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Preliminary examination of glucagon‐like peptide‐1 levels in women with purging disorder and bulimia nervosa
Author(s) -
Dossat Amanda M.,
Bodell Lindsay P.,
Williams Diana L.,
Eckel Lisa A.,
Keel Pamela K.
Publication year - 2015
Publication title -
international journal of eating disorders
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.785
H-Index - 138
eISSN - 1098-108X
pISSN - 0276-3478
DOI - 10.1002/eat.22264
Subject(s) - postprandial , bulimia nervosa , meal , binge eating , glucagon like peptide 1 , medicine , psychology , endocrinology , binge eating disorder , gastrointestinal hormone , eating disorders , hormone , clinical psychology , peptide hormone , insulin , diabetes mellitus , type 2 diabetes
Objective This study examined pre‐ and postprandial glucagon‐like peptide 1 (GLP‐1) levels in women with bulimia nervosa (BN), purging disorder (PD), and non‐eating disorder control women to better understand whether alterations in satiation‐related hormones in BN may be linked to binge‐eating episodes or other altered ingestive behaviors. Method Participants included women with BN ( n  = 19), PD ( n  = 14), or controls ( n  = 14). Participants provided subjective ratings for hunger and fullness and plasma samples before and after consumption of a standardized test meal. Results As expected, GLP‐1 levels increased significantly following test meal consumption; however, participants with BN displayed significantly lower GLP‐1 levels compared to PD and control participants both before and after consumption of the test meal. There were no significant differences between PD and control participants in GLP‐1 levels, but individuals with PD displayed significantly higher levels of fullness throughout the test meal as compared to both control and BN participants. Discussion Our findings provide preliminary evidence that reduced GLP‐1 levels in individuals with BN may be associated with binge‐eating episodes. Additionally, increased fullness in individuals with PD does not appear to be accounted for by exaggerated postprandial GLP‐1 release. © 2014 Wiley Periodicals, Inc. Int J Eat Disord 2015; 48:199–205

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