CCK response in bulimia nervosa and following remission

Abstract

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 postprandial 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 minutes 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.

Different Effects of Cholestyramine on Postprandial Secretions of Cholecystokinin and Peptide YY in Women with Bulimia Nervosa

“…Although consistent with a recent study [20], this finding is actually divergent from previous studies where postprandial CCK response was reported to be lower in BN than in the control group [17,18,19]. As stated in the introduction, the reasons for this discrepancy could be related to differences in the study samples with respect to the severity of the disease (the number of binge and purge episodes per week, illness duration, recruitment from inpatient or outpatient treatment settings, acute phase or remission, etc.)…”

“…Similarly, in symptomatic patients with BN, postprandial CCK response was found to be significantly decreased by some authors [17,18,19] but not by others [20]. Several variables, including the severity of BN and differences in both the composition of test meals and methodological procedures, have been put forward to explain such a discrepancy in postprandial CCK response in BN.…”

Central and Peripheral Peptides Regulating Eating Behaviour and Energy Homeostasis in Anorexia Nervosa and Bulimia Nervosa: A Literature Review

“…In BN patients, circulating CCK levels have been reported to be similar to healthy controls (Hannon‐Engel, Filin, & Wolfe, ) or lower than normal in plasma (Lydiard et al, ), in the CSF and in polymorphonucleate blood mononuclear cells (Brambilla et al, 1995). A normal or diminished CCK release after a test meal has been observed (Walsh, ).…”

Current Aspects of the Role of Autoantibodies Directed Against Appetite-Regulating Hormones and the Gut Microbiome in Eating Disorders

“…Depressed and blunted PYY levels may result from reduced and impaired CCK secretion in BN. The anorexigenic hormone CCK is a stimulant of PYY secretion (107). PYY 3-36 is known as meal terminator opposed to ghrelin considered as meal initiator in the feeding behavior.…”