Dorton Hilary M, Luo Shan, Monterosso John R, Page Kathleen A
Neuroscience Graduate Program, University of Southern California, Los Angeles, CA, United States.
Diabetes and Obesity Research Institute, University of Southern California, Los Angeles, CA, United States.
Front Psychiatry. 2018 Jan 4;8:297. doi: 10.3389/fpsyt.2017.00297. eCollection 2017.
Sugar consumption in the United States exceeds recommendations from the American Heart Association. Overconsumption of sugar is linked to risk for obesity and metabolic disease. Animal studies suggest that high-sugar diets alter functions in brain regions associated with reward processing, including the dorsal and ventral striatum. Human neuroimaging studies have shown that these regions are responsive to food cues, and that the gut-derived satiety hormones, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY), suppress striatal food-cue responsivity. We aimed to determine the associations between dietary added sugar intake, striatal responsivity to food cues, and postprandial GLP-1 and PYY levels. Twenty-two lean volunteers underwent a functional magnetic resonance imaging (fMRI) scan during which they viewed pictures of food and non-food items after a 12-h fast. Before scanning, participants consumed a glucose drink. A subset of 19 participants underwent an additional fMRI session in which they consumed water as a control condition. Blood was sampled for GLP-1, and PYY levels and hunger ratings were assessed before and ~75 min after drink consumption. In-person 24-h dietary recalls were collected from each participant on three to six separate occasions over a 2-month period. Average percent calories from added sugar were calculated using information from 24-h dietary recalls. A region-of-interest analysis was performed to compare the blood oxygen level-dependent (BOLD) response to food vs. non-food cues in the bilateral dorsal striatum (caudate/putamen) and ventral striatum (nucleus accumbens). The relationships between added sugar, striatal responses, and hormone changes after drink consumption were assessed using Spearman's correlations. We observed a positive correlation between added sugar intake and BOLD response to food cues in the dorsal striatum and a similar trend in the nucleus accumbens after glucose, but not water, consumption. Added sugar intake was negatively associated with GLP-1 response to glucose. analysis revealed a negative correlation between GLP-1 response to glucose and BOLD response to food cues in the dorsal striatum. Our findings suggest that habitual added sugar intake is related to increased striatal response to food cues and decreased GLP-1 release following glucose intake, which could contribute to susceptibility to overeating.
美国的糖消费量超过了美国心脏协会的建议。糖的过度消费与肥胖和代谢疾病风险相关。动物研究表明,高糖饮食会改变与奖励处理相关的脑区功能,包括背侧和腹侧纹状体。人类神经影像学研究表明,这些区域对食物线索有反应,并且肠道衍生的饱腹感激素胰高血糖素样肽-1(GLP-1)和肽YY(PYY)会抑制纹状体对食物线索的反应性。我们旨在确定饮食中添加糖的摄入量、纹状体对食物线索的反应性以及餐后GLP-1和PYY水平之间的关联。22名体型偏瘦的志愿者在禁食12小时后进行了功能磁共振成像(fMRI)扫描,期间他们观看食物和非食物物品的图片。在扫描前,参与者饮用了葡萄糖饮料。19名参与者的一个子集进行了额外的fMRI实验,其中他们饮用了水作为对照条件。采集血液样本检测GLP-1,并在饮用饮料前和饮用后约75分钟评估PYY水平和饥饿评分。在2个月的时间里,从每位参与者身上分别收集三到六次24小时饮食回忆。使用24小时饮食回忆中的信息计算添加糖提供的平均卡路里百分比。进行感兴趣区域分析,以比较双侧背侧纹状体(尾状核/壳核)和腹侧纹状体(伏隔核)对食物与非食物线索的血氧水平依赖(BOLD)反应。使用斯皮尔曼相关性评估饮用饮料后添加糖、纹状体反应和激素变化之间的关系。我们观察到添加糖摄入量与背侧纹状体对食物线索的BOLD反应之间存在正相关,在饮用葡萄糖而非水后,伏隔核也有类似趋势。添加糖摄入量与GLP-1对葡萄糖的反应呈负相关。分析显示GLP-1对葡萄糖的反应与背侧纹状体对食物线索的BOLD反应之间存在负相关。我们的研究结果表明,习惯性添加糖的摄入量与纹状体对食物线索反应增加以及葡萄糖摄入后GLP-1释放减少有关,这可能导致暴饮暴食的易感性。