Hedonic and incentive signals for body weight control.

Hedonic and incentive signals for body weight control.
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DOI:
10.1007/s11154-011-9166-4
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发表时间:
2011-09
影响因子:
8.2
通讯作者:
Dickson, Suzanne L.
Dickson, Suzanne L.
中科院分区:
医学2区
文献类型:
--
作者:
Egecioglu, Emil;Skibicka, Karolina P.;Hansson, Caroline;Alvarez-Crespo, Mayte;Friberg, P. Anders;Jerlhag, Elisabet;Engel, Jorgen A.;Dickson, Suzanne L.

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在这里,我们回顾了新兴的神经生物学的理解的作用,大脑的奖励系统在调节体重的健康和疾病。普通肥胖的特征是过度食用可口/有益的食物,反映了享乐信号与稳态信号的相对重要性的不平衡。流行的食物奖励的“激励显着性理论”不仅承认享乐/快乐成分(“喜欢”),而且还承认激励动机成分(“想要”或“寻求奖励”)。奖励机制的神经生物学的核心是中脑多巴胺系统,它不仅为自然奖励(如食物),而且还为人工奖励(如食物)提供激励动机。成瘾药物)。事实上,这个中脑多巴胺系统接收并整合了食物的激励(奖励)价值和代谢状态的信息。有问题的暴饮暴食可能反映了下丘脑与奖励回路所施加的控制的平衡变化,并且/或者它可能反映了食物奖励的享乐设定点的非稳态转变。当然,肥胖症的流行,代谢饱足信号,如瘦素和胰岛素未能重新控制食欲的大脑网络,包括那些涉及食物奖励。另一方面,代谢控制可能反映了胃源性食欲素(ghrelin)信号的增加。我们已经证明,生长激素释放肽激活中脑多巴胺系统,中枢生长激素释放肽信号是化学药物(如酒精)和可口食物的奖赏所必需的。未来治疗过度饮食和肥胖的药物可能包括干扰激励动机的药物,如ghrelin拮抗剂。
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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