TY - JOUR
T1 - Hedonic and incentive signals for body weight control
AU - Egecioglu, Emil
AU - Skibicka, Karolina P.
AU - Hansson, Caroline
AU - Alvarez-Crespo, Mayte
AU - Anders Friberg, P.
AU - Jerlhag, Elisabet
AU - Engel, Jörgen A.
AU - Dickson, Suzanne L.
N1 - Funding Information:
Acknowledgements The Swedish Research Council for Medicine (2009-S266, K2006-21X-04247-33-3 and 2009-2782), European Commission 7th Framework (FP7-HEALTH-2009-241592; FP7-KBBE-2009-3-245009 and FP7-KBBE-2010-4-266408), FOU/ALF Göteborg (ALFGBG-138741, ALFGBG-7341), The Swedish Brain Foundation, Torsten and Ragnar Söderberg foundation and the Swedish Foundation for Strategic Research to Sahlgrenska Center for Cardiovascular and Metabolic Research (A305-188). Dr Johan Alsiö and Prof Roger Adan for helpful discussion regarding section IV.
PY - 2011/9
Y1 - 2011/9
N2 - Here we review the emerging neurobiological understanding of the role of the brain's reward system in the regulation of body weight in health and in disease. Common obesity is characterized by the over-consumption of palatable/rewarding foods, reflecting an imbalance in the relative importance of hedonic versus homeostatic signals. The popular 'incentive salience theory' of food reward recognises not only a hedonic/pleasure component ('liking') but also an incentive motivation component ('wanting' or 'reward-seeking'). Central to the neurobiology of the reward mechanism is the mesoaccumbal dopamine system that confers incentive motivation not only for natural rewards such as food but also by artificial rewards (eg. addictive drugs). Indeed, this mesoaccumbal dopamine system receives and integrates information about the incentive (rewarding) value of foods with information about metabolic status. Problematic over-eating likely reflects a changing balance in the control exerted by hypothalamic versus reward circuits and/or it could reflect an allostatic shift in the hedonic set point for food reward. Certainly, for obesity to prevail, metabolic satiety signals such as leptin and insulin fail to regain control of appetitive brain networks, including those involved in food reward. On the other hand, metabolic control could reflect increased signalling by the stomach-derived orexigenic hormone, ghrelin. We have shown that ghrelin activates the mesoaccumbal dopamine system and that central ghrelin signalling is required for reward from both chemical drugs (eg alcohol) and also from palatable food. Future therapies for problematic over-eating and obesity may include drugs that interfere with incentive motivation, such as ghrelin antagonists.
AB - Here we review the emerging neurobiological understanding of the role of the brain's reward system in the regulation of body weight in health and in disease. Common obesity is characterized by the over-consumption of palatable/rewarding foods, reflecting an imbalance in the relative importance of hedonic versus homeostatic signals. The popular 'incentive salience theory' of food reward recognises not only a hedonic/pleasure component ('liking') but also an incentive motivation component ('wanting' or 'reward-seeking'). Central to the neurobiology of the reward mechanism is the mesoaccumbal dopamine system that confers incentive motivation not only for natural rewards such as food but also by artificial rewards (eg. addictive drugs). Indeed, this mesoaccumbal dopamine system receives and integrates information about the incentive (rewarding) value of foods with information about metabolic status. Problematic over-eating likely reflects a changing balance in the control exerted by hypothalamic versus reward circuits and/or it could reflect an allostatic shift in the hedonic set point for food reward. Certainly, for obesity to prevail, metabolic satiety signals such as leptin and insulin fail to regain control of appetitive brain networks, including those involved in food reward. On the other hand, metabolic control could reflect increased signalling by the stomach-derived orexigenic hormone, ghrelin. We have shown that ghrelin activates the mesoaccumbal dopamine system and that central ghrelin signalling is required for reward from both chemical drugs (eg alcohol) and also from palatable food. Future therapies for problematic over-eating and obesity may include drugs that interfere with incentive motivation, such as ghrelin antagonists.
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U2 - 10.1007/s11154-011-9166-4
DO - 10.1007/s11154-011-9166-4
M3 - Article
C2 - 21340584
AN - SCOPUS:80054866688
SN - 1389-9155
VL - 12
SP - 141
EP - 151
JO - Reviews in Endocrine and Metabolic Disorders
JF - Reviews in Endocrine and Metabolic Disorders
IS - 3
ER -