Neural representations of hunger and satiety in Prader-Willi syndrome
Neural representations of hunger and satiety in Prader-Willi syndrome
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DOI：
10.1038/sj.ijo.0803128
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发表时间：
2006-02-01
影响因子：
4.9
通讯作者：
Owen, AM
中科院分区：
文献类型：
--
作者：
Hinton, EC;Holland, AJ;Owen, AM
目的：应用脑成像技术探讨Prader-Willi综合征(PWS)患者进食行为异常的神经基础。我们预测，PWS患者的饱腹感反应将延迟，并且对食物摄入不敏感。设计和参与者：这项研究的设计基于先前对非肥胖、非PWS组与禁食和食物摄入条件相关的神经激活的调查。这些发现被用来产生关于当前研究中感兴趣的大脑区域的特定假设，13名患有PWS的成年人参与了这项研究(Mean+/-S.D.年龄29+/-6；BMI=31.5+/-5.1；智商71+/-8，6名女性)。测量：用正电子发射断层扫描分三次测量局部脑血流量：一次在隔夜禁食后，两次在伪装的能量控制下，相似的体积和外观-一次1674kJ(400kcal)和另一次5021kJ(1200kcal)。在每次成像会议前后测量饥饿、饱腹感和食欲的主观评分，以及血糖、胰岛素、瘦素、Ghrelin和PYY的血浆水平。结果：在隔夜禁食后，饥饿的神经表现与对照研究中非肥胖者的相似。相比之下，在摄入食物后，即使在较高的能量负荷之后，也没有发现以前与饱腹感有关的神经激活模式。外侧和内侧眶前叶皮质的激活分别与400千卡和1200千卡的膳食消耗有关。然而，只有在高能量饮食后饱腹度评分有较大百分比变化的人中，才能发现眼眶前额内侧的激活。结论：我们得出结论：PWS患者的饱腹感系统存在功能障碍。这些发现表明，在患有这种综合征的人中，与饱腹感相关的大脑区域甚至对高能量食物的摄入也不敏感。这可能是PWS出现吞噬亢进的神经基础。
Objective: To investigate the neural basis of the abnormal eating behaviour in Prader-Willi syndrome (PWS), using brain imaging. We predicted that the satiety response in those with PWS would be delayed and insensitive to food intake.Design and participants: The design of this study was based on a previous investigation of the neural activation associated with conditions of fasting and food intake in a nonobese, non-PWS group. The findings were used to generate specific hypotheses regarding brain regions of interest for the current study, in which 13 adults with PWS took part (mean +/- s.d. age=29 +/- 6; BMI=31.5 +/- 5.1; IQ 71 +/- 8, six were female).Measurements: Regional cerebral blood flow was measured using positron emission tomography in three sessions: one following an overnight fast and two following disguised energy controlled meals of similar volume and appearance-one of 1674 kJ (400 kcal) and another of 5021 kJ (1200 kcal). Subjective ratings of hunger, fullness and desire to eat, and blood plasma levels of glucose, insulin, leptin, ghrelin and PYY were measured before and after each imaging session.Results: The neural representation of hunger, after an overnight fast, was similar to that found in nonobese individuals in the control study. In contrast, after food intake, the patterns of neural activation previously associated with satiety were not found, even after the higher-energy load. Lateral and medial orbitofrontal cortical activation was associated with consumption of the 400- and 1200-kcal meals, respectively. The medial orbitofrontal activation, however, was only found in those who had shown a large percentage change in fullness ratings following the higher-energy meal.Conclusion: We conclude that there is a dysfunction in the satiety system in those with PWS. These findings suggest that brain regions associated with satiety are insensitive even to high-energy food intake in those with the syndrome. This may be the neural basis of the hyperphagia seen in PWS.