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Modulation of Adiponectin and Leptin during Refeeding of Female Anorexia Nervosa Patients

Pediatric Endocrinology Unit (D.M.-M.), Pediatric Psychosomatic Department (D.S., A.Y., M.F.), Institute of Endocrinology (C.P., R.H., H.K.), Adult Eating Disorders Department (A.R.), and Tissue Typing Laboratory (R.L.), Sheba Medical Center, Tel Hashomer, 52621 Israel; Sackler School of Medicine (D.M.-M., D.S., A.Y., R.L.), Tel-Aviv University, Tel-Aviv, 69978 Israel; and The Mina and Everard Goodman Faculty of Life Sciences (E.Y.), Bar-Ilan University, Ramat-Gan, 52900 Israel

Address all correspondence and requests for reprints to: Dalit Modan-Moses, M.D., Division of Pediatrics, Chaim Sheba Medical Center, Tel-Hashomer, 52621 Israel. E-mail: dmodan{at}sheba.health.gov.il.

Context: Several studies assessed adiponectin levels in anorexia nervosa (AN) patients, however, data regarding the dynamics of changes in adiponectin levels during refeeding of these patients is limited and contradicting.

Objective: Our objective was to assess adiponectin levels and the distribution of its different isoforms in AN patients before and after long-term refeeding, and to relate them to alterations in body mass index, leptin, insulin sensitivity, and additional endocrine parameters.

Design, Setting, and Participants: We conducted a longitudinal controlled study of 38 female adolescent malnourished AN inpatients, with 13 young, lean, healthy women serving as controls. Blood samples were obtained upon admission and thereafter at 1, 3, and 5 months (at target weight).

Main Outcome Measures: Changes in body mass index, leptin, adiponectin, insulin sensitivity, and adiponectin multimeric forms were measured.

Results: At admission, leptin levels of AN patients were significantly lower, whereas insulin sensitivity (assessed by homeostasis model assessment-insulin resistance), adiponectin levels, and the ratio of high molecular weight (HMW) adiponectin to total adiponectin were significantly higher compared with controls. During weight recovery, leptin levels and homeostasis model assessment-insulin resistance increased significantly, whereas adiponectin and HMW adiponectin/total adiponectin ratio decreased significantly, to levels similar to controls. An initial increase in adiponectin levels was observed after 1 month of refeeding. There was no correlation between adiponectin and either T₄ or cortisol levels.

Conclusions: Our study demonstrates hyperadiponectinemia, increased adiponectin HMW isoform, and increased insulin sensitivity in adolescent AN female patients and reversal of these findings with weight rehabilitation. We hypothesize that increased adiponectin levels may have a protective role in maintaining energy homeostasis during extreme malnourishment.

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