Glucocorticoid Regulation of Food-Choice Behavior in Humans: Evidence from Cushing's Syndrome.
Glucocorticoid Regulation of Food-Choice Behavior in Humans: Evidence from Cushing's Syndrome.
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DOI：
10.3389/fnins.2016.00021
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发表时间：
2016
影响因子：
4.3
通讯作者：
Geer EB
中科院分区：
文献类型：
--
作者：
Moeller SJ;Couto L;Cohen V;Lalazar Y;Makotkine I;Williams N;Yehuda R;Goldstein RZ;Geer EB
糖皮质激素调节食物摄入和人体体重的机制尚不清楚。一个潜在的机制可能涉及奖励处理的调制，但人类压力模型检查糖皮质激素对行为的影响包含重要的混淆。在这里，我们研究了患有库欣综合征的个体，库欣综合征是一种罕见的内分泌疾病，其特征是慢性内源性糖皮质激素过量。库欣综合征23例（13例活动性疾病; 10名疾病缓解期患者）和15名体重指数（BMI）较高的对照组完成了两项模拟食物选择任务（一个具有“明确的”任务偶然性，一个具有“概率性”任务偶然性），在此期间，他们表示他们对观看高热量食物图像与标准化的愉快，不愉快，中性的图像。所有参与者还完成了对食物渴望的测量，大约一半的参与者提供了24小时尿样，用于评估皮质醇和可的松浓度。结果表明，在外显任务（而不是概率任务），积极的库欣综合征的参与者比参与者更少的食物相关的选择与缓解期的库欣综合征，谁反过来又比超重对照组更少的食物相关的选择。证实了这一群体效应，较高的尿可的松与食物相关的选择在子样本的所有参与者，这些数据是可用的负相关。在概率任务，尽管缺乏组间差异，较高的食物相关的选择与较高的状态和特质的食物渴望活跃的库欣的患者。总的来说，相对于超重对照组，库欣患者，特别是那些患有活动性疾病的患者，表现出对食物奖励的反应活力降低，这可能归因于糖皮质激素异常。除了库欣，这些结果可能与阐明糖皮质激素对食物寻求行为的贡献，增强对与口服糖皮质激素治疗和/或慢性应激相关的体重波动的机械理解，以及告知以异常皮质醇动力学为标志的神经精神疾病的神经生物学（例如，严重抑郁症、阿尔茨海默病）。
The mechanisms by which glucocorticoids regulate food intake and resulting body mass in humans are not well-understood. One potential mechanism could involve modulation of reward processing, but human stress models examining effects of glucocorticoids on behavior contain important confounds. Here, we studied individuals with Cushing's syndrome, a rare endocrine disorder characterized by chronic excess endogenous glucocorticoids. Twenty-three patients with Cushing's syndrome (13 with active disease; 10 with disease in remission) and 15 controls with a comparably high body mass index (BMI) completed two simulated food-choice tasks (one with “explicit” task contingencies and one with “probabilistic” task contingencies), during which they indicated their objective preference for viewing high calorie food images vs. standardized pleasant, unpleasant, and neutral images. All participants also completed measures of food craving, and approximately half of the participants provided 24-h urine samples for assessment of cortisol and cortisone concentrations. Results showed that on the explicit task (but not the probabilistic task), participants with active Cushing's syndrome made fewer food-related choices than participants with Cushing's syndrome in remission, who in turn made fewer food-related choices than overweight controls. Corroborating this group effect, higher urine cortisone was negatively correlated with food-related choice in the subsample of all participants for whom these data were available. On the probabilistic task, despite a lack of group differences, higher food-related choice correlated with higher state and trait food craving in active Cushing's patients. Taken together, relative to overweight controls, Cushing's patients, particularly those with active disease, displayed a reduced vigor of responding for food rewards that was presumably attributable to glucocorticoid abnormalities. Beyond Cushing's, these results may have relevance for elucidating glucocorticoid contributions to food-seeking behavior, enhancing mechanistic understanding of weight fluctuations associated with oral glucocorticoid therapy and/or chronic stress, and informing the neurobiology of neuropsychiatric conditions marked by abnormal cortisol dynamics (e.g., major depression, Alzheimer's disease).