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

A E Rigamonti,S Bini,F Piscitelli,A Lauritano,V Di Marzo,C Vanetti,F Agosti,A De Col,E Lucchetti,G Grugni,A Sartorio

doi:10.1080/16546628.2017.1297553

Abstract

ABSTRACTHedonic and homeostatic hunger represent two different forms of eating: just for pleasure or following energy deprivation, respectively. Consumption of food for pleasure was reported to be associated with increased circulating levels of both the orexigenic peptide ghrelin and some specific endocannabinoids in normal-weight subjects and patients with morbid obesity. To date, the effects of palatable food on these mediators in Prader–Willi syndrome (PWS) are still unknown. To explore the role of some gastrointestinal orexigenic and anorexigenic peptides and endocannabinoids (and some related congeners) in chocolate consumption, we measured changes in circulating levels of ghrelin, cholecystokinin (CCK), peptide YY (PYY), anandamide (AEA), 2-arachidonoyl-glycerol (2-AG), palmitoylethanolamide (PEA) and oleoylethanolamide (OEA) in eight satiated adult PWS patients after consumption of chocolate and, on a separate day, of a non-palatable isocaloric food with the same macronutrient composition. Evaluation of hunger and satiety was also performed by visual analogic scale. The anticipatory phase and the consumption of food for pleasure were associated with decreased circulating levels of PYY. An increase in PEA levels was also observed. By contrast, circulating levels of ghrelin, CCK, AEA, 2-AG and OEA did not differ before and after the exposure/ingestion of either chocolate or non-palatable foods. Hunger and satiety were similar in the hedonic and non-palatable sessions. In conclusion, when motivation to eat is promoted by highly palatable foods, a depressed post-prandial PYY secretion is observed in PWS. Although preliminary, these findings seem to hypothesize a possible role of PYY agonists in the management of PWS patients.Abbreviations: AEA, Anandamide; 2-AG, 2-arachidonoyl-glycerol; CB1, cannabinoid receptor type 1; OEA, oleoylethanolamide; PEA, palmitoylethanolamide; PWS: Prader-Willi syndrome; VAS, visual analog scales

Highlights

In animals and humans, eating is stimulated by the need to restore energy homeostasis, and by the rewarding properties of highly palatable foods, mainly fatty and/or sugar-sweet meals, despite a state of satiety and positive energy balance [1]
A mild mental retardation was present in all individuals and, in this respect, the requirement for participating in the study was a score over the cut-off value of 24 in the Mini Mental State Examination (MMSE) [32]
The main finding of the present study carried out in Prader–Willi syndrome (PWS) patients was that circulating levels of peptide YY (PYY) were persistently found depressed during the entire hedonic session, which included the administration of a satiating breakfast and, one hour after, a chocolate tablet, which was initially served for stimulating an intense sensorial experience and freely eaten

Summary

Introduction

In animals and humans, eating is stimulated by the need to restore energy homeostasis (homeostatic hunger), and by the rewarding properties of highly palatable foods, mainly fatty and/or sugar-sweet meals, despite a state of satiety and positive energy balance (hedonic hunger) [1]. A huge number of gastrointestinal endocrine cells produces and secretes satiety hormones in response to food consumption and digestion. These hormones, including cholecystokinin (CCK), peptide YY (PYY) and glucagon-like peptide 1 (GLP-1), suppress homeostatic hunger and promote satiety [4]. In addition to these anorexigenic peptides, there is an orexigenic peptide produced by the stomach, named ghrelin, which is capable to stimulate homeostatic, and hedonic hunger [5,6]. These effects are mediated by activation of the receptor, GHS-R1a, which is expressed in the hypothalamus

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