MEG Center, University of Tübingen, Tübingen, Germany.
J Clin Endocrinol Metab. 2011 Aug;96(8):E1283-7. doi: 10.1210/jc.2010-2713. Epub 2011 May 18.
Mutations that lead to congenital leptin deficiency cause severe obesity, hyperphagia, and impaired satiety due to malfunctions of peripheral and brain-related mechanisms.
In a leptin-deficient adolescent girl, we investigated brain-related changes before and at two time points after leptin therapy (3 d and 6 months). Functional magnetic resonance imaging was performed during visual stimulation with food (high and low caloric) and nonfood pictures.
Results show acute and long-term effects in the amygdala, the orbitofrontal cortex, and the substantia nigra/ventral tegmental area for the comparison of food and nonfood pictures. For the comparison of high and low caloric pictures, pure acute effects in the ventral striatum and the orbitofrontal cortex could be observed as well as acute and long-term effects in the hypothalamus.
This study gives additional insight in the influence of leptin therapy on brain functions in leptin deficiency.
导致先天性瘦素缺乏的突变会导致严重的肥胖、食欲过盛和饱腹感受损,这是由于外周和与大脑相关的机制发生故障。
在一名瘦素缺乏的青春期女孩中,我们在接受瘦素治疗前(3 天和 6 个月)和两个时间点研究了与大脑相关的变化。在视觉刺激下进行功能性磁共振成像,刺激物为食物(高热量和低热量)和非食物图片。
结果显示,在比较食物和非食物图片时,杏仁核、眶额皮质和黑质/腹侧被盖区会出现急性和长期的影响。对于高热量和低热量图片的比较,除了腹侧纹状体和眶额皮质的纯急性影响外,还可以观察到下丘脑的急性和长期影响。
这项研究进一步了解了瘦素治疗对瘦素缺乏症患者大脑功能的影响。