William F. Connell School of Nursing, Boston College, Chestnut Hill, MA, United States.
Physiol Behav. 2013 Oct 2;122:56-61. doi: 10.1016/j.physbeh.2013.08.014. Epub 2013 Aug 27.
The core defining features of bulimia nervosa (BN) are repeated binge eating episodes and inappropriate compensatory (e.g., purging) behavior. Previous studies suggest an abnormal post-prandial response in the satiety-signaling peptide cholecystokinin (CCK) in persons with BN. It is unknown whether this altered response persists following remission or if it may be a potential target for the development of clinical treatment strategies. To examine the nature of this altered response, this study assessed whether CCK normalizes following remission from BN (RBN). This study prospectively evaluated the plasma CCK response and corresponding eating behavior-related ratings (e.g., satiety, fullness, hunger, urge to binge and vomit) in individuals with BN-purging subtype (n=10), RBN-purging subtype (n=14), and healthy controls (CON, n=13) at baseline, +15, +30, and +60 min following the ingestion of a standardized liquid test meal. Subject groups did not significantly differ in CCK response to the test meal. A significant relationship between CCK response and satiety ratings was observed in the RBN group (r=.59, p<.05 two-tailed). A new and unanticipated finding in the BN group was a significant relationship between CCK response and ratings of "urge to vomit" (r=.86, p<.01, two-tailed). Unlike previous investigations, CCK response did not differ in BN and CON groups. Thus the role of symptom severity remains an area of further investigation. Additionally, findings suggest that in this sample, CCK functioning following remission from BN-purging subtype is not different from controls. It remains unknown whether or not CCK functioning may be a protective or liability factor in the stabilization and recovery process. Replication studies utilizing a larger sample size are needed to further elucidate the role of CCK in recovery from BN and its potential target of related novel treatment strategies.
神经性贪食症（BN）的核心特征是反复发作的暴食发作和不适当的补偿（例如，催吐）行为。先前的研究表明，BN 患者的餐后饱腹感信号肽胆囊收缩素（CCK）反应异常。尚不清楚这种改变的反应是否在缓解后持续存在，或者它是否可能成为开发临床治疗策略的潜在目标。为了研究这种改变的反应的本质，本研究评估了 BN 缓解后（RBN）CCK 是否恢复正常。本研究前瞻性评估了个体的血浆 CCK 反应和相应的与进食行为相关的评分（例如，饱腹感、饱足感、饥饿感、暴食冲动和呕吐冲动），这些个体患有 BN-催吐亚型（n=10）、RBN-催吐亚型（n=14）和健康对照组（CON，n=13），在摄入标准化液体测试餐后基线、+15、+30 和+60 分钟时。在 CCK 对测试餐的反应方面，各组之间没有显著差异。在 RBN 组观察到 CCK 反应与饱腹感评分之间存在显著关系（r=.59，p<.05，双侧）。在 BN 组中一个新的和意外的发现是 CCK 反应与“呕吐冲动”评分之间存在显著关系（r=.86，p<.01，双侧）。与之前的研究不同，BN 和 CON 组的 CCK 反应没有差异。因此，症状严重程度仍然是进一步研究的一个领域。此外，研究结果表明，在该样本中，BN-催吐亚型缓解后 CCK 的功能与对照组无差异。CCK 的功能是否可能成为 BN 稳定和恢复过程中的保护或致病因素尚不清楚。需要更大样本量的复制研究来进一步阐明 CCK 在 BN 恢复中的作用及其相关新型治疗策略的潜在靶点。
