Effects of leptin deficiency and replacement on cerebellar response to food-related cues.
Effects of leptin deficiency and replacement on cerebellar response to food-related cues.
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DOI：
10.1007/s12311-012-0360-z
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发表时间：
2013-02
期刊：
影响因子：
3.5
通讯作者：
London, Edythe D.
中科院分区：
文献类型：
--
作者：
Berman, Steven M.;Paz-Filho, Gilberto;Wong, Ma-Li;Kohno, Milky;Licinio, Julio;London, Edythe D.
瘦素部分通过改变大脑对食物相关刺激的反应来影响饮食行为。瘦素对大脑结构的影响已经在小脑中观察到，小脑是瘦素受体表达最密集的地方，但瘦素在小脑中的功能尚不清楚。我们对三名患有遗传性瘦素缺乏症的成年人进行了一项非随机、前瞻性干预研究。在瘦素替代治疗的第5年和第6年，每年记录3次功能磁共振成像。每年的第一阶段是在连续10个月每天更换后，第二阶段是在33-37天不使用瘦素后，第三阶段是在恢复每天更换后的14-23天。采用统计参数映射软件（SPM5）对比高热量食物图像和砖墙图像对fMRI血氧水平依赖性的反应。协变量分析量化了瘦素替代持续时间和伴随的体重变化对大脑反应的影响。更换时间越长，小脑后叶腹侧的食物图像激活程度越高，而体重同时减少，小脑后叶背侧的激活程度越低。这些发现表明，瘦素替代可可逆地改变小脑后部的神经功能，并调节对食物线索的可塑性依赖的大脑生理。研究结果表明，小脑后部在调节瘦素介导的与食物摄入相关的过程中的作用尚未得到充分的研究。
Leptin affects eating behavior partly by altering the response of the brain to food-related stimuli. Effects of leptin on brain structure have been observed in the cerebellum, where leptin receptors are most densely expressed, but the function of leptin in the cerebellum remains unclear. We performed a nonrandomized, prospective interventional study of three adults with genetically-mediated leptin deficiency. FMRI was recorded three times each year during years 5 and 6 of leptin replacement treatment. Session one of each year occurred after 10 months of continuous daily replacement, session two after 33–37 days without leptin, and session three 14–23 days after daily replacement was restored. Statistical parametric mapping software (SPM5) was employed to contrast the fMRI blood-oxygenation level-dependent response to images of high-calorie foods versus images of brick walls. Covariate analyses quantified the effects of the duration of leptin replacement and concomitant changes in body mass on the cerebral responses. Longer duration of replacement was associated with more activation by food images in a ventral portion of the posterior lobe of the cerebellum, while simultaneous decreases in body mass were associated with decreased activation in a more dorsal portion of the same lobe. These findings indicate that leptin replacement reversibly alters neural function within the posterior cerebellum, and modulates plasticity-dependent brain physiology in response to food cues. The results suggest an underexplored role for the posterior cerebellum in the regulation of leptin-mediated processes related to food intake.
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