Shapira N A, Lessig M C, He A G, James G A, Driscoll D J, Liu Y
Department of Psychiatry, University of florida, Gainesville, FL, USA.
J Neurol Neurosurg Psychiatry. 2005 Feb;76(2):260-2. doi: 10.1136/jnnp.2004.039024.
The neurobiology relating to the insatiable appetite observed in Prader-Willi syndrome (PWS) has not been fully characterised. Two functional magnetic resonance imaging (fMRI) scans were performed on each of three adults with PWS. The scans were carried out pre- and post-treatment with the antiepileptic topiramate, which had little effect on body weight and appetite in these subjects. Subjects fasted overnight and drank a 75 g dextrose solution prior to fMRI scans for measurement of brain activation levels during/after glucose ingestion. Following glucose administration, there was a significant delay in activation at the hypothalamus and other brain regions associated with satiety compared with previous data on obese volunteers. These regions include the insula, ventromedial prefrontal cortex, and nucleus accumbens. Individuals with PWS showed a mean latency of 24 min while in a previous study obese volunteers had shown a latency of 15 min and lean volunteers a latency of 10 min in the hypothalamus. Our results provide evidence towards a satiety dysfunction in the central nervous system of PWS patients.
与普拉德-威利综合征(PWS)中观察到的贪食症相关的神经生物学尚未得到充分表征。对三名患有PWS的成年人分别进行了两次功能磁共振成像(fMRI)扫描。扫描在使用抗癫痫药物托吡酯治疗前后进行,该药物对这些受试者的体重和食欲几乎没有影响。受试者在fMRI扫描前禁食过夜并饮用75克葡萄糖溶液,以测量葡萄糖摄入期间/之后的大脑激活水平。与之前关于肥胖志愿者的数据相比,给予葡萄糖后,下丘脑和其他与饱腹感相关的脑区的激活出现了显著延迟。这些区域包括脑岛、腹内侧前额叶皮层和伏隔核。PWS患者在下丘脑中的平均延迟为24分钟,而在之前的一项研究中,肥胖志愿者的延迟为15分钟,瘦志愿者的延迟为10分钟。我们的结果为PWS患者中枢神经系统中的饱腹感功能障碍提供了证据。