cholecystokinin and Bulimia-Nervosa

Individuals with bulimia nervosa (BN) report altered perceptions in hunger, fullness, and satiety. This article reviews the role of cholecystokinin (CCK), a satiety-producing hormone, in the regulation of binge eating in those who suffer from BN.. Studies have shown that CCK is decreased in individuals with BN when compared with healthy controls. Decreased CCK functioning may contribute to impaired satiety and thus binge eating in this patient population. Depending on the macronutrient composition of food choices, CCK release can be differentially influenced. For instance, protein is a potent stimulator of a CCK response. Eating more protein-rich meals increases the release of CCK, increasing satiety and ending a meal.. Knowledge of CCK functioning and the utility of manipulating the macronutrient composition of meals may inform standard behavioral treatment strategies for those who suffer from BN.

Topics: Bulimia Nervosa; Cholecystokinin; Feeding Behavior; Humans; Hunger; Satiation

Previous studies have suggested that delayed gastric emptying and abnormal postprandial release of hormones that influence satiation, particularly cholecystokinin (CCK), may play an important role in the pathophysiology of bulimia nervosa (BN). This study was designed to test these hypotheses as well as the efficacy of the prokinetic agent erythromycin in patients with BN.. Thirty-two normal-weight women with BN and 24 control participants consumed a large liquid test meal. Gastric emptying and pre- and postprandial release of CCK, peptide YY (PYY), and ghrelin were determined. Participants with BN were then recruited for double-blind treatment with erythromycin up to 500 mg three times daily vs. placebo for 6 weeks, following which they consumed a repeat test meal with gastric emptying and appetitive hormone measurements.. CCK release at 15 min following the meal was marginally lower (p=0.1) in BN than in control participants. Rate of gastric emptying and postprandial hormone release were similar in BN and controls. BN patients assigned to erythromycin compared to those assigned to placebo had more rapid gastric emptying following treatment, but there were no differences in release of CCK, PYY, or ghrelin following the post-treatment test meal. Moreover, treatment with erythromycin was not associated with clinical response.. The current study does not support the clinical utility of moderate dose erythromycin in treating BN. Furthermore, the findings suggest that a modest increase in gastric emptying rate is associated neither with altered postprandial hormonal release nor with clinical benefit in these patients. While providing no evidence for the effectiveness of prokinetic agents in this setting, our findings do not preclude the possibility that a greater increase in gastric emptying rate might prove beneficial.

Topics: Adolescent; Adult; Bulimia Nervosa; Cholecystokinin; Double-Blind Method; Erythromycin; Female; Gastric Emptying; Gastrointestinal Agents; Ghrelin; Humans; Middle Aged; Motilin; Peptide YY

High androgen levels in women with bulimia nervosa may promote bulimic behavior. The aim of the present study was to investigate the effects of an antiandrogenic oral contraceptive (OC) on appetite and eating behavior in women with bulimia nervosa compared to healthy controls. Twenty-one women with bulimia nervosa and 17 healthy controls matched for age and body mass index participated in the study. Basal and meal-related appetite and secretions of the satiety peptide cholecystokinin (CCK) and the appetite-stimulating peptide ghrelin were studied before and after 3 months of treatment with an antiandrogenic OC (30 microg ethinyl estradiol combined with 3 mg drospirenone). Bulimic behavior was evaluated in relation to changes in hormone levels. Before treatment, bulimic women had higher frequency of menstrual disturbances, acne and hirsutism and higher levels of testosterone but lower meal-related CCK secretion than controls. OC treatment reduced meal-related hunger and gastric distention in bulimics. CCK secretion in response to the meal was unchanged in bulimic women but decreased in the controls. Ghrelin secretion was comparable between groups and did not change in response to OC treatment. The treatment improved bulimic behavior in relation to a decline in testosterone levels in the entire group. Our results support the suggestion that androgens play a role in bulimic behavior. Treatment with an antiandrogenic OC may serve as a new strategy for treatment of bulimia nervosa and particularly in those patients with hyperandrogenic symptoms.

Topics: Adult; Androgen Antagonists; Androstenes; Appetite; Appetite Regulation; Area Under Curve; Bulimia Nervosa; Case-Control Studies; Cholecystokinin; Contraceptives, Oral, Hormonal; Eating; Feeding Behavior; Female; Ghrelin; Humans; Matched-Pair Analysis; Peptide Hormones; Reference Values; Sex Hormone-Binding Globulin; Testosterone

Patients with bulimia nervosa (BN) are reported to have decreased postprandial levels of cholecystokinin (CCK) and peptide YY (PYY). Fatty nutrients are the most powerful stimulus for releasing these peptides. Cholestyramine is an anion exchanger which adsorbs bile salts and reduces the digestion of lipids, affecting the secretion of both CCK and PYY. To further characterise the physiology of these peptides in BN, we aimed to investigate the effects of cholestyramine (12 g, per os) or placebo administered with a high-fat meal on CCK and PYY secretions in bulimic versus healthy women.. Postprandial CCK levels significantly increased in both healthy and bulimic women after placebo + the high-fat meal, without any significant difference between the two groups. Cholestyramine administration significantly increased postprandial CCK responses in both healthy and bulimic women; however, significantly lower CCK levels were observed in BN. Postprandial PYY levels significantly increased after placebo administration in healthy women after the high-fat meal, whereas no significant changes were found in bulimic women. Cholestyramine, administered with the high-fat meal, significantly reduced postprandial PYY response in healthy women, but not in bulimic women. Finally, there was a negative correlation of the area under the curve with respect to the increase of PYY (after placebo administration) with binge frequency in the bulimic women.. In BN an altered postprandial secretion of CCK may be evidenced when cholestyramine is combined with a high-fat meal. Instead, the postprandial secretion of PYY is significantly blunted and not affected by cholestyramine administration.

Topics: Adult; Anion Exchange Resins; Bulimia Nervosa; Cholecystokinin; Cholestyramine Resin; Diet, High-Fat; Female; Humans; Peptide YY; Postprandial Period

The core defining features of bulimia nervosa (BN) are repeated binge eating episodes and inappropriate compensatory (e.g., purging) behavior. Previous studies suggest an abnormal post-prandial response in the satiety-signaling peptide cholecystokinin (CCK) in persons with BN. It is unknown whether this altered response persists following remission or if it may be a potential target for the development of clinical treatment strategies. To examine the nature of this altered response, this study assessed whether CCK normalizes following remission from BN (RBN). This study prospectively evaluated the plasma CCK response and corresponding eating behavior-related ratings (e.g., satiety, fullness, hunger, urge to binge and vomit) in individuals with BN-purging subtype (n=10), RBN-purging subtype (n=14), and healthy controls (CON, n=13) at baseline, +15, +30, and +60 min following the ingestion of a standardized liquid test meal. Subject groups did not significantly differ in CCK response to the test meal. A significant relationship between CCK response and satiety ratings was observed in the RBN group (r=.59, p<.05 two-tailed). A new and unanticipated finding in the BN group was a significant relationship between CCK response and ratings of "urge to vomit" (r=.86, p<.01, two-tailed). Unlike previous investigations, CCK response did not differ in BN and CON groups. Thus the role of symptom severity remains an area of further investigation. Additionally, findings suggest that in this sample, CCK functioning following remission from BN-purging subtype is not different from controls. It remains unknown whether or not CCK functioning may be a protective or liability factor in the stabilization and recovery process. Replication studies utilizing a larger sample size are needed to further elucidate the role of CCK in recovery from BN and its potential target of related novel treatment strategies.

Topics: Adolescent; Adult; Bulimia; Bulimia Nervosa; Cholecystokinin; Eating; Female; Humans; Hunger; Middle Aged; Postprandial Period; Prospective Studies; Satiation

Several abnormalities of peripheral neuropeptide release in obese and obese patients with binge eating disorder (BED) compared to controls have been reported: lower baseline, meal-induced, and post-meal ghrelin concentrations, decreased baseline PYY, and a blunted PYY response to meals. In contrast, obese BED individuals show comparable CCK releases. We aimed at clarifying the role of peripheral hormones in BED, to assess the impact of a cognitive behavioral treatment (CBT) for BED on neuropeptides and to investigate the predictive value of neuropeptide concentrations on binge eating status after treatment.. Blood samples of 14 female and 4 male overweight to obese participants with BED were collected repeatedly for CCK, PYY, and ghrelin analysis in the morning after an 8-h fasting period. BED participants and 19 controls matched for age and body mass index (BMI) were served a standardized breakfast. The release of neuropeptides was compared to corresponding measures of controls.. Fasting baseline values of all three peptides were comparable between BED participants and controls. BED participants revealed a higher meal-induced increase in CCK and PYY compared to controls, whereas ghrelin was not affected. Following a short-term CBT the neuropeptide concentration of the BED participants was comparable to before CBT. The hormone release prior to treatment had no predictive value on binge eating status after the treatment.. With respect to CCK and PYY our results point to a combined conditioned response from the central nervous system and the gut to initiate the release of satiety hormones in order to prevent further bingeing after initial food intake. The release of neuropeptides does not predict short-term treatment outcome. Future prospective studies should investigate whether neuropeptide secretion influences the course of BED in the long term.

Topics: Bulimia Nervosa; Case-Control Studies; Cholecystokinin; Cognitive Behavioral Therapy; Eating; Female; Ghrelin; Humans; Male; Middle Aged; Obesity; Peptide YY; Severity of Illness Index

Recent data suggest that purging disorder, a recently characterized form of eating disorder not otherwise specified, may be worthy of specific delineation in nosological schemes. However, more data are needed to determine how purging disorder differs from bulimia nervosa.. To examine clinical features and subjective as well as objective physiological responses to a standardized test meal in purging disorder compared with bulimia nervosa and controls.. Study visit 1 included psychological assessments with structured clinical interviews and questionnaires. Study visit 2 included assessment of test-meal responses.. Participants recruited from the community completed test-meal studies in a General Clinical Research Center.. Women with DSM-IV bulimia nervosa-purging subtype (n = 37) and purging disorder (n = 20) and non-eating disorder controls (n = 33) with a body mass index (calculated as weight in kilograms divided by height in meters squared) between 18.5 and 26.5 who were free of psychotropic medications.. Assessments of eating disorder severity, postprandial cholecystokinin response, and subjective responses to test meals.. Eating abnormalities were significantly elevated in participants with purging disorder and bulimia nervosa compared with controls but did not differ between eating disorder groups. Participants with purging disorder demonstrated significantly greater postprandial cholecystokinin release compared with participants with bulimia nervosa (t(76.44) = 2.51; P = .01) and did not differ significantly from controls (t(75.93) = 0.03; P = .98). Participants with purging disorder reported significantly greater postprandial fullness and gastrointestinal distress compared with participants with bulimia nervosa and controls.. Purging disorder is a clinically significant disorder of eating that appears to be distinct from bulimia nervosa on subjective and physiological responses to a test meal. Findings support further consideration of purging disorder for inclusion in the classification of eating disorders. Future studies on the psychobiology of purging disorder are needed to understand the propensity to purge in the absence of binge eating.

Topics: Adult; Appetite; Body Mass Index; Bulimia Nervosa; Cholecystokinin; Control Groups; Diagnosis, Differential; Diagnostic and Statistical Manual of Mental Disorders; Eating; Feeding and Eating Disorders; Female; Humans; Hunger; Personality Inventory; Postprandial Period; Psychiatric Status Rating Scales; Satiation; Severity of Illness Index; Surveys and Questionnaires; Vomiting

Eating disorders (EDs) have a highly heterogeneous etiology and multiple genetic factors might contribute to their pathogenesis. Ghrelin, a novel growth hormone-releasing peptide, enhances appetite and increases food intake, and human ghrelin plasma levels are inversely correlated with body mass index. In the present study, we examined the 171T/C polymorphism of the ghrelin receptor (growth hormone secretagogue receptor, GHSR) gene in patients diagnosed with EDs, because the subjects having ghrelin gene polymorphism (Leu72Met) was not detected in a Japanese population, previously. In addition, beta3 adrenergic receptor gene polymorphism (Try64Arg) and cholecystokinin (CCK)-A receptor (R) gene polymorphism (-81A/G, -128G/T), which are both associated with obesity, were investigated. The subjects consisted of 228 Japanese patients with EDs [96 anorexia nervosa (AN), 116 bulimia nervosa (BN) and 16 not otherwise specified (NOS)]. The age- and gender-matched control group consisted of 284 unrelated Japanese subjects. The frequency of the CC type of the GHSR gene was significantly higher in BN subjects than in control subjects (chi(2) = 4.47, p = 0.035, odds ratio = 2.05, Bonferroni correction: p = 0.070), while the frequency in AN subjects was not different from that in controls. The distribution of neither beta3 adrenergic receptor gene nor CCK-AR polymorphism differed between EDs and control subjects. Therefore, the CC type of GHSR gene polymorphism (171T/C) is a risk factor for BN, but not for AN.

Topics: Adult; Aged; Body Mass Index; Bulimia Nervosa; Cholecystokinin; DNA; Feeding and Eating Disorders; Female; Genotype; Humans; Japan; Male; Middle Aged; Panic Disorder; Polymorphism, Single Nucleotide; Receptors, Adrenergic, beta-3; Receptors, Cholecystokinin; Receptors, G-Protein-Coupled; Receptors, Ghrelin; Reverse Transcriptase Polymerase Chain Reaction; Risk Factors