
目前,在大多数西方国家人口中,肥胖症的患病率逐年上升。众所周知,能量摄入过多会导致肥胖的发生,但迄今为止我们仍不清楚为什么有些人更容易出现暴饮暴食的现象,导致自身体重的增加。
我们知道大脑中枢神经系统处理饥饿信号并控制着我们食物的摄入量,因此科学家猜测我们体重的增加以及肥胖的发生或许与大脑有关。最近,刊登在PLoS ONE杂志上的一项研究发现了大脑在肥胖发生中发挥关键作用的有力证据。
研究人员将研究对象分成病态肥胖组、消瘦组和健康对照组三组,运用多重大脑成像科学技术对三组研究对象的功能性大脑环路分别进行了检测,检测胰岛素信号转导情况判定机体是否处于饱食状态,运用正电子放射断层造影术检测研究对象大脑葡萄糖代谢情况。
结果发现:与消瘦组相比,肥胖组的研究对象大脑纹状体区的糖代谢水平明显提高。这可能导致体他们经常性的暴饮暴食,最终自身体重飙升。研究人员表示即使肥胖的人已经吃饱了,已经不再需要摄入能量时,这些人的大脑中可能仍会一直产生促进肥胖的人进食的信号。

Dorsal Striatum and Its Limbic Connectivity Mediate Abnormal Anticipatory Reward Processing in Obesity
Lauri Nummenmaa, Jussi Hirvonen, Jarna C. Hannukainen, Heidi Immonen, Markus M. Lindroos, et al.
Obesity is characterized by an imbalance in the brain circuits promoting reward seeking and those governing cognitive control. Here we show that the dorsal caudate nucleus and its connections with amygdala, insula and prefrontal cortex contribute to abnormal reward processing in obesity. We measured regional brain glucose uptake in morbidly obese (n = 19) and normal weighted (n = 16) subjects with 2-[18F]fluoro-2-deoxyglucose ([18F]FDG) positron emission tomography (PET) during euglycemic hyperinsulinemia and with functional magnetic resonance imaging (fMRI) while anticipatory food reward was induced by repeated presentations of appetizing and bland food pictures. First, we found that glucose uptake rate in the dorsal caudate nucleus was higher in obese than in normal-weight subjects. Second, obese subjects showed increased hemodynamic responses in the caudate nucleus while viewing appetizing versus bland foods in fMRI. The caudate also showed elevated task-related functional connectivity with amygdala and insula in the obese versus normal-weight subjects. Finally, obese subjects had smaller responses to appetizing versus bland foods in the dorsolateral and orbitofrontal cortices than did normal-weight subjects, and failure to activate the dorsolateral prefrontal cortex was correlated with high glucose metabolism in the dorsal caudate nucleus. These findings suggest that enhanced sensitivity to external food cues in obesity may involve abnormal stimulus-response learning and incentive motivation subserved by the dorsal caudate nucleus, which in turn may be due to abnormally high input from the amygdala and insula and dysfunctional inhibitory control by the frontal cortical regions. These functional changes in the responsiveness and interconnectivity of the reward circuit could be a critical mechanism to explain overeating in obesity.
文献链接:https://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0031089

