Charumathi Baskaran1, Kamryn T Eddy2, Karen K Miller2, Erinne Meenaghan2, Madhusmita Misra3, Elizabeth A Lawson2. 1. Pediatric Endocrine UnitMassachusetts General Hospital for Children and Harvard Medical School, 101 Merrimac, Suite 615, Boston, Massachusetts 02114, USANeuroendocrine UnitEating Disorder Clinical Research ProgramMassachusetts General Hospital for Children and Harvard Medical School, Boston, Massachusetts, USA Pediatric Endocrine UnitMassachusetts General Hospital for Children and Harvard Medical School, 101 Merrimac, Suite 615, Boston, Massachusetts 02114, USANeuroendocrine UnitEating Disorder Clinical Research ProgramMassachusetts General Hospital for Children and Harvard Medical School, Boston, Massachusetts, USA cbaskaran@mgh.harvard.edu. 2. Pediatric Endocrine UnitMassachusetts General Hospital for Children and Harvard Medical School, 101 Merrimac, Suite 615, Boston, Massachusetts 02114, USANeuroendocrine UnitEating Disorder Clinical Research ProgramMassachusetts General Hospital for Children and Harvard Medical School, Boston, Massachusetts, USA. 3. Pediatric Endocrine UnitMassachusetts General Hospital for Children and Harvard Medical School, 101 Merrimac, Suite 615, Boston, Massachusetts 02114, USANeuroendocrine UnitEating Disorder Clinical Research ProgramMassachusetts General Hospital for Children and Harvard Medical School, Boston, Massachusetts, USA Pediatric Endocrine UnitMassachusetts General Hospital for Children and Harvard Medical School, 101 Merrimac, Suite 615, Boston, Massachusetts 02114, USANeuroendocrine UnitEating Disorder Clinical Research ProgramMassachusetts General Hospital for Children and Harvard Medical School, Boston, Massachusetts, USA.
Abstract
OBJECTIVE: Leptin secretory dynamics across the weight spectrum and their relationship with disordered eating psychopathology have not been studied. Our objective was to compare leptin secretory dynamics in 13 anorexia nervosa (AN), 12 overweight/obese (OB) and 12 normal-weight women using deconvolution analysis. METHODS: In this cross-sectional study conducted at a tertiary referral center, serum leptin levels were obtained every 20 min from 2000 to 0800 h. Dual energy X-ray absorptiometry was used to measure percent body fat. Disordered eating psychopathology was assessed by the Eating Disorders Examination-Questionnaire (EDE-Q) and the Eating Disorders Inventory-2 (EDI-2). RESULTS: The groups differed for basal leptin secretion (BASAL) (P=0.02). Mean leptin pulse amplitude, pulse mass, total pulsatile secretion (TPS) and area under the curve (AUC) were significantly different between groups before and after adjustment for BASAL (P<0.0001 for all). Leptin AUC correlated strongly with TPS (r=0.97, P<0.0001) and less with BASAL (r=0.35, P=0.03). On multivariate analysis, only TPS was a significant predictor of leptin AUC (P<0.0001). TPS was inversely associated with most EDE-Q and EDI-2 parameters and the associations remained significant for EDE-Q eating concern (P=0.01), and EDI-2 asceticism, ineffectiveness and social insecurity (P<0.05) after adjusting for BASAL. These relationships were not significant when controlled for percent body fat. CONCLUSION: Secretory dynamics of leptin differ across weight spectrum, with mean pulse amplitude, mean pulse mass and TPS being low in AN and high in OB. Pulsatile, rather than basal secretion, is the major contributor to leptin AUC. Decreased pulsatile leptin is associated with disordered eating psychopathology, possibly reflecting low percent body fat in AN.
OBJECTIVE:Leptin secretory dynamics across the weight spectrum and their relationship with disordered eating psychopathology have not been studied. Our objective was to compare leptin secretory dynamics in 13 anorexia nervosa (AN), 12 overweight/obese (OB) and 12 normal-weight women using deconvolution analysis. METHODS: In this cross-sectional study conducted at a tertiary referral center, serum leptin levels were obtained every 20 min from 2000 to 0800 h. Dual energy X-ray absorptiometry was used to measure percent body fat. Disordered eating psychopathology was assessed by the Eating Disorders Examination-Questionnaire (EDE-Q) and the Eating Disorders Inventory-2 (EDI-2). RESULTS: The groups differed for basal leptin secretion (BASAL) (P=0.02). Mean leptin pulse amplitude, pulse mass, total pulsatile secretion (TPS) and area under the curve (AUC) were significantly different between groups before and after adjustment for BASAL (P<0.0001 for all). Leptin AUC correlated strongly with TPS (r=0.97, P<0.0001) and less with BASAL (r=0.35, P=0.03). On multivariate analysis, only TPS was a significant predictor of leptin AUC (P<0.0001). TPS was inversely associated with most EDE-Q and EDI-2 parameters and the associations remained significant for EDE-Q eating concern (P=0.01), and EDI-2 asceticism, ineffectiveness and social insecurity (P<0.05) after adjusting for BASAL. These relationships were not significant when controlled for percent body fat. CONCLUSION: Secretory dynamics of leptin differ across weight spectrum, with mean pulse amplitude, mean pulse mass and TPS being low in AN and high in OB. Pulsatile, rather than basal secretion, is the major contributor to leptin AUC. Decreased pulsatile leptin is associated with disordered eating psychopathology, possibly reflecting low percent body fat in AN.
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