peptide-yy and Feeding-and-Eating-Disorders

Disturbances in gastrointestinal hormones have been implicated in the pathogenesis of eating disorders such as anorexia nervosa and bulimia nervosa. However, the contribution of these hormonal changes to the onset and maintenance of eating disorder remains unclear. We focus our review on a selective number of gastrointestinal hormones that are known to play a role in the regulation of short-term or long-term energy balance and examine their association with eating disorder in recently published literature.. Several new studies reported differential changes of ghrelin isoforms during fasting and following nutrient ingestion. New findings on other appetite-regulating hormones (peptide YY, cholecystokinin, incretin hormones and pancreatic polypeptide) at different nutritional states and disease stage have also been reported in subtypes of eating disorder. Most of the changes in peripheral hormones disappeared or partially recovered after the restoration of weight with nutritional and behavioral therapy.. Dysregulation of gastrointestinal hormones is more likely to contribute to the maintenance of the disordered eating behavior and related metabolic outcomes as well as the clinical course rather than causing them. A better understanding of this relationship also carries implications for developing targeted hormone-base treatment for eating disorder.

Topics: Animals; Cholecystokinin; Feeding and Eating Disorders; Gastrointestinal Hormones; Ghrelin; Glucagon-Like Peptide 1; Humans; Peptide Hormones; Peptide YY

Disturbances in gastrointestinal hormones have been widely identified in persons with eating disorders (EDs) and have been implicated in their clinical pathologies.. The objective was to identify, critically examine, and summarize studies investigating the short-term response of gastrointestinal hormones to food in persons with an ED, including the subtypes anorexia nervosa and bulimia nervosa.. A priori inclusion and exclusion criteria were set and included a procedure in which a test meal or glucose load was given and blood hormone concentrations measured. All studies included a healthy control group for comparison. The outcome variable was defined as the mean difference between fasting plasma hormone concentrations and the maximum postprandial peak or nadir. The difference in baseline values between groups was also examined. Pooled standardized mean differences were calculated and analyzed where possible.. A total of 28 studies were identified, including sufficient studies to perform a meta-analysis for ghrelin, peptide YY, cholecystokinin, insulin, and pancreatic polypeptide. Persons with an ED had higher baseline concentrations of ghrelin (large effect), peptide YY (medium effect), and cholecystokinin (medium effect for ED, large effect for anorexia nervosa). The response of insulin to food was decreased in persons with an ED (medium effect). No further differences were found in the release of gut peptides to a standardized test meal.. All of the studies had low power for the different subtypes of EDs. High heterogeneity among the studies was observed, and limitations are discussed. The findings suggest that the physiologic changes observed in patients with EDs are highly variable and subject to multiple confounding factors.

Topics: Cholecystokinin; Feeding and Eating Disorders; Gastrointestinal Hormones; Gastrointestinal Tract; Ghrelin; Humans; Insulin; Pancreatic Polypeptide; Peptide YY

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

Obesity is a major cause of premature death in the UK, and may contribute to as many as 30 000 deaths a year in the UK. Although effective treatment for obesity is still awaited, many developments have occurred to improve our understanding of neuroendocrine regulation of food intake and weight gain, especially regarding the role of gut hormones. One such gut hormone is peptide tyrosine-tyrosine also known as PYY where Y depicts the abbreviation for tyrosine. PYY is a 36 amino acid hormone, first isolated from porcine intestine. PYY, along with few other gut hormones, has been suggested as a potential therapeutic agent for obesity. This review examines the relationship of PYY to appetite regulation, energy homeostasis and the relevant neuroendocrine feedback mechanism.

Topics: Animals; Anti-Obesity Agents; Appetite Regulation; Bariatric Surgery; Feeding and Eating Disorders; Genetic Predisposition to Disease; Humans; Obesity; Peptide Fragments; Peptide YY; Satiation

Health problems resulting from obesity could offset many of the recent health gains achieved by modern medicine, and obesity may replace tobacco as the number one health risk for developed societies. An estimated 300,000 deaths per year and significant morbidity are directly attributable to obesity, mainly due to heart disease, diabetes, cancer, asthma, sleep apnea, arthritis, reproductive complications and psychological disturbances. In parallel with the increasing prevalence of obesity, there has been a dramatic increase in the number of scientific and clinical studies on the control of energy homeostasis and the pathogenesis of obesity to further our understanding of energy balance. It is now recognized that there are many central and peripheral factors involved in energy homeostasis, and it is expected that the understanding of these mechanisms should lead to effective treatments for the control of obesity. This brief review discusses the potential role of several recently discovered molecular pathways involved in the control of energy homeostasis, obesity and eating disorders.

Topics: Adiponectin; Animals; Appetite; Child; Energy Metabolism; Feeding and Eating Disorders; Ghrelin; Homeostasis; Humans; Insulin; Intercellular Signaling Peptides and Proteins; Leptin; Obesity; Peptide Fragments; Peptide Hormones; Peptide YY; Proteins

Peptide YY (PYY) is the most potent orexigenic peptide or substance known. However, neither the underlying physiology of this hyperphagia nor PYY's natural role in brain are well understood. Thus, this review details the neuroanatomical sites, the neurochemical and systemic interactions, the food-related properties and the motivational factors that characterize hyperphagia elicited by central PYY. Emphasis also is given to evidence that central PYY has properties functionally distinct from neuropeptide Y. Finally, future research directions are outlined that aim at accelerating our understanding of the roles that brain PYY and PYY-preferring receptors occupy in normal and abnormal feeding behavior.

Topics: Amino Acid Sequence; Animals; Brain; Central Nervous System; Feeding and Eating Disorders; Feeding Behavior; Female; Humans; Hyperphagia; Male; Molecular Sequence Data; Neurotransmitter Agents; Peptide YY; Rats

Eating disorders (EDs) are increasingly frequent. Their pathophysiology involves disturbance of peptide signaling and the microbiota-gut-brain axis. This study analyzed peptides and corresponding immunoglobulin (Ig) concentrations in groups of ED. In 120 patients with restrictive (R), bulimic (B), and compulsive (C) ED, the plasma concentrations of leptin, glucagon-like peptide-1 (GLP-1), peptide YY (PYY), and insulin were analyzed by Milliplex and those of acyl ghrelin (AG), des-acyl ghrelin (DAG), and α-melanocyte-stimulating hormone (α-MSH) by ELISA kits. Immunoglobulin G (in response to an antigen) concentrations were analyzed by ELISA, and their affinity for the respective peptide was measured by surface plasmon resonance. The concentrations of leptin, insulin, GLP-1, and PYY were higher in C patients than in R patients. On the contrary, α-MSH, DAG, and AG concentrations were higher in R than in C patients. After adjustment for body mass index (BMI), differences among peptide concentrations were no longer different. No difference in the concentrations of the IgG was found, but the IgG concentrations were correlated with each other. Although differences of peptide concentrations exist among ED subtypes, they may be due to differences in BMI. Changes in the concentration and/or affinity of several anti-peptide IgG may contribute to the physiopathology of ED or may be related to fat mass.

Topics: Body Mass Index; Cohort Studies; Enzyme-Linked Immunosorbent Assay; Feeding and Eating Disorders; Female; France; Glucagon-Like Peptide 1; Humans; Immunoglobulin G; Insulin; Leptin; Longitudinal Studies; Male; Peptide YY; Peptides

Objective To evaluate the eating behavior of obese adolescents and its association with biochemical, anthropometric and peptide YY (PYY) measures. Methods Fifty-one obese adolescents received counseling for weight management at 12 monthly appointments. Fasting serum PYY levels, total cholesterol (TC), high density lipoprotein cholesterol (HDL-C), triglycerides (TG), low density lipoprotein cholesterol (LDL-C), insulin and glucose levels, waist circumference (WC) and results from the Three-Factor Eating Questionnaire (TFEQ-21) were assessed. Results Over one year there was a significant increase in PYY levels (p = 0.026), reduction in TC (p = 0.003), TG (p = 0.022), BMI (p = 0.002), BMI z-score (p < 0.001) and WC (p = 0.003). During this period there was a decrease in the uncontrolled eating score (UE), illustrating that adolescents displayed more self-control (p = 0.008) at the end of the study; however, this result was independent of BMI and BMI z-score (p = 0.407). The reduction in UE was associated with a significant improvement in insulin levels (rs = 0.326; p = 0.020). The reduction in UE was also associated with lower levels of blood glucose (r = 0.332; p = 0.017), and the increase of cognitive restriction, with the reduction of insulin insulin (rs = -0.294; p = 0.036) and TG (r = -0.368; p = 0.008) and an increase in Cognitive Restraint. Conclusions Our results show that after a year of monitoring weight loss, adolescents had more controlled eating behaviors, increased PYY levels, and reduced weights.

Topics: Adolescent; Ambulatory Care; Biomarkers; Body Mass Index; Body Weights and Measures; Child; Cohort Studies; Feeding and Eating Disorders; Feeding Behavior; Female; Humans; Male; Obesity, Morbid; Pediatric Obesity; Peptide YY

Little is known about biological factors that contribute to purging after normal amounts of food-the central feature of purging disorder (PD). This study comes from a series of nested studies examining ingestive behaviors in bulimic syndromes and specifically evaluated the satiety peptide YY (PYY) and the hunger peptide ghrelin in women with PD (n = 25), bulimia nervosa-purging (BNp) (n = 26), and controls (n = 26). Based on distinct subjective responses to a fixed meal in PD (Keel, Wolfe, Liddle, DeYoung, & Jimerson, ), we tested whether postprandial PYY response was significantly greater and ghrelin levels significantly lower in women with PD compared to controls and women with BNp.. Participants completed structured clinical interviews, self-report questionnaires, and laboratory assessments of gut peptide and subjective responses to a fixed meal.. Women with PD demonstrated a significantly greater postprandial PYY response compared to women with BNp and controls, who did not differ significantly. PD women also endorsed significantly greater gastrointestinal distress, and PYY predicted gastrointestinal intestinal distress. Ghrelin levels were significantly greater in PD and BNp compared to controls, but did not differ significantly between eating disorders. Women with BNp endorsed significantly greater postprandial hunger, and ghrelin predicted hunger.. PD is associated with a unique disturbance in PYY response. Findings contribute to growing evidence of physiological distinctions between PD and BNp. Future research should examine whether these distinctions account for differences in clinical presentation as this could inform the development of specific interventions for patients with PD.

Topics: Adolescent; Adult; Feeding and Eating Disorders; Female; Gastrointestinal Absorption; Humans; Middle Aged; Peptide YY; Satiation; Young Adult

Basal release of GUT peptides has been found to be altered in restrained eaters. Stress-induced secretion, however, has not yet been described, but could be a biological basis of overeating that exposes restrained eaters to a higher risk of becoming obese. The aim of the present study was to compare restrained and unrestrained eaters with respect to stress-induced release of the GUT peptides ghrelin and PYY. 46 young women were studied. Blood sampling for peptides was done before and after the Trier Social Stress Test. Ghrelin secretion after stress was significantly elevated in the restrained eaters, whereas no significant differences were detected for PYY. Stress-induced release of GUT peptides can be interpreted as a cause as well as a consequence of restrained eating.

Topics: Case-Control Studies; Feeding and Eating Disorders; Feeding Behavior; Female; Ghrelin; Humans; Peptide YY; Stress, Psychological; Surveys and Questionnaires; Young Adult

Many patients with major depression refer a decreased appetite and weight loss among their symptoms. Peptide YY (PYY) and ghrelin belong to the family of peptides of the gut-brain axis implicated in the regulation of appetite and energy metabolism. PYY stimulates a powerful central satiety response and ghrelin increases food intake and weight gain. Brain-derived neurotrophic factor (BDNF) also contributes to the central control of food intake as an anorexigenic factor.. To study fasting plasma total and acylated ghrelin, plasma PYY and serum BDNF levels in patients with major depression with weight loss as one of their symptoms and compare them with matched healthy controls.. Fifteen adult patients, 9 male and 6 female, with recent diagnosis of major depression, and 16 healthy adult subjects, matched by age and anthropometric parameters were studied. All depressed patients referred weight loss and were not under antidepressant therapy. Fasting total PYY, total ghrelin and acylated ghrelin and BDNF were determined.. Fasting total PYY was higher in patients than controls (2.01±0.09 vs 1.29±0.16 pmol/l). There were no differences in fasting total ghrelin, acylated ghrelin or BDNF levels.. Major depressed patients, with weight loss at diagnosis, showed higher fasting plasma PYY levels that could contribute to their reduced appetite.

Topics: Acetylation; Adult; Appetite Regulation; Body Mass Index; Brain-Derived Neurotrophic Factor; Case-Control Studies; Cohort Studies; Depressive Disorder, Major; Feeding and Eating Disorders; Female; Ghrelin; Humans; Male; Middle Aged; Peptide YY; Self Report; Weight Loss

Disordered eating occurs in women at both weight extremes of anorexia nervosa (AN) and obesity. Cortisol, peptide YY (PYY), leptin, and ghrelin are hormones involved in appetite and feeding behavior that vary with weight and body fat. Abnormal levels of these hormones have been reported in women with AN, functional hypothalamic amenorrhea (HA), and obesity. The relationship between appetite-regulating hormones and disordered eating psychopathology is unknown. We therefore studied the relationship between orexigenic and anorexigenic hormones and disordered eating psychopathology in women across a range of weights.. A cross-sectional study of 65 women, 18-45 years: 16 with AN, 12 normal-weight with HA, 17 overweight or obese, and 20 normal-weight in good health.. Two validated measures of disordered eating psychopathology, the Eating Disorders Examination-Questionnaire (EDE-Q) and Eating Disorders Inventory-2 (EDI-2), were administered. Fasting PYY, leptin, and ghrelin levels were measured; cortisol levels were pooled from serum samples obtained every 20 min from 2000 to 0800 h.. Cortisol and PYY levels were positively associated with disordered eating psychopathology including restraint, eating concerns, and body image disturbance, independent of body mass index (BMI). Although leptin levels were negatively associated with disordered eating psychopathology, these relationships were not significant after controlling for BMI. Ghrelin levels were generally not associated with EDE-Q or EDI-2 scores.. Higher levels of cortisol and PYY are associated with disordered eating psychopathology independent of BMI in women across the weight spectrum, suggesting that abnormalities in appetite regulation may be associated with specific eating disorder pathologies.

Topics: Adolescent; Adult; Analysis of Variance; Body Image; Body Mass Index; Cross-Sectional Studies; Feeding and Eating Disorders; Female; Ghrelin; Humans; Hydrocortisone; Leptin; Middle Aged; Peptide YY; Radioimmunoassay; Surveys and Questionnaires

The purpose of this study was twofold: (1) to determine if gastrointestinal hormones, associated with energy intake and energy balance, are altered in exercising women with hypothalamic amenorrhea and (2) to assess the association between gastrointestinal hormones and behavioural indicators of subclinical disordered eating in exercising women with hypothalamic amenorrhea. This cross-sectional study analyzed serum ghrelin, peptide YY (PYY), glucagon-like peptide-1 (GLP-1), menstrual status (by E1G and PdG), resting energy expenditure (REE), and subclinical eating behaviours in sedentary ovulatory (SedOv), exercising ovulatory (ExOv), and exercising amenorrheic (ExAmen) women. Groups were similar with respect to age (23.8+/-0.6 years) and BMI (21.4+/-0.3 kg/m(2)). The ratio of REE to predicted REE (REE:predicted REE) was 0.94+/-0.02, 0.94+/-0.02, and 0.88+/-0.02 in the SedOv, ExOv, and ExAmen groups, respectively. The REE:predicted REE in the ExAmen group was consistent with an energy deficiency. LogPYY, ghrelin, dietary cognitive restraint, and drive for thinness were elevated in the ExAmen group compared to other groups. GLP-1 concentrations were similar among groups. LogPYY correlated with drive for thinness and REE/FFM. In conclusion, fasting PYY and ghrelin concentrations are elevated in exercising women with FHA and both gastrointestinal peptides may serve as a proxy indicator of energy deficiency in this population.

Topics: Adolescent; Adult; Amenorrhea; Body Mass Index; Cross-Sectional Studies; Energy Intake; Energy Metabolism; Exercise; Feeding and Eating Disorders; Female; Ghrelin; Glucagon-Like Peptide 1; Humans; Hypothalamus; Menstrual Cycle; Peptide YY; Thinness

Central injection of peptide YY (PYY) in sated rats produces the most powerful stimulating effect of food intake known to date. The neural mechanisms by which PYY regulates appetite are not clear but may be important because abnormal levels of PYY have been implicated in the neurobiology of bulimia nervosa. Interactions between brain acetylcholine (ACh) and PYY had not been studied. Therefore, the present experiments were designed to explore the in vivo release of ACh from the hippocampus (HPC) of rats in response to hypothalamic infusion of PYY. Hippocampal ACh release was found to increase 400% in response to 10 microg PYY. In a separate experiment, blockade of the same area of the HPC with bilateral intracerebral injections of 3.5 microg scopolamine did not affect intake stimulated by intrahypothalamic injection of 4 microg PYY. Furthermore, a third experiment showed, for the first time, that PYY (2.5-10.0 microg) can elicit robust feeding when infused directly into the HPC. The significance of these findings to the activation of limbic functions such as memory, reinforcement, and obsessional processes that accompany human binge-eating syndromes is discussed.

Topics: Acetylcholine; Animals; Choline; Cholinergic Antagonists; Drinking Behavior; Feeding and Eating Disorders; Feeding Behavior; Female; Hypothalamus; Limbic System; Male; Motor Activity; Peptide YY; Rats; Rats, Sprague-Dawley; Scopolamine