY; Peptides; Serotonin

Potential mechanisms of abnormal food intake, such as dysregulation of meal-related appetite hormones, including acyl ghrelin (AG) and des-acyl ghrelin (DAG), were investigated among men and women with obesity, with and without binge eating (BE).. Participants (n = 42: 19 female, 23 male) were assigned to a liquid meal and water condition in counterbalanced order, and blood samples for measuring hormones were obtained before and after these conditions.. Participants with BE had significantly lower fasting and postingestive AG concentrations than participants without BE in both conditions. During the meal condition, postprandial decreases in AG concentrations were significantly smaller for the BE group than for the non-BE group. There were no significant differences in DAG by BE group. Leptin increased significantly less after meals for those with BE compared with those without BE. There were no differences in other hormones by BE group. Fasting and postmeal hunger ratings were significantly higher for those with BE than for those without BE.. In individuals with BE, lower fasting AG may be due to downregulation by habitual overeating, and a smaller postmeal decline in AG may contribute to overeating. Lower postmeal leptin concentrations may also contribute to overeating.

Topics: Adult; Appetite; Binge-Eating Disorder; Bulimia; Cholecystokinin; Eating; Female; Ghrelin; Glucagon-Like Peptide 1; Humans; Hyperphagia; Insulin; Leptin; Male; Meals; Middle Aged; Obesity; Peptide YY; Postprandial Period; Young Adult

Gut-derived peptides, such as peptide YY (PYY) and ghrelin that regulate the initiation and termination of meals, could play a role in the altered eating behavior of patients with bulimia nervosa (BN). Therefore, we aimed to assess plasma PYY and ghrelin responses to a test meal in symptomatic bulimics.. Ten healthy women and nine women with BN underwent blood sample collections before and after the ingestion of a test meal of 1300 Kcal (with 15% carbohydrates, 10% proteins, and 75% fat) at 12:00 noon. Plasma total PYY, ghrelin, insulin, and glucose were assayed.. As compared with healthy women, bulimics exhibited a significantly blunted increase of circulating PYY (p < .007) and a significantly reduced suppression of plasma ghrelin (p < .0004) after the test meal. No significant differences emerged in food-induced plasma insulin and glucose changes between the two groups. Plasma ghrelin suppression after the meal was significantly correlated with plasma PYY increase.. We replicated our previous findings of an altered ghrelin response to food ingestion in people with BN and showed for the first time a blunted PYY increase after food consumption in these patients. These findings support the occurrence in BN of a profound dysregulation of some peripheral regulatory mechanisms involved in the short-term regulation of feeding behavior that might be involved in the pathophysiology of their binge eating behavior.

Topics: Adult; Blood Glucose; Body Composition; Body Mass Index; Bulimia; Dietary Fats; Eating; Female; Ghrelin; Humans; Insulin; Nutritional Physiological Phenomena; Peptide Hormones; Peptide YY

In recent years great advances have been made in our understanding of the peripheral signals produced within the gastrointestinal tract that regulate appetite, such as ghrelin and peptide YY (PYY). While ghrelin elicites hunger signals, PYY elicites satiety. Therefore, alterations in hormone physiology may play a role in the pathogenesis of bulimia nervosa (BN). In this study, we investigated the postprandial profile of ghrelin and PYY levels in patients with BN.. Postprandial plasma ghrelin and PYY levels and insulin and glucose responses were measured in 10 patients with BN and 12 control patients in response to a standard 400 kcal meal.. Basal ghrelin levels present in BN subjects (265.0 +/- 25.5 pmol/l) were significantly higher than those in healthy controls (199.3 +/- 18.4 pmol/l, P < 0.05), while basal PYY levels were equivalent in BN (14.6 +/- 1.3 pmol/l) and control (12.8 +/- 1.1 pmol/l, P = 0.30) subjects. Postprandial ghrelin suppression (decremental ghrelin area under the curve) was significantly attenuated in BN patients, compared to controls (-96.3 +/- 26.8 pmol/l x 3 h vs. -178.2 +/- 25.7 pmol/l x 3 h, P < 0.05). After a meal, the incremental PYY area under the curve in BN patients was significantly blunted from that observed in controls (9.2 +/- 2.6 pmol/l x 3 h vs. 26.8 +/- 3.2 pmol/l x 3 h, P < 0.01). Glucose and insulin responses to meals were similar between the two groups.. BN patients exhibit elevated ghrelin levels before meals with reduced ghrelin suppression after eating. In bulimia nervosa subjects, the rise in PYY levels after meals is also blunted. A gut-hypothalamic pathway involving peripheral signals, such as ghrelin and PYY, may be involved in the pathophysiology of BN.

Topics: Adult; Analysis of Variance; Blood Glucose; Bulimia; Case-Control Studies; Eating; Female; Ghrelin; Humans; Insulin; Peptide Hormones; Peptide YY; Postprandial Period

Whether or not peptide YY (PYY)-induced hyperphagia is modified by the histaminergic system in the brain is not yet known.. We investigated the effect on feeding of intracerebroventricular (ICV) administration of a specific histamine H3 receptor antagonist prior to ICV administration of PYY in rats.. PYY (1, 3, and 10 micrograms/10 microL) strongly induced feeding behavior in a dose-dependent manner in sated rats. The 4-hour food intake induced by 3 micrograms/10 microL of PYY was equal to that induced by a 16-hour fast. The ICV administration of thioperamide (40.8, 122.4, and 408.5 micrograms/10 microL) did not suppress the 4-hour food intake induced by 16-hour fasting; however, thioperamide produced dose-dependent and strong inhibition of hyperphagia induced by a 3-microgram dose of PYY.. These results suggest that the effect of PYY on appetite is different than that induced by fasting and may involve a histaminergic mechanism.

Topics: Analysis of Variance; Animals; Appetite Regulation; Bulimia; Disease Models, Animal; Dose-Response Relationship, Drug; Drinking; Eating; Fasting; Histamine Antagonists; Hyperphagia; Injections, Intraventricular; Male; Peptide YY; Piperidines; Rats; Rats, Wistar; Receptors, Histamine H3; Satiation; Time Factors

Disturbances of leptin, neuropeptide Y (NPY), and peptide YY (PYY) have been found in women who are ill with anorexia or bulimia nervosa. It is not certain whether peptide disturbances are cause or consequence of eating disorders.. Plasma leptin and cerebrospinal fluid leptin, NPY, and PYY concentrations were measured in women who were recovered from anorexia or bulimia nervosa to determine whether alterations persisted after recovery.. NPY, PYY, and leptin concentrations were similar across all diagnostic groups.. Alterations in NPY, PYY, and serum leptin concentrations are probably secondary to pathological eating behaviors. Alterations of these peptides are unlikely to be trait-related disturbances that contribute to the etiology of eating disorders.

Topics: Adipose Tissue; Adult; Anorexia Nervosa; Body Image; Body Mass Index; Bulimia; Convalescence; Female; Humans; Neuropeptide Y; Peptide YY; Proteins; Severity of Illness Index; Spinal Puncture

The related central nervous system peptides neuropeptide Y and peptide YY have been found to be among the most potent endogenous stimulants of feeding behavior. We measured these neuropeptides in cerebrospinal fluid to determine whether they contributed to the pathophysiologic characteristics of anorexia and bulimia nervosa. Cerebrospinal fluid neuropeptide Y concentrations were significantly elevated in underweight anorectic patients and in many of the anorectic patients studied at intervals after weight restoration. These levels normalized in long-term weight-restored anorectic patients who had a return of normal menstrual cycles. Increased neuropeptide Y activity may contribute to several characteristic disturbances in anorexia, including menstrual dysregulation. Cerebrospinal fluid peptide YY concentrations were significantly elevated in normal-weight bulimic patients abstinent from pathological eating behavior for a month compared with themselves when actively bingeing and vomiting or compared with healthy volunteers. Increased peptide YY activity may contribute to a drive to overfeed in normal-weight bulimic patients.

Topics: Adult; Anorexia Nervosa; Body Weight; Bulimia; Drive; Eating; Female; Gastrointestinal Hormones; Humans; Menstrual Cycle; Neuropeptide Y; Peptide YY; Peptides

Peptide YY (PYY), a recently discovered peptide, is a potent stimulant of eating behavior in rats. We developed a radioimmunoassay for PYY and measured cerebrospinal fluid (CSF) levels in subjects with anorexia nervosa, bulimia and matched normal controls. Bulimics who had abstained from bingeing for 30 days showed a dramatic increase in CSF PYY levels compared to normal values (p less than 0.001) or their own values when actively bingeing (p less than 0.01, paired t test). No differences were seen for anorexia nervosa. These results suggest that bulimic behavior may correct a central nervous system abnormality in PYY.

Topics: Adolescent; Adult; Anorexia Nervosa; Bulimia; Chromatography, High Pressure Liquid; Female; Follow-Up Studies; Humans; Peptide YY; Peptides; Radioimmunoassay