peptide-yy and Bulimia-Nervosa

Anorexia nervosa (AN) and bulimia nervosa (BN) are psychiatric disorders characterized by abnormal eating behaviors and imbalance of energy homeostasis. Changes of both central and peripheral neuroendocrine substances involved in the modulation of food intake and energy expenditure have been described in acutely ill patients with eating disorders. This review selectively focuses on the most recent findings supporting abnormal changes in the physiology of some peripheral adipokines and gut-secreted peptides, brain-derived neurotrophic factor and endocannabinoids in patients with AN or BN. Literature data do suggest a dysregulation of these neuroendocrine feeding regulators but, at the moment, they do not allow to establish the state or trait-dependent nature of those aberrations. It has been proposed, although not definitively proved, that neuroendocrine alterations, even when secondary to malnutrition and/or to aberrant eating behaviors, might contribute to the genesis and the maintenance of some symptomatic aspects of AN and BN, thus affecting the course and the prognosis of these disorders. Future studies should clarify whether neuroendocrine alterations are part of the genetically transmitted biological vulnerability to eating disorders.

Topics: Adipokines; Adolescent; Adult; Anorexia Nervosa; Brain-Derived Neurotrophic Factor; Bulimia Nervosa; Cannabinoid Receptor Modulators; Eating; Feeding and Eating Disorders; Female; Ghrelin; Humans; Neurosecretory Systems; Peptide YY

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

BED is characterized by overeating with a loss of control. The primary aim of the study was to measure plasma concentrations of three key gut peptides influencing hunger (ghrelin) and satiety (PYY, GLP-1) to ascertain potential abnormalities in BED. The participants were 10 obese BED and 9 obese nonBED premenopausal women. They did not differ in age, 30.1+/-8.1 SD, BMI, 36.2+/-5.9, or % body fat, 43.3+/-5.7. Following a13-h overnight fast, blood was drawn (-15, 0, 5, 15, 30, 60, 90, 120 min) for measurement of total plasma concentrations of ghrelin, PYY and GLP-1, pre and post ingestion of a nutritionally complete liquid meal (1256 kJ) at 9 am (0-5 min). Ratings of hunger and fullness preceded each blood draw. Ghrelin was significantly lower premeal at -15 min (P=.05) and postmeal at 90 min (P=.027) and 120 min (P=.025) in the BED group as compared to the nonBED group. Ghrelin also declined less postprandially in the BED group (P=.019) with a longer time to the nadir value (P=.004). However, fasting and meal-related changes in levels of PYY and GLP-1 did not differ between the groups nor did ratings of hunger and fullness. Following a randomized cognitive behavior and dietary intervention, the ghrelin values in BED normalized. Prior to treatment, the lower fasting ghrelin in BED may be a consequence of down regulation by overeating. The lack of differences in the satiety promoting hormones, PYY and GLP-1, makes them unlikely contributors to the binge eating in BED.

Topics: Adult; Analysis of Variance; Appetite Regulation; Bulimia Nervosa; Cognitive Behavioral Therapy; Counseling; Female; Ghrelin; Glucagon-Like Peptide 1; Humans; Linear Models; Obesity; Peptide YY; Postprandial Period; Satiation

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

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