neuropeptide-y and Bulimia

The eating disorders anorexia nervosa and bulimia nervosa are best conceptualized as syndromes and are classified on the basis of the clusters of symptoms they present. According to the multidimensional model, eating disorders begin with dieting, which is propelled into a full-blown disorder by antecedent conditions of biological vulnerability and genetics, premorbid psychological characteristics, family interactions, and social climate. The medical abnormalities present in individuals with eating disorders are due to starvation conditions and purging behaviors and will resolve with nutritional rehabilitation and the cessation of purging. Comorbid psychiatric conditions such as affective disorders, anxiety disorders, substance abuse, and personality disorders are frequently present. For anorexia nervosa, the most effective strategy is multidimensional treatment, consisting of nutritional rehabilitation, medical attention, individual cognitive psychotherapy, and family counseling or therapy if the patient is younger than age 18 years. For bulimia nervosa, the treatment of choice is cognitive-behavioral therapy with directions in a manual for therapists. A second choice for treatment is an antidepressant, beginning with fluoxetine.

Topics: Anorexia Nervosa; Bulimia; Cholecystokinin; Dopamine; Female; Humans; Neuropeptide Y; Serotonin

Topics: Anorexia Nervosa; Body Image; Bulimia; Cognitive Behavioral Therapy; Family; Homovanillic Acid; Humans; Hypothalamus; Neuropeptide Y; Neurotransmitter Agents; Psychiatric Status Rating Scales; Research

The consumption of a large food bolus leads to stomach distension. Gastric distension potently signals the termination of a meal by stimulating gastric mechanoreceptors and activating neuroendocrine circuitry. The ability to terminate a meal is altered in disorders such as bulimia nervosa (BN), binge-eating disorder (BED) and certain subtypes of obesity in which large quantities of food are frequently ingested. When a large meal is consumed, the stomach is rapidly stretched. We modeled this rapid distension of the stomach in order to determine if the neuroendocrine abnormalities present in these disorders, including increased gastric capacit3y, leptin dysregulation, and alterations in neuropeptide Y (NPY), and proopiomelanocortin (POMC) expression, were influenced by the rapid stretch aspect of repeatedly consuming a large meal. To test the effects of repeated gastric distension (RGD) on neuroendocrine factors involved in energy homeostasis, a permanent intra-gastric balloon was implanted in rats, and briefly inflated daily for 4 weeks. Though body weights and daily food intakes remained equivalent in RGD and control rats, a significant delay in the onset of feeding was present during the first and second, but not the third and fourth weeks of inflations. Despite equivalent body weights and daily caloric consumption, RGD animals had significantly decreased leptin levels (p<0.05), and tended to have increased fasting arcuate NPY levels (p=0.08), which were suppressed more than control animals following food intake (control and RGD decreases from baseline were 184.95% and 257.42%, respectively). NPY expression in the nucleus of the solitary tract followed a similar pattern. These data demonstrate that the act of regularly distending the stomach can have effects on the regulation of energy balance that are independent from those related to caloric consumption, and may be related to disorders such as BN, BED, and certain types of obesity in which meal termination is impaired.

Topics: Animals; Arcuate Nucleus of Hypothalamus; Body Weight; Bulimia; Eating; Energy Metabolism; Feeding Behavior; Gastric Balloon; Hyperphagia; Leptin; Male; Neuropeptide Y; Pro-Opiomelanocortin; Rats; Rats, Long-Evans; Solitary Nucleus; Stomach

It has been reported that leptin and neuropeptide Y (NPY) play a role in the control of appetite and in the regulation of hormonal secretion.. Plasma leptin, neuropeptide Y (NPY) and galanin concentrations were estimated in 13 women with bulimia nervosa (BN) 19 women with anorexia nervosa (AN) and in 19 healthy women of the control group (CG).. Plasma leptin concentration in BN was significantly higher than that in AN and it was lower as compared with the control group, despite the same BMI (body mass index) in both the groups. Plasma leptin level in AN was significantly lower as compared with the controls. Plasma galanin concentrations in AN and BN did not differ significantly from the control group. Plasma NPY concentration in AN was lower than that in the control group. However, plasma NPY level in BN was significantly higher as compared with AN and with the control group (CG). The observed increase of NPY in BN was independent of BMI because BMI in bulimia nervosa was normal.. The data may suggest that other factors than body weight changes may be involved in the modulation of leptin and NPY release in BN. The pathological behaviour of patients with bulimia nervosa may result from disturbed NPY release which is the strongest orexigenic factor.

Topics: Adolescent; Adult; Anorexia Nervosa; Body Mass Index; Bulimia; Female; Galanin; Humans; Leptin; Neuropeptide Y; Reference Values

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