Hedonic Eating and the "Delicious Circle": From Lipid-Derived Mediators to Brain Dopamine and Back.

Hedonic Eating and the "Delicious Circle": From Lipid-Derived Mediators to Brain Dopamine and Back.
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DOI:
10.3389/fnins.2018.00271
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发表时间:
2018
影响因子:
4.3
通讯作者:
Maccarrone M
Maccarrone M
中科院分区:
医学2区
文献类型:
--
作者:
Coccurello R;Maccarrone M

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美味的食物可能是诱人的,享乐主义的饮食可能会变得无法抗拒,超越饥饿和负面后果。这可以从饮食和奖励导致的暴饮暴食之间的微妙平衡中得到证明。近年来,人们投入了大量的精力来研究神经回路,并确定导致动态平衡进食向享乐性进食和成瘾性进食行为转变的潜在因素。在这里,我们检查了最近的文献,关于“新的”和“新的”玩家对奖励导致的暴饮暴食和可能的饮食成瘾负责的文献。因此,中脑多巴胺的作用位于参与食物奖励信息处理的选定激素信号(即瘦素、Ghrelin和胰岛素)和脂源性神经介质(如内源性大麻素)之间的交叉点。综述了高脂肪可口食物和膳食脂肪对内源性大麻素形成的影响,其潜在的致病作用是扰乱摄食平衡。接下来,我们讨论了调节突触可塑性的内源性大麻素信号,它是作用于下丘脑和中脑边缘环路的关键机制,影响多巴胺功能以及瘦素和Ghrelin信号之间的相互作用。除了典型的下丘脑与能量平衡有关的喂养回路和“喂养中心”的概念外,我们关注的是下丘脑外侧作为神经底物,能够面对食物相关的稳态信息,包括食物的突出性、进食动机、寻求奖励和强迫性进食的发展。因此,重新检查外侧下丘脑-腹侧被盖区-伏核的神经回路,以询问Ghrelin、多巴胺、增食欲素和内源性大麻素信号之间的功能相互作用。我们认为,内源性大麻素在下丘脑外侧区的食物奖赏处理中起着关键作用,食欲素神经元将内分泌信号与食物强化和享乐进食相结合。此外,还从内源性大麻素的产生、食欲素受体的激活和多巴胺神经元的去抑制来考虑不同应激源在恢复对美味食物的偏好和寻找食物行为中所起的作用。最后,依赖1型大麻素受体抑制GABA能释放和对奖赏相关刺激的复发与下丘脑外侧-腹侧被盖区-伏隔核网络中的Ghrelin和增食欲素信号有关,以突出其对食物成瘾样行为的病理潜力。
Palatable food can be seductive and hedonic eating can become irresistible beyond hunger and negative consequences. This is witnessed by the subtle equilibrium between eating to provide energy intake for homeostatic functions, and reward-induced overeating. In recent years, considerable efforts have been devoted to study neural circuits, and to identify potential factors responsible for the derangement of homeostatic eating toward hedonic eating and addiction-like feeding behavior. Here, we examined recent literature on “old” and “new” players accountable for reward-induced overeating and possible liability to eating addiction. Thus, the role of midbrain dopamine is positioned at the intersection between selected hormonal signals involved in food reward information processing (namely, leptin, ghrelin, and insulin), and lipid-derived neural mediators such as endocannabinoids. The impact of high fat palatable food and dietary lipids on endocannabinoid formation is reviewed in its pathogenetic potential for the derangement of feeding homeostasis. Next, endocannabinoid signaling that regulates synaptic plasticity is discussed as a key mechanism acting both at hypothalamic and mesolimbic circuits, and affecting both dopamine function and interplay between leptin and ghrelin signaling. Outside the canonical hypothalamic feeding circuits involved in energy homeostasis and the notion of “feeding center,” we focused on lateral hypothalamus as neural substrate able to confront food-associated homeostatic information with food salience, motivation to eat, reward-seeking, and development of compulsive eating. Thus, the lateral hypothalamus-ventral tegmental area-nucleus accumbens neural circuitry is reexamined in order to interrogate the functional interplay between ghrelin, dopamine, orexin, and endocannabinoid signaling. We suggested a pivotal role for endocannabinoids in food reward processing within the lateral hypothalamus, and for orexin neurons to integrate endocrine signals with food reinforcement and hedonic eating. In addition, the role played by different stressors in the reinstatement of preference for palatable food and food-seeking behavior is also considered in the light of endocannabinoid production, activation of orexin receptors and disinhibition of dopamine neurons. Finally, type-1 cannabinoid receptor-dependent inhibition of GABA-ergic release and relapse to reward-associated stimuli is linked to ghrelin and orexin signaling in the lateral hypothalamus-ventral tegmental area-nucleus accumbens network to highlight its pathological potential for food addiction-like behavior.
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