Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 758-775-Beta Cells, Glucose Control & Complications
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-770
Jenny Tong*1, Abbigail Tissot2, Ronald Prigeon3, James Peugh2, David A D'Alessio1 and Jennifer Bahr Hillman4
1Univ of Cincinnati, Cincinnati, OH, 2Cincinnati Children's Hospital Medical Center, 3VA Medical Center, Baltimore, MA, Baltimore, MD, 4Cincinnati Children's Hospital, Cincinnati, OH
Treatment of restrictive eating disorders (ED) often require medical stabilization due to severe malnutrition. Short-term medical refeeding attempts to normalize physiologic function, but causes psychological disturbance and stresses the metabolic system. Understanding physiologic recovery in ED is critical for improving care for patients with this potentially fatal condition. Methods: Females (aged 13-21) newly diagnosed with ED and requiring inpatient stabilization were recruited. Healthy controls were matched for sex, age, age at menarche, BMI percentile (BMIp), socioeconomic status, and race. A 150-min meal tolerance tests (MTT) was performed after an overnight fast at admission and 5-7 days after refeeding for ED girls, and once for controls. Glucose and insulin responses were summed as area under the curve (AUC). Insulin secretion rate (ISR) was derived from plasma C-peptide levels during MTT; insulin sensitivity was estimated with the Matsuda index; disposition index (DI) was calculated as ISR x Matsuda index; insulin clearance was estimated by AUC ISR/AUC Insulin; β-cell sensitivity was calculated as slope of ISR to glucose.  Data were analyzed using nonparametric comparison tests and linear regression. Results: Fifteen ED girls (age: 15.5±1.9 y [mean±SD], BMIp: 16.9±18.8, admission weight: 44.6±7.5 kg) and 15 controls (age: 15.7±1.9 y, BMIp: 33.4±14.9, weight: 50.3±5.1 kg) completed the study. Weight for the ED group was 45.4±7.9 kg after an average of 6.4 days (SD 0.91) of refeeding. On admission, ED girls had relative glucose intolerance compared to post-refeeding (AUC glucose 1947±1606 vs. -85.8±1308, p=0.0009). Insulin secretion was higher on admission (AUC ISR-meal: 39.4±17.5 vs. 25.9±10.5, p=0.002) even after adjustment for plasma glucose, but insulin sensitivity and insulin clearance were similar at admission and post-refeeding. Compared to controls, ED girls at admission had similar fasting glucose and insulin levels and meal-induced ISR. However, ED girls were more insulin sensitive (63.5±26.2 vs. 98.9±43.4, p<0.05), had greater insulin clearance (p<0.01), and higher DI (19.4±3.7 vs. 34.1±15.3, p<0.01) compared to controls. ED girls at admission and post-refeeding showed lower β-cell sensitivity ([R2=.09; CI95%:-.135, -.318] and [R2=.17; CI95%:.004-.326]) than controls (R2=.22; CI95%:.006-.425). Conclusion: Severely malnourished females with new ED have a metabolic phenotype similar to what has been described for starvation, with relative glucose intolerance. This corrected within a week of refeeding.  The glucose intolerance seen with active caloric restriction cannot be readily explained by abnormalities of insulin secretion or insulin action. This suggests that an important role for insulin-independent glucose metabolism in active ED.

Disclosure: DAD: Ad Hoc Consultant, Amylin, Ad Hoc Consultant, Eli Lilly, Investigator, Johnson and Johnson, Speaker, Merck, Ad Hoc Consultant, Novo Nordisk, Investigator, Procter and Gamble, Clinical Researcher, Sanofi. Nothing to Disclose: JT, AT, RP, JP, JBH

*Please take note of The Endocrine Society's News Embargo Policy at

Sources of Research Support: NIH/NIDDK (5K23DK80081, 1R03DK89090)