Food cue reactivity: Neurobiological and behavioral underpinnings.
Food cue reactivity: Neurobiological and behavioral underpinnings.
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DOI：
10.1007/s11154-022-09724-x
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发表时间：
2022-08
影响因子：
8.2
通讯作者：
Boutelle, Kerri N.
中科院分区：
文献类型：
--
作者：
Kanoski, Scott E.;Boutelle, Kerri N.
现代肥胖环境包含丰富的食物线索（例如食物的视觉、气味）以及通过学习和记忆过程与食物相关的线索。食物暗示暴露可能导致原本已经饱食的个体寻求食物和过度消费，而高水平的食物暗示反应是超重和肥胖的危险因素。在实验啮齿动物模型中观察到类似的食物提示反应，因此这些模型可用于机械地识别介导食物提示反应的神经回路。这篇综述根据实验啮齿动物模型和人类数据来描述食物相关刺激导致暴饮暴食和体重增加的行为和生物过程。强调了两种啮齿动物模型——线索增强喂养和巴甫洛夫仪器转移——它们提供了对食物线索反应性背后的神经回路和肽系统的深入了解。来自人类的数据被强调，揭示了将食物提示反应与暴饮暴食和体重增加联系起来的生理、心理和神经机制。集体文献确定了啮齿动物和人类食物线索反应性增强与肥胖之间的联系，并确定了这两个物种调节食物线索反应性的潜在大脑区域（伏隔核、杏仁核、眶额皮质、海马体）和内分泌系统（生长素释放肽）。这些物种的相似性令人鼓舞，有可能进行机械啮齿动物模型研究和进一步的人类研究，从而找到针对人类过度食物线索反应的新疗法。
The modern obesogenic environment contains an abundance of food cues (e.g., sight, smell of food) as well cues that are associated with food through learning and memory processes. Food cue exposure can lead to food seeking and excessive consumption in otherwise food-sated individuals, and a high level of food cue responsivity is a risk factor for overweight and obesity. Similar food cue responses are observed in experimental rodent models, and these models are therefore useful for mechanistically identifying the neural circuits mediating food cue responsivity. This review draws from both experimental rodent models and human data to characterize the behavioral and biological processes through which food-associated stimuli contribute to overeating and weight gain. Two rodent models are emphasized – cue-potentiated feeding and Pavlovian-instrumental transfer – that provide insight in the neural circuits and peptide systems underlying food cue responsivity. Data from humans are highlighted that reveal physiological, psychological, and neural mechanisms that connect food cue responsivity with overeating and weight gain. The collective literature identifies connections between heightened food cue responsivity and obesity in both rodents and humans, and identifies underlying brain regions (nucleus accumbens, amygdala, orbitofrontal cortex, hippocampus) and endocrine systems (ghrelin) that regulate food cue responsivity in both species. These species similarities are encouraging for the possibility of mechanistic rodent model research and further human research leading to novel treatments for excessive food cue responsivity in humans.
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