Hedonic eating in Prader–Willi syndrome is associated with blunted PYY secretion

Rigamonti, Antonello E.; Bini, Silvia; Piscitelli, Fabiana; Lauritano, Anna; Marzo, Vincenzo Di; Vanetti, Claudia; Agosti, Fiorenza; Col, Alessandra De; Lucchetti, Elisa; Grugni, Graziano; Sartório, Alessandro

doi:10.1080/16546628.2017.1297553

Cited by 12 publications

(8 citation statements)

References 47 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In PWS children, the fasting levels of NPY ( 30 ) and AEA ( 41 ) were not different compared to BMI)-matched controls. After a meal, AEA decreased ( 42 ). Fasting levels of beta-endorphin ( 43 ) and 2-AG ( 41 ) were higher in children with PWS compared to controls and 2-AG levels remained unchanged after a meal ( 42 ).…”

Section: Neuroendocrine Factors Stimulating Food Intake and Body Weightmentioning

confidence: 99%

“…After a meal, AEA decreased ( 42 ). Fasting levels of beta-endorphin ( 43 ) and 2-AG ( 41 ) were higher in children with PWS compared to controls and 2-AG levels remained unchanged after a meal ( 42 ). Levels of brain-derived neurotrophic factor (BDNF) ( 44 , 45 ) were lower in children with PWS compared to controls.…”

Section: Neuroendocrine Factors Stimulating Food Intake and Body Weightmentioning

confidence: 99%

“…Studies in children and adults with PWS showed no difference in fasting or postprandial CCK levels compared to obese controls ( 42 , 67 , 79 , 89 ), although in one study a greater increase in CCK during a meal compared to control adults was observed ( 90 ). This greater increase was not related to a reduced food intake in PWS patients ( 90 ).…”

Section: Neuroendocrine Factors Inhibiting Food Intake and Body Weightmentioning

confidence: 99%

See 2 more Smart Citations

Appetite- and weight-inducing and -inhibiting neuroendocrine factors in Prader–Willi syndrome, Bardet–Biedl syndrome and craniopharyngioma versus anorexia nervosa

Vlaardingerbroek

Akker

Hokken-Koelega

2021

Endocrine Connections

View full text Add to dashboard Cite

Obesity is reaching endemic state and has a major impact on health and economy. In most cases obesity is caused by life style factors. However, the risk of becoming obese differs highly between people. Individual differences in life style, genetic, and neuroendocrine factors play a role in satiety, hunger and regulation of body weight. In a small percentage of children and adults with obesity, an underlying hormonal or genetic cause can be found. The aim of this review is to present and compare data on the extreme ends of the obesity and undernutrition spectrum in patients with Prader-Willi syndrome (PWS), Bardet-Biedl syndrome (BBS), acquired hypothalamic obesity in craniopharyngioma patients, and anorexia nervosa. This may give more insight in the role of neuroendocrine factors and might give direction for future research in conditions of severe obesity and underweight.

show abstract

Section: Neuroendocrine Factors Stimulating Food Intake and Body Weightmentioning

confidence: 99%

Section: Neuroendocrine Factors Stimulating Food Intake and Body Weightmentioning

confidence: 99%

Section: Neuroendocrine Factors Inhibiting Food Intake and Body Weightmentioning

confidence: 99%

See 1 more Smart Citation

Appetite- and weight-inducing and -inhibiting neuroendocrine factors in Prader–Willi syndrome, Bardet–Biedl syndrome and craniopharyngioma versus anorexia nervosa

Vlaardingerbroek

Akker

Hokken-Koelega

2021

Endocrine Connections

View full text Add to dashboard Cite

show abstract

“…In fact, fast feeding leads to higher concentrations of both GLP-1 and PYY, favoring the appearance of satiety in PWS adult patients, this pattern not being evident in obese controls. 37 Moreover, reduced postprandial PYY secretion is detected in PWS when motivation to eat is induced by highly appetizing foods, suggesting a possible role of PYY agonists in the pharmacological strategy in these patients. 38 …”

Section: Endocrine Control Of Eating Behavior In Pwsmentioning

confidence: 99%

Obesity management in Prader–Willi syndrome: current perspectives

Crinò¹,

Fintini²,

Bocchini³

et al. 2018

DMSO

106

View full text Add to dashboard Cite

Prader–Willi syndrome (PWS) is a complex multisystem disorder due to the absent expression of the paternally active genes in the PWS critical region on chromosome 15 (15q11.2-q13). The syndrome is considered the most common genetic cause of obesity, occurring in 1:10,000–1:30,000 live births. Its main characteristics include neonatal hypotonia, poor feeding, and lack of appetite in infancy, followed by weight gain, lack of satiety, and uncontrolled appetite, frequently after the age of 2–3 years. The clinical picture includes short stature, multiple endocrine abnormalities (hypogonadism, growth hormone/insulin-like growth factor-I axis dysfunction, hypothyroidism, central adrenal insufficiency), dysmorphic features, scoliosis, osteoporosis, mental retardation, and behavioral and psychiatric problems. Subjects with PWS will become severely obese unless their food intake is strictly controlled. Constant and obsessive food seeking behavior can make life very difficult for both the family and caretakers. Prevention of obesity is mandatory in these patients from the first years of life, because once obesity develops it is difficult to maintain the control of food intake. In fact, PWS subjects die prematurely from complications conventionally related to obesity, including diabetes mellitus, metabolic syndrome, sleep apnea, respiratory insufficiency, and cardiovascular disease. The mechanisms underlying hyperphagia in PWS are not completely known, and to date no drugs have proven their efficacy in controlling appetite. Consequently, dietary restriction, physical activity, and behavior management are fundamental in the prevention and management of obesity in PWS. In spite of all available therapeutic tools, however, successful weight loss and maintenance are hardly accomplished. In this context, clinical trials with new drugs have been initiated in order to find new possibilities of a therapy for obesity in these patients. The preliminary results of these studies seem to be encouraging. On the other hand, until well-proven medical treatments are available, bariatric surgery can be taken into consideration, especially in PWS patients with life-threatening comorbidities.

show abstract

“…The hyperphagia and adiposity in PWS children are associated with hyperleptinemia, hyperghrelinemia and a blunted peptide YY response to high‐fat (58%) feeding . Likewise, the rise in PYY was attenuated in PWS adults following a high calorie chocolate snack containing 61% carbohydrate and 31% fat . Fasting insulin concentrations are lower in PWS than in nonsyndromic obesity and insulin sensitivity, as assessed by HOMA‐IR, adiponectin and the ratio of TG to HDL, is higher …”

Section: Discussionmentioning

confidence: 99%

Hormonal and metabolic effects of carbohydrate restriction in children with Prader‐Willi syndrome

Irizarry

Mager

Triador

et al. 2019

Clinical Endocrinology

View full text Add to dashboard Cite

Objective: Macronutrient regulation of hyperphagia and adiposity in Prader-Willi syndrome (PWS) is poorly understood. We compared fasting and postprandial concentrations of hormones and metabolites in eight PWS children (age 9-18 years) fed, in random order, low carbohydrate, high-fat (LC, 15% carb; 65% fat; 20% protein) and low-fat, high carbohydrate (LF, 65% carb, 15% fat, 20% protein) diets matched for calories and protein.Methods: Participants were randomized to consume either the LC or LF diet during a first hospital admission and the second diet during a subsequent admission. Blood samples were obtained after overnight fasting and 1 hour after a mixed meal.Results: Relative to subjects consuming the LF diet, subjects consuming the LC diet had: lower postprandial insulin concentrations (P = 0.02); higher fasting GLP-1 AND GIP concentrations and increased postprandial GLP-1 (P < 0.02); reduced ratio of fasting ghrelin to GLP-1 (P = 0.0078); increased FFA and fatty acid oxidation, as assessed by concentrations of even-chain acylcarnitines (P < 0.001); lower fasting TG and TG/HDL ratio (P < 0.01); and higher concentrations of branch chain amino acids (P < 0.01). There were no changes in glucose, PYY, or adiponectin. CRP, AST and ALT were all higher (P < 0.01) on the LC diet.Conclusions: Increases in GLP-1 with low carbohydrate feeding and reductions in the ratio of ghrelin to GLP-1 might limit food intake and improve glycaemic control in PWS. Other potential benefits of carbohydrate restriction may include fat mobilization and oxidation and reductions in the TG/HDL ratio, a marker of insulin resistance.However, increases in CRP, AST and ALT necessitate longer-term studies of low carbohydrate efficacy and safety. K E Y W O R D Sbranch chain amino acids, ghrelin, GLP-1, GIP, insulin, low carbohydrate diet, Prader-Willi syndrome, PYY

show abstract

Hedonic eating in Prader–Willi syndrome is associated with blunted PYY secretion

Cited by 12 publications

References 47 publications

Appetite- and weight-inducing and -inhibiting neuroendocrine factors in Prader–Willi syndrome, Bardet–Biedl syndrome and craniopharyngioma versus anorexia nervosa

Appetite- and weight-inducing and -inhibiting neuroendocrine factors in Prader–Willi syndrome, Bardet–Biedl syndrome and craniopharyngioma versus anorexia nervosa

Obesity management in Prader–Willi syndrome: current perspectives

Hormonal and metabolic effects of carbohydrate restriction in children with Prader‐Willi syndrome

Contact Info

Product

Resources

About

Hedonic eating in Prader–Willi syndrome is associated with blunted PYY secretion

Cited by 12 publications

References 47 publications

Appetite- and weight-inducing and -inhibiting neuroendocrine factors in Prader–Willi syndrome, Bardet–Biedl syndrome and craniopharyngioma versus anorexia nervosa

Appetite- and weight-inducing and -inhibiting neuroendocrine factors in Prader–Willi syndrome, Bardet–Biedl syndrome and craniopharyngioma versus anorexia nervosa

Obesity management in Prader&ndash;Willi syndrome: current perspectives

Hormonal and metabolic effects of carbohydrate restriction in children with Prader‐Willi syndrome

Contact Info

Product

Resources

About

Obesity management in Prader–Willi syndrome: current perspectives