Fang Zhuo, Spaeth Andrea M, Ma Ning, Zhu Senhua, Hu Siyuan, Goel Namni, Detre John A, Dinges David F, Rao Hengyi
Center for Functional Neuroimaging, Department of Neurology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Center for Sleep and Circadian Neurobiology, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Sci Rep. 2015 Feb 3;5:8215. doi: 10.1038/srep08215.
Although insufficient sleep is a well-recognized risk factor for overeating and weight gain, the neural mechanisms underlying increased caloric (particularly fat) intake after sleep deprivation remain unclear. Here we used resting-state functional magnetic resonance imaging and examined brain connectivity changes associated with macronutrient intake after one night of total sleep deprivation (TSD). Compared to the day following baseline sleep, healthy adults consumed a greater percentage of calories from fat and a lower percentage of calories from carbohydrates during the day following TSD. Subjects also exhibited increased brain connectivity in the salience network from the dorsal anterior cingulate cortex (dACC) to bilateral putamen and bilateral anterior insula (aINS) after TSD. Moreover, dACC-putamen and dACC-aINS connectivity correlated with increased fat and decreased carbohydrate intake during the day following TSD, but not during the day following baseline sleep. These findings provide a potential neural mechanism by which sleep loss leads to increased fat intake.
尽管睡眠不足是公认的暴饮暴食和体重增加的风险因素,但睡眠剥夺后热量(尤其是脂肪)摄入增加背后的神经机制仍不清楚。在这里,我们使用静息态功能磁共振成像,研究了完全睡眠剥夺(TSD)一晚后与大量营养素摄入相关的大脑连接变化。与基线睡眠后的那天相比,健康成年人在TSD后的那天从脂肪中摄入的热量百分比更高,从碳水化合物中摄入的热量百分比更低。TSD后,受试者的显著网络中从背侧前扣带回皮质(dACC)到双侧壳核和双侧前脑岛(aINS)的大脑连接也增加。此外,dACC-壳核和dACC-aINS连接与TSD后那天脂肪摄入增加和碳水化合物摄入减少相关,但与基线睡眠后那天无关。这些发现提供了一种潜在的神经机制,通过该机制睡眠不足导致脂肪摄入增加。