Functional Magnetic Resonance Imaging Analysis of Food-Related Brain Activity in Patients with Lipodystrophy Undergoing Leptin Replacement Therapy
Functional Magnetic Resonance Imaging Analysis of Food-Related Brain Activity in Patients with Lipodystrophy Undergoing Leptin Replacement Therapy
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DOI：
10.1210/jc.2012-1872
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发表时间：
2012-10-01
影响因子：
5.8
通讯作者：
Nakao, Kazuwa
中科院分区：
文献类型：
--
作者：
Aotani, Daisuke;Ebihara, Ken;Nakao, Kazuwa
背景：脂肪代谢障碍是一种以脂肪组织缺乏和脂肪细胞源性瘦素低循环浓度为特征的疾病。瘦素替代疗法改善脂肪代谢障碍患者的进食和代谢障碍目的：本研究旨在阐明脂肪代谢障碍患者进食障碍的发病机制以及瘦素对食欲调节的作用机制。我们调查了食物-应用功能性磁共振成像对接受或未接受瘦素替代治疗的脂肪营养不良患者和健康人的相关神经活动进行研究对照我们还测量了主观感觉的nappet.Results：虽然有一点差异，在增强患者和对照组之间的食物刺激的神经活动禁食，餐后抑制的神经活动是不够的，在许多地区的利益，包括杏仁核，杏仁核，尾状核，壳核，苍白球的患者相比，与对照组。瘦素治疗有效地抑制了这些感兴趣的区域中的许多区域的餐后神经活动，而在患者禁食下几乎没有效果。与这些结果相一致，餐后形成的饱腹感不足的患者相比，与对照组，这是有效地加强瘦素treatment.Conclusions：本研究表明，不足的餐后抑制食物相关的神经活动和形成的饱腹感在脂肪营养不良的患者，这是有效地恢复瘦素。本研究的发现强调了瘦素在脂肪代谢障碍中的重要病理作用，为了解瘦素在人体中的作用机制提供了线索，并可能为肥胖的预防和治疗提供新的策略。（临床内分泌代谢杂志97：3663-3671，2012）
Context: Lipodystrophy is a disease characterized by a paucity of adipose tissue and low circulating concentrations of adipocyte-derived leptin. Leptin-replacement therapy improves eating and metabolic disorders in patients with lipodystrophy.Objective: The aim of the study was to clarify the pathogenic mechanism of eating disorders in lipodystrophic patients and the action mechanism of leptin on appetite regulation.Subjects and Interventions: We investigated food-related neural activity using functional magnetic resonance imaging in lipodystrophic patients with or without leptin replacement therapy and in healthy controls. We also measured the subjective feelings of appetite.Results: Although there was little difference in the enhancement of neural activity by food stimuli between patients and controls under fasting, postprandial suppression of neural activity was insufficient in many regions of interest including amygdala, insula, nucleus accumbens, caudate, putamen, and globus pallidus in patients when compared with controls. Leptin treatment effectively suppressed postprandial neural activity in many of these regions of interest, whereas it showed little effect under fasting in patients. Consistent with these results, postprandial formation of satiety feeling was insufficient in patients when compared with controls, which was effectively reinforced by leptin treatment.Conclusions: This study demonstrated the insufficiency of postprandial suppression of food-related neural activity and formation of satiety feeling in lipodystrophic patients, which was effectively restored by leptin. The findings in this study emphasize the important pathological role of leptin in eating disorders in lipodystrophy and provide a clue to understanding the action mechanism of leptin in human, which may lead to development of novel strategies for prevention and treatment of obesity. (J Clin Endocrinol Metab 97: 3663-3671, 2012)