Preliminary Examination of Glucagon-Like Peptide-1 Levels in Women with Purging Disorder and Bulimia Nervosa

Bulimia nervosa (BN) is characterized by recurrent objectively large binge-eating episodes, defined by a “loss of control” during consumption of excessive quantities of food. These objectively large feeding bouts are accompanied by compensatory behaviors (e.g., self-induced vomiting), which are used in an effort to prevent weight gain and/or influence body shape (1). Several studies have reported that individuals with BN experience altered perceptions of hunger, satiation, and fullness (2, 3, 4, 5, 6). These experiences suggest deficits in satiation which have been implicated in the propensity to consume large quantities of food, and investigators have sought possible physiological alterations that could account for satiation deficits. Examination of pre- and post-prandial levels of feeding-related hormones (e.g., cholecystokinin [CCK]) has revealed reductions in individuals with BN compared to controls, providing insight about the physiological correlates for the reported alterations in satiation in this group (7, 4, 5, 8). However, most studies have compared individuals with BN to healthy control participants. Thus, differences in satiation-related hormones may be linked to binge-eating episodes in BN or other altered ingestive behaviors in this group, such as dietary restriction or purging behavior. Purging disorder (PD) is another specified feeding and eating disorder (OSFED) (1) that is characterized by purging behaviors (e.g., self-induced vomiting) after consumption of normal or small amounts of food among individuals who are not underweight (9). Thus, a key difference between PD and BN is the absence of objectively large binge-eating episodes in PD, making PD an excellent comparison group for understanding factors that are uniquely related to the presence of binge-eating episodes in BN. Keel and colleagues (5) found that individuals with BN reported both lower satiation and postprandial fullness in response to a standardized test meal compared to individuals with PD. Furthermore, individuals with BN demonstrated significantly lower post-prandial CCK response compared to individuals with PD. Of interest, participants with PD reported greater levels of post-prandial fullness as compared to controls. This elevation in post-prandial fullness could not be completely attributed to alterations in CCK levels, as those with PD did not differ from controls on postprandial CCK response. To follow up on these observations, the goal of this preliminary investigation was to examine pre- and post-prandial glucagon-like peptide-1 (GLP-1) levels in individuals with BN, PD, and non-eating disorder controls. GLP-1 is a feeding-related hormone that is synthesized in intestinal enteroendocrine L cells and released in response and in proportion to nutrient stimulation of the gut (10, 11). Delivery of GLP-1 reduces food intake and increases satiation in a dose-dependent manner in humans (12). Furthermore, rodent studies have provided evidence that peripherally released GLP-1 plays a physiological role in satiation (13) and central GLP-1 receptors mediate nutrient-induced satiation (14, 15). Thus, alterations in GLP-1 release may be a physiological mechanism that underlies deficits in satiation in individuals with BN, elevated fullness in individuals with PD, or both.