TEDP (Temple Eating Disorders Program), Department of Psychology, Temple University, 1701 N 13th Street, Philadelphia, PA, 19122, USA.
University of Maryland School of Medicine, Baltimore, MD, USA.
Int J Obes (Lond). 2020 Aug;44(8):1636-1652. doi: 10.1038/s41366-020-0608-5. Epub 2020 Jun 18.
Consuming sweet foods, even when sated, can lead to unwanted weight gain. Contextual factors, such as longer time fasting, subjective hunger, and body mass index (BMI), may increase the likelihood of overeating. Nevertheless, the neural mechanisms underlying these moderating influences on energy intake are poorly understood.
We conducted both categorical meta-analysis and meta-regression of factors modulating neural responses to sweet stimuli, using data from 30 functional magnetic resonance imaging (fMRI) articles incorporating 39 experiments (N = 995) carried out between 2006 and 2019.
Responses to sweet stimuli were associated with increased activity in regions associated with taste, sensory integration, and reward processing. These taste-evoked responses were modulated by context. Longer fasts were associated with higher posterior cerebellar, thalamic, and striatal activity. Greater self-reported hunger was associated with higher medial orbitofrontal cortex (OFC), dorsal striatum, and amygdala activity and lower posterior cerebellar activity. Higher BMI was associated with higher posterior cerebellar and insular activity.
Variations in fasting time, self-reported hunger, and BMI are contexts associated with differential sweet stimulus responses in regions associated with reward processing and homeostatic regulation. These results are broadly consistent with a hierarchical model of taste processing. Hunger, but not fasting or BMI, was associated with sweet stimulus-related OFC activity. Our findings extend existing models of taste processing to include posterior cerebellar regions that are associated with moderating effects of both state (fast length and self-reported hunger) and trait (BMI) variables.
即使吃饱了,吃甜食也会导致体重增加。语境因素,如较长的禁食时间、主观饥饿感和体重指数(BMI),可能会增加暴饮暴食的可能性。然而,这些调节能量摄入的因素的神经机制尚不清楚。
我们使用了 2006 年至 2019 年间进行的 30 项功能性磁共振成像(fMRI)研究的 39 项实验数据(N=995),进行了分类元分析和元回归,以调节对甜味刺激的神经反应的因素。
对甜味刺激的反应与与味觉、感觉整合和奖励处理相关的区域的活动增加有关。这些味觉诱发的反应受到环境的调节。较长的禁食时间与后小脑、丘脑和纹状体的活性增加有关。自我报告的饥饿感越强,与内侧眶额皮质(OFC)、背侧纹状体和杏仁核的活性增加以及后小脑的活性降低有关。较高的 BMI 与后小脑和岛叶的活性增加有关。
禁食时间、自我报告的饥饿感和 BMI 的变化是与与奖励处理和体内平衡调节相关的区域的甜味刺激反应不同的环境。这些结果与味觉处理的层次模型基本一致。饥饿感,但不是禁食或 BMI,与与甜味刺激相关的 OFC 活动有关。我们的发现将现有的味觉处理模型扩展到包括与状态(禁食时间和自我报告的饥饿感)和特质(BMI)变量的调节作用相关的后小脑区域。